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Big Pharma > Pharm Quiz 5 > Flashcards

Pharm Quiz 5 Flashcards

1
Q
  1. What is the most common side effect of traditional antihistamine medicines such as Benadryl?
A

Drowsiness, sedation, fatigue, and psychomotor slowing.

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2
Q
  1. What type of receptors (hint: alpha? beta?1or2?) in the nasal mucosa do most common nasal decongestants act on?
A

Alpha-1

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3
Q
  1. How can high doses and prolonged use of nasal decongestants effect blood pressure?
A

Alpha-1 agonists can mimic the effects of increased sympathetic nervous system activity and can cause serious cardiovascular and CNS excitation

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4
Q
  1. What are drugs that antagonize H1 histamine receptor sites useful treating?
A

H1 antagonists are useful in decreasing nasal congestion, mucosal irritation and discharge (rhinitis, sinusitis), and conjunctivitis that are caused by inhaled allergens.

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5
Q
  1. Why are second-generation antihistamines such as loratadine (Claritin) are preferred to traditional antihistamines?
A

They are more selective for the H1 receptor subtype and have fewer side effects (less risk of sedation and other CNS side effects)

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6
Q
  1. What are drugs called that decrease respiratory secretions? What are drugs called that facilitate the production and ejection of mucous called?
A

Mucolytics decrease respiratory secretions. Expectorants facilitate the production and ejection of mucous.

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7
Q
  1. To selectively produce bronchodilation, what type of receptors in the airways of smooth muscle are stimulated?
A

Beta-2 receptor agonists.

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8
Q
  1. Why should patients with bronchospastic disease avoid overuse of beta-agonist drugs?
A

With prolonged or excessive use, inhaled beta-2 agonists may actually increase bronchial responses to allergens and other irritants, thus increasing the incidence and severity of bronchospastic attacks. Prolonged use may also cause tolerance

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9
Q
  1. Do drugs that break down phosphodiesterase and increase cAMP cause bronchodilation or bronchoconstriction?
A

Bronchodialtion

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10
Q
  1. To avoid muscle wasting, bone loss and other serious glucocorticoid side effects, what is the best method of administering medications to control airway inflammation in asthma and COPD?
A

Inhalation

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11
Q
  1. How do cromones help to prevent airway irritation and bronchospasm in patients with asthma?
A
  • Cromones are NOT bronchodilators and will not reverse bronchoconstriction during an asthma attack. These drugs should be taken prior to the onset of bronchoconstriction and they must typically be administered prophylactically to prevent asthma attacks that are initiated by specific, well-defined activities.
  • Cromones are generally regarded as mast cell stabilizers because they desensitize these cells to allergens and other substances if the drug is administered before the mast cell is exposed to the precipitated factor.
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12
Q
  1. Why are drugs the inhibit the production of leukotrienes helpful in treating bronchospastic diseases?
A

Because leukotrienes are inflammatory compounds that are especially important in mediating the airway inflammation that underlies bronchoconstrictive disease.

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13
Q
  1. What drug classes are often used to treat bronchospasm in asthma? Sometimes in combination with what other drug class(es)?
A

Leukotriene inhibitors

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14
Q
  1. Most antacid medications contain a chemical base that neutralizes this excessive ion in the stomach. Is it hydrogen, calcium, sodium, or potassium?
A

Hydrogen

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15
Q
  1. Why should prolonged or excessive use of antacids be avoided?
A

Prolonged use can cause electrolyte imbalances and altered pharmacokinetics, and can cause an increase in urinary pH that affects drug elimination.

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16
Q
  1. How do selective H2 receptor blockers (such as famotidine) affect the stomach parietal cells?
A

H2 receptor blockers bind to histamine receptors on parietal cells to decrease gastric acid secretion.

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17
Q
  1. Why are proton pump inhibitors (PPI) such as pantoprazole (Protonix) useful in reducing gastric acid?
A

PPIs inhibit the H+, K+-ATPase enzyme that is ultimately responsible for secreting acid from gastric parietal cells into the lumen of the stomach

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18
Q
  1. Antibacterial drugs are often used in combination with a PPI to help eliminate what type of infection that is a risk factor for ulcer formation?
A

H. pylori

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19
Q
  1. Do natural/synthetic opioid drugs increase or decrease GI motility? What acutely is this useful for treating?
A

Decrease GI motility. They are useful in treating diarrhea.

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20
Q
  1. Why should excessive laxatives be avoided?
A

With prolonged use, serious lower GI irritation, including spastic colitis, may occur. Fluid and electrolyte abnormalities are also a potential problem.
Also, chronic administration may result in laxative dependence when bowel evaluation has become so subservient to laxative use that the normal mechanisms governing evacuation and defecation are impaired

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21
Q
  1. To improve the health and well-being of cystic fibrosis patients, what type of enzymes and other medications can be given?
A
  • Because of the thick secretions pancreatic enzymes are deficient.
  • Giving them an oral preparations (a digestant medication) containing the enzymes and bile salt can help.
  • For respiratory issues, bronchodilators, mucolytic, glucocorticoids, and NSAIDS are all used to help the pt breath.
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22
Q
  1. What kind of hormones are released from the anterior pituitary gland?
A

The ant. pituitary secretes 6 peptide hormones:
1. Growth hormone (GH)
2. Luteinizing hormone (LH)
3. Follicle-stimulating hormone (FSH)
4. Thyroid-stimulating hormone (TSH)
5. Adrenocorticotropic hormone (ACTH)
6. Prolactin

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23
Q
  1. Where do the hormones that are released from the posterior pituitary that are synthesized by neurons originate from?
A

Hormones released in the post. pituitary are synthesized in the hypothalamus.

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24
Q
  1. If the alpha cells of the pancreas are destroyed, the production of this would be impaired?
A

Glucagon

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25
Q
  1. Anti-inflammatory steroids produced by the adrenal cortex are under the control of what hormone from the hypothalamus? This stimulates the release of what hormone from the anterior pituitary?
A

CRH from the hypothalamus stimulated ACTH release from the ant. Pituitary, which in turn stimulates the synthesis of glucocorticoids.

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26
Q
  1. What common chemical framework are steroid hormones derived from?
A

Lipids, such as cholesterol.

27
Q
  1. The self-control mechanism of hormonal release that commonly occurs in the endocrine system is an example of what type of feedback mechanism?
A

Negative feedback

28
Q
  1. In humans, what is the primary mineralocorticoid that is produced by the adrenal cortex? What is the primary glucocorticoid produced by the adrenal cortex?
A

The primary mineralocorticoid produced by the adrenal cortex is aldosterone.
The primary glucocorticoid produced by the adrenal cortex is cortisol.

29
Q
  1. Why are the glucocorticoids released from the adrenal cortex?
A

In normal situation cortisol is released to help regulate the sleep-wake cycle in humans (circadian rhythm)
In addition cortisol is released for basically any type of stressful stimulus.

30
Q
  1. Steroids alter protein synthesis in responsive cells through a direct effect on this part of the cell?
A

Steroids alter protein synthesis through a direct effect on the nucleus

31
Q
  1. How do glucocorticoids exert their anti-inflammatory effect?
A

By entering the target cell and binding to a receptor located in cytosol, this creates an activated hormone-receptor complex that travels to the nucleus of the cell to bind directly to a specific DNA segment to control inflammation

32
Q
  1. What paradoxical effect do cortisol and other glucocorticoids exert on circulating glucose levels? How do they affect glycogen storage in the liver?
A
  • They cause an increase of circulating levels of glucose at the same time that glucose storage is enhanced.
  • Glucocorticoids affect the metabolism of glucose, fat, and protein.
  • Cortisol breaks down muscle into amino acids and lipids into free fatty acids, which can be transported to the liver to form glucose (gluconeogenesis).
  • Glucose that is synthesized in the liver can either be stored as glycogen or released back into the bloodstream to increase blood glucose levels.
  • Cortisol also inhibits the uptake of glucose into muscle and fat cells, thus allowing more glucose to remain available in the bloodstream.
33
Q
  1. What is an important adverse effect seen in patients in patients taking systemic glucocorticoid drugs? Hint: something you as a PT would be concerned about
A

Loss of bone strength

34
Q
  1. What side effects are common in patients taking prolonged systemic glucocorticoids?
A
  • Adrenocortical suppression
  • Breakdown of supporting tissues (muscle, bone, ligaments, tendons, skin)
  • Peptic ulcer formation
  • Glaucoma
  • Mood changes and psychosis
35
Q
  1. Why are glucocorticoids slowly withdrawn after prolonged use (several weeks to months)? Hint: what gland do they affect?
A

Because the patient’s normal production of glucocorticoids is shut down by the exogenous hormones, patients will not be able to resume production of glucocorticoids immediately.

36
Q
  1. How do the mineralocorticoids act on the kidneys?
A
  • Aldosterone binds on the epithelial cells that line the distal tubules of the nephron.
  • Sodium is actively transported out the cell and reabsorbed into the bloodstream.
  • Water reabsorption is increased as water follows the sodium movement back into the bloodstream.
  • As sodium is reabsorbed, potassium is secreted by a sodium-potassium exchange, thus increasing potassium excretion.
37
Q
  1. How are drugs with mineralocorticoid-like activity generally administered?
A

Orally

38
Q
  1. Mineralocorticoid antagonists such as spironolactone are used primarily for this purpose.
A

Diuretics for treating hypertension and heart failure.

39
Q
  1. What type of steroids are typically administered to maintain optimal health in patients with Addison’s disease?
A

Mineralcorticoids and glucocordicoids.

40
Q
  1. What type of hormone in men stimulates synthesis of testosterone? This occurs via direct effect on what cells in the testes?
A

LH and FSH
LH targets Leydig cells

41
Q
  1. At the onset of puberty increased testosterone production produces what effects?
A

It brings about the development of most of the physical characteristics associated with men (increased body hair, increased skeletal muscle mass, voice change, and maturation of external genitalia)

42
Q
  1. In some men, what cancer can small doses of testosterone increase risk of?
A

Prostate cancer

43
Q
  1. What conditions can physiologic doses of testosterone be useful?
A

-Replacement therapy
-Catabolic states (to treat muscle catabolism and protein loss)
-Delayed puberty
-Breast cancer
-Anemia
-Hereditary angioedema

44
Q
  1. Why should both male and female athletes be discouraged from taking male androgens?
A

The side effects

Women:
-Hirsutim
-Hoarseness or deepening of the voice
-Changes to external genitalia
-Irregular menstrual periods
-Acne
Men:
-Bladder irritation
-Breast swelling and soreness
-Testicular atrophy and impaired sperm production

45
Q
  1. What hormone controlled the first half of the menstrual cycle? Where is estrogen released from?
A

FSH starts the menstrual cycle.
Estrogen is released by the ovarian follicle.

46
Q
  1. In post-menopausal women, what are the benefits of estrogen replacement? Increased risk?
A
  • Benefit:Stop vasomotor hot flashes, help stop osteoporosis, help against dementia and alzheimers, and reporductive organ hypertrophy.
  • Risks: MI, Stroke, thromboembolism, cancer, abnormal blood clotting.nausea, and swelling of feet and ankles.
47
Q
  1. Selective estrogen modulators (SERMS) are beneficial because they stimulate estrogen receptors on the bone and tissue. What tissues do estrogen antagonize?
A

Uterine and breast tissue

48
Q
  1. How do traditional oral hormonal contraception exert their effects?
A
  • Inhibiting ovulation and impairing the normal development of the uterine endometrium.
  • Hormonal contraceptives maintain fairly high plasma levels of estrogen and progestin, limiting the release of LH and FSH through a negative feedback system.
  • Inhibition of LH release prevents ovulation, thus preventing fertilization.
49
Q
  1. Clinically how can drugs that block progesterone receptors be used?
A
  • They can be used to detach the placenta and terminate the pregnancy.
  • Decease pain and bleeding in the uterus
  • Treat endometriosis
  • Treat Cushing’s syndrome
50
Q
  1. What in small amounts should be ingested in the diet so that the thyroid gland can synthesize thyroid hormone?
A

Iodine

51
Q
  1. What are common symptoms associated with hyperthyroidism?
A
  • Goiter
  • Graves disease
  • Nervousness
  • Weight loss
  • Diarrhea
  • Tachycardia
  • Insomnia
  • Increase appetite
  • Heat intolerance
  • Oligomenorrhea
  • Muscle wasting
  • Exopthalamus
52
Q
  1. What is the common treatment of hypothyroidism?
A

The primary method of treatment is to administer natural thyroid hormones and synthetic analogs, such as preparations containing T4 (levothyroxine), T3 (liothyronine), or both.

53
Q
  1. How do parathyroid hormone affect plasma calcium levels? How does it affect calcium reabsorption from bone?
A

It controls it by releasing PTH. It increases bone turnover and causes more bone to breakdown and release calcium.

54
Q
  1. Does prolonged large doses of parathyroid hormone increase or decrease bone breakdown?
A

High levels of PTH accelerate bone breakdown (catabolic effect) to mobilize calcium for other physiological needs.

55
Q
  1. Does Vitamin D enhance bone formation by increasing or decreasing intestinal absorption of calcium and phosphate?
A

Increasing

56
Q
  1. How do bisphosphonates reduce bone resorption in osteoporosis?
A

These compounds appear to adsorb directly into calcium crystals in the bone and reduce bone resorption by inhibiting osteoclast activity.

57
Q
  1. What medications can be used to increase bone mineral density in post-menopausal women?
A
  • Calcium Supplements
  • Estrogen therapy
  • Vitamin D
  • Bisphosphonates
  • Calcitonin
  • Teriparatide
  • Denosumab
58
Q
  1. Do calcimimetics increase or decrease parathyroid hormone release? Will this decrease or increase the excessive bone loss associated with parathyroid hormones?
A

Decrease PTH release
Decrease excessive bone breakdown

59
Q
  1. Does insulin increase or decrease the storage of glucose in the skeletal muscle and other tissue? What happens to glucose levels after a meal?
A

Insulin increases the storage into other tissues.
Following a meal blood glucose sharply increases

60
Q
  1. What is the primary problem with type II diabetes mellitus?
A

Insulin resistance
Altered protein phosphorylation, impaired production of chemical mediators, and a lack of glucose transporter

61
Q
  1. Why are certain forms of biosynthetic insulin absorbed more rapidly than regular human insulin?
A

They have an altered amino acid sequence

62
Q
  1. Why can insulin only be administered by parenteral route?
A

Insulin is a large polypeptide and is too large to be absorbed through the GI wall.

63
Q
  1. What are risk factors for patients for hypoglycemia?
A

Insulin therapy, insulin therapy + exercise, inconsistent eating schedule with too many fasted periods

Big Pharma (3 decks)

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