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1
Q

The gene responsible for the final activating step of vitamin D3 is called 25- Hydroxyvitamin D 1-alpha-hydroxylase. People with mutations in this gene are unable to produce active vitamin D3. Which of the following symptoms would you expect to see?

A. High levels of 1,25-hydroxy vitamin D3

B. Low levels of circulating Ca2+

C. Low levels of PTH

D. High levels of circulating Ca2+

E. Dietary insufficiency of vitamin D3

A

The gene responsible for the final activating step of vitamin D3 is called 25- Hydroxyvitamin D 1-alpha-hydroxylase. People with mutations in this gene are unable to produce active vitamin D3. Which of the following symptoms would you expect to see?

A. High levels of 1,25-hydroxyvitamin D3

B. Low levels of circulating Ca2+ (↑Ca2+ resorption)

C. Low levels of PTH ☓

D. High levels of circulating Ca2+ (opposite)

E. Dietary insufficiency of vitamin D3 (unrelated)

2
Q

Excess circulating amounts of PTH due to chronically low circulating Ca2+ levels is referred to as:

A. secondary hyperparathyroidism

B. vitamin D3 deficiency

C. primary hyperparathyroidism

D. hypocalcemia

E. hypoparathyroidism

A

Excess circulating amounts of PTH due to chronically low circulating Ca2+ levels is referred to as:

A. secondary hyperparathyroidism

B. vitamin D3 deficiency → may be cause, but not what question is asking = related to D

C. primary hyperparathyroidism (↑PTH secretion)

D. hypocalcemia (see B)

E. hypoparathyroidism (hypo = decrease PTH)

3
Q

Fill in the blanks in this sentence. Teriparatide is closely related to ____________ and primarily functions by activating receptors on ___________

A. Vitamin D3; osteoclasts

B. RANKL; osteoclasts

C. PTH; osteoblasts

D. PTH; osteoclasts

E. Vitamin D; osteoblasts

A

Fill in the blanks in this sentence. Teriparatide is closely related to ____________ and primarily functions by activating receptors on ___________

A. Vitamin D3; osteoclasts

B. RANKL; osteoclasts

C. PTH; osteoblasts

D. PTH; osteoclasts

E. Vitamin D; osteoblasts

Teriparatide

  • analog of PTH
  • not a long-term drug (once daily)
    • ​activating osteoblasts in the short term; pharmacokinetic effect
4
Q

Denosumab is effective for the treatment of osteoporosis because:

A. Denosumab promotes bone remodeling by activating osteoclasts

B. Denosumab promotes bone remodeling by activating osteoblasts

C. Denosumab inhibits bone resorption by binding to RANKL

D. Denosumab inhibits bone resorption by binding to RANK

E. Denosumab inhibits bone deposition by binding to RANKL

A

Denosumab is effective for the treatment of osteoporosis because:

A. Denosumab promotes bone remodeling by activating osteoclasts → not direct effect

B. Denosumab promotes bone remodeling by activating osteoclasts→ not direct effect

C. Denosumab inhibits bone resorption by binding to RANKL

D. Denosumab inhibits bone resorption by binding to RANK

E. Denosumab inhibits bone deposition by binding to RANKL → does not inhibit bone deposition

5
Q

Which of the following is not a physiological function of PTH

A. Promotion of bone remodeling

B. Increased activity of 25-Hydroxyvitamin D 24-alpha-hydroxylase (formation of 24,25-hydroxy vitamin D3)

C. Increased activity of 25-Hydroxyvitamin D 1-alpha-hydroxylase (formation of 1,25-hydroxy vitamin D3)

D. Increased reabsorption of Ca2+ in the kidney

E. Increased excretion of PO4 3- in the kidney

A

Which of the following is not a physiological function of PTH

A. Promotion of bone remodeling → Yes - activate osteoblast PTH receptors

B. Increased activity of 25-Hydroxyvitamin D 24-alpha-hydroxylase (formation of 24,25-hydroxy vitamin D3)inactive D3

C. Increased activity of 25-Hydroxyvitamin D 1-alpha-hydroxylase (formation of 1,25-hydroxy vitamin D3) ✓

D. Increased reabsorption of Ca2+ in the kidney ✓

E. Increased excretion of PO4 3- in the kidney ✓

6
Q

Bisphosphonates are effective for the treatment of osteoporosis because:

A. Bisphosphonates accumulate in bone and promote osteoblast activity

B. Bisphosphonates inhibit RANKL activation of osteoclasts

C. Bisphosphonates selectively accumulate in weak bones and promote repair

D. Bisphosphonates accumulate in bone and promote osteoclast apoptosis

E. Bisphosphonates promote bone deposition via suppression of PTH

A

Bisphosphonates are effective for the treatment of osteoporosis because:

A. Bisphosphonates accumulate in bone and promote osteoblast activity → does not promote osteoblast activity

B. Bisphosphonates inhibit RANKL activation of osteoclasts → does not inhibit RANKL activation

C. Bisphosphonates selectively accumulate in weak bones and promote repair → does not promote repair

D. Bisphosphonates accumulate in bone and promote osteoclast apoptosis

E. Bisphosphonates promote bone deposition via suppression of PTH

7
Q

Prednisone is a glucocorticoid drug that can be administered orally because:

A. It prevents excessive side effects that occur when it is applied topically

B. Oral administration allows for a more rapid response

C. It has a weak effect on the liver

D. It has weak activity but can be activated by metabolic conversion to prednisolone

E. It requires specific transporters in the gut to be absorbed into the body

A

Prednisone is a glucocorticoid drug that can be administered orally because:

A. It prevents excessive side effects that occur when it is applied topically

B. Oral administration allows for a more rapid response

C. It has a weak effect on the liver

D. It has weak activity but can be activated by metabolic conversion to prednisolone

E. It requires specific transporters in the gut to be absorbed into the body

8
Q

Humanized or chimeric therapeutic antibodies are:

A. Modified mouse antibodies designed to evade destruction by the human immune system

B. Modified human antibodies designed to bind to antigens of pathogenic microorganisms

C. Antibodies designed to heighten the sensitivity of our immune system to pathogens

D. Modified mouse antibodies that have been engineered for enhanced activation of the T-cell receptor

E. Antibodies purified from chimeric mouse/human cell types

A

Humanized or chimeric therapeutic antibodies are:

A. Modified mouse antibodies designed to evade destruction by the human immune system

B. Modified human antibodies designed to bind to antigens of pathogenic microorganisms

C. Antibodies designed to heighten the sensitivity of our immune system to pathogens

D. Modified mouse antibodies that have been engineered for enhanced activation of the T-cell receptor

E. Antibodies purified from chimeric mouse/human cell types

9
Q

Immunosuppressive effects of glucocorticoids are primarily related to:

A. Interfering with the antigen presentation phase of the immune response

B. Interaction of steroid hormone receptors with NFAT

C. Inhibition of thromboxane A2 generation

D. Suppressed expression/generation of cytokines

E. Off-target effects on the mineralocorticoid receptor

A

Immunosuppressive effects of glucocorticoids are primarily related to:

A. Interfering with the antigen presentation phase of the immune response

B. Interaction of steroid hormone receptors with NFAT

C. Inhibition of thromboxane A2 generation

D. Suppressed expression/generation of cytokines

E. Off-target effects on the mineralocorticoid receptor

10
Q

Human or mouse antibodies contain:

A. 2 heavy chains that underlie antigen specificity, and 2 light chains that are recognized by immune cells.

B. A Fab region that underlies antigen specificity, and an Fc region that is recognized by immune cells.

C. 2 heavy chains and 2 light chains that form a single antigen binding site.

D. A Fab region that is required for complement activation, and an Fc region that is required for antigen binding.

E. One uninterrupted protein that is essential for binding antigens and immune cell receptors.

A

Human or mouse antibodies contain:

A. 2 heavy chains that underlie antigen specificity, and 2 light chains that are recognized by immune cells.

B. A Fab region that underlies antigen specificity, and an Fc region that is recognized by immune cells.

C. 2 heavy chains and 2 light chains that form a single antigen binding site.

D. A Fab region that is required for complement activation, and an Fc region that is required for antigen binding.

E. One uninterrupted protein that is essential for binding antigens and immune cell receptors.

11
Q

Which of the following statements about the T-cell receptor signaling cascade is false?

A. Calcineurin is a phosphatase that causes dephosphorylation of NFAT.

B. A Ca2+ signal is an early step after activation of the T-cell receptor.

C. Alemtuzumab is a monoclonal antibody that directly inhibits the T-cell receptor.

D. Dephosphorylated NFAT can translocate to the nucleus and influence gene transcription.

E. T-cell receptors are activated during the antigen presentation phase by interactions with an antigen-presenting cell.

A

Which of the following statements about the T-cell receptor signaling cascade is false?

A. Calcineurin is a phosphatase that causes dephosphorylation of NFAT.

B. A Ca2+ signal is an early step after activation of the T-cell receptor.

C. Alemtuzumab is a monoclonal antibody that directly inhibits the T-cell receptor.

D. Dephosphorylated NFAT can translocate to the nucleus and influence gene transcription.

E. T-cell receptors are activated during the antigen presentation phase by interactions with an antigen-presenting cell.

12
Q

Drugs that interfere with DNA synthesis or replication commonly lead to immunosuppression because:

A. The immune response requires generation of antibodies.

B. Gene transcription is required for immune cell function.

C. Immunosuppression is a side-effect of byproducts of DNA synthesis.

D. Immune cells rapidly divide during the clonal expansion phase of an immune response.

E. DNA synthesis is required for replication of infectious agents like viruses or bacteria.

A

Drugs that interfere with DNA synthesis or replication commonly lead to immunosuppression because:

A. The immune response requires generation of antibodies.

B. Gene transcription is required for immune cell function.

C. Immunosuppression is a side-effect of byproducts of DNA synthesis.

D. Immune cells rapidly divide during the clonal expansion phase of an immune response.

E. DNA synthesis is required for replication of infectious agents like viruses or bacteria.

13
Q

Activation of the T-cell receptor during the antigen presentation phase of an immune response:

A. Leads to activation of a calcineurin and NFAT-dependent signaling cascade that is inhibited by cyclosporine

B. Leads to activation of a calcineurin and NFAT-dependent signaling cascade that is inhibited by interleukin-2

C. Triggers secretion of antibodies from memory B cells for a rapid and specific response

D. Requires interleukin-2 for maximal stimulation of NFAT target genes

E. Is directly inhibited by prednisone or other glucocorticoids

A

Activation of the T-cell receptor during the antigen presentation phase of an immune response:

A. Leads to activation of a calcineurin and NFAT-dependent signaling cascade that is inhibited by cyclosporine

B. Leads to activation of a calcineurin and NFAT-dependent signaling cascade that is inhibited by interleukin-2

C. Triggers secretion of antibodies from memory B cells for a rapid and specific response

D. Requires interleukin-2 for maximal stimulation of NFAT target genes

E. Is directly inhibited by prednisone or other glucocorticoids

14
Q

Which of the following statements regarding Tacrolimus and Cyclosporine is false?

A. Tacrolimus and cyclosporine are immunosuppressive drugs

B. Tacrolimus and cyclosporine prevent signaling associated with T-cell receptor activation

C. Tacrolimus and cyclosporine enhance expression of interleukin-2

D. Tacrolimus and cyclosporine suppress the induction phase of the immune response

E. Tacrolimus and cyclosporine influence NFAT signaling

A

Which of the following statements regarding Tacrolimus and Cyclosporine is false?

A. Tacrolimus and cyclosporine are immunosuppressive drugs

B. Tacrolimus and cyclosporine prevent signaling associated with T-cell receptor activation

C. Tacrolimus and cyclosporine enhance expression of interleukin-2

D. Tacrolimus and cyclosporine suppress the induction phase of the immune response

E. Tacrolimus and cyclosporine influence NFAT signaling

15
Q

Which of the following statements about interleukin-2 (IL-2) is false?

A. IL-2 synthesis is enhanced by activation of NFAT

B. IL-2 can act in an autocrine manner to stimulate T-cell maturation and differentiation

C. IL-2 receptor activation requires FKBP binding

D. IL-2 receptors activate a signaling cascade that affects transcription of target genes

E. IL-2 signaling can be inhibited (indirectly) by rapamycin

A

Which of the following statements about interleukin-2 (IL-2) is false?

A. IL-2 synthesis is enhanced by activation of NFAT

B. IL-2 can act in an autocrine manner to stimulate T-cell maturation and differentiation

C. IL-2 receptor activation requires FKBP binding

D. IL-2 receptors activate a signaling cascade that affects transcription of target genes

E. IL-2 signaling can be inhibited (indirectly) by rapamycin

16
Q

Which of the following statements regarding NFAT (Nuclear Factor of Activated T-cells) is correct:

A. NFAT is a transcription factor that is directly inhibited by tacrolimus.

B. NFAT is a phosphatase that is required for activation of target genes involved in T-cell proliferation.

C. NFAT is a transcription factor that translocates to the nucleus following calcineurin-mediated dephosphorylation.

D. Inhibition of NFAT signaling by rapamycin prevents the IL-2 receptor signaling cascade.

E. NFAT is phosphorylated by calcineurin

A

Which of the following statements regarding NFAT (Nuclear Factor of Activated T-cells) is correct:

A. NFAT is a transcription factor that is directly inhibited by tacrolimus.

B. NFAT is a phosphatase that is required for activation of target genes involved in T-cell proliferation.

C. NFAT is a transcription factor that translocates to the nucleus following calcineurin-mediated dephosphorylation.

D. Inhibition of NFAT signaling by rapamycin prevents the IL-2 receptor signaling cascade.

E. NFAT is phosphorylated by calcineurin

17
Q

Autocrine activation of the IL-2 receptor is:

A. Directly inhibited by basiliximab.

B. Triggered by basiliximab binding to Th cells.

C. A step during antigen presentation that is inhibited by cyclosporine.

D. A requirement for rapamycin activation of target genes.

E. Required for T-cell receptor activation

A

Autocrine activation of the IL-2 receptor is:

A. Directly inhibited by basiliximab.

B. Triggered by basiliximab binding to Th cells.

C. A step during antigen presentation that is inhibited by cyclosporine.

D. A requirement for rapamycin activation of target genes.

E. Required for T-cell receptor activation

18
Q

In a patient undergoing treatment with a therapeutic dose of a glucocorticoid like dexamethasone, which of the following would be expected?

A. Elevated circulating levels of ACTH/corticotropin

B. Hypoglycemia

C. Hyperplasia (increased size) of the adrenal gland

D. Reduced circulating levels of corticotropin-releasing factor (i.e. CRF or CRH)

E. Enhanced production of endogenous cortisol

A

In a patient undergoing treatment with a therapeutic dose of a glucocorticoid like dexamethasone, which of the following would be expected?

A. Elevated circulating levels of ACTH/corticotropin

B. Hypoglycemia

C. Hyperplasia (increased size) of the adrenal gland

D. Reduced circulating levels of corticotropin-releasing factor (i.e. CRF or CRH)

E. Enhanced production of endogenous cortisol

19
Q

Pseudohyperaldosteronism arising from inhibition of 11-β-hydroxysteroid dehydrogenase (type 2) is caused by:

A. Excessive activation of glucocorticoid receptors due to activation of aldosterone

B. Inhibition of glucocorticoid receptor expression

C. Excessive activation of aldosterone receptors in the kidney by cortisol

D. Failure to generate active cortisol in appropriate target tissues

E. Excessive negative feedback on ACTH generation in the anterior pituitary

A

Pseudohyperaldosteronism arising from inhibition of 11-β-hydroxysteroid dehydrogenase (type 2) is caused by:

A. Excessive activation of glucocorticoid receptors due to activation of aldosterone

B. Inhibition of glucocorticoid receptor expression

C. Excessive activation of aldosterone receptors in the kidney by cortisol

D. Failure to generate active cortisol in appropriate target tissues

E. Excessive negative feedback on ACTH generation in the anterior pituitary

20
Q

Which of the following effects would most likely not be observed in a patient treated with a therapeutic glucocorticoid?

A. Inhibition of COX-2 expression

B. Induction of lipocortin/annexin expression

C. Enhanced generation of prostanoids

D. Reduced PLA2 (phospholipase A2)-mediated generation of arachidonic acid

E. Hyperglycemia

A

Which of the following effects would most likely not be observed in a patient treated with a therapeutic glucocorticoid?

A. Inhibition of COX-2 expression

B. Induction of lipocortin/annexin expression

C. Enhanced generation of prostanoids

D. Reduced PLA2 (phospholipase A2)-mediated generation of arachidonic acid

E. Hyperglycemia

21
Q

Immediately stopping a therapeutic dose of glucocorticoids is dangerous because:

A. Failure to take the recommended dosage may lead to weight gain

B. Endogenous glucocorticoid production is likely suppressed due to negative feedback

C. Inhibition of glucocorticoid receptors interferes with glucose regulation

D. Suppression of COX-2 could lead to susceptibility to an opportunistic infection

E. Glucocorticoids are required for normal salt and water balance in the body

A

Immediately stopping a therapeutic dose of glucocorticoids is dangerous because:

A. Failure to take the recommended dosage may lead to weight gain

B. Endogenous glucocorticoid production is likely suppressed due to negative feedback

C. Inhibition of glucocorticoid receptors interferes with glucose regulation

D. Suppression of COX-2 could lead to susceptibility to an opportunistic infection

E. Glucocorticoids are required for normal salt and water balance in the body

22
Q

The cellular signaling mechanism underlying glucocorticoid actions involves:

A. Binding to a transmembrane receptor and activation of a signaling cascade

B. Triggering of Ca2+ release from the ER due to activation IP3 receptors

C. Direct inhibition of enzymes including COX-2 and lipocortin

D. Binding to an intracellular receptor followed by altered expression of target genes

E. Exerting negative feedback on the adrenal cortex

A

The cellular signaling mechanism underlying glucocorticoid actions involves:

A. Binding to a transmembrane receptor and activation of a signaling cascade

B. Triggering of Ca2+ release from the ER due to activation IP3 receptors

C. Direct inhibition of enzymes including COX-2 and lipocortin

D. Binding to an intracellular receptor followed by altered expression of target genes

E. Exerting negative feedback on the adrenal cortex

23
Q

Acyclovir blocks:

a) viral adhesion
b) DNA synthesis
c) protein translation
d) virion release

A

Acyclovir blocks:

a) viral adhesion

b) DNA synthesis

c) protein translation
d) virion release

24
Q

Which statement is true about the viral capsid:

  1. .it is a protein coat surrounding viral genetic material
  2. it is the lipid envelope of the virus
  3. it never contains antigenic proteins
  4. it is made of host cell material
A

Which statement is true about the viral capsid:

  1. .it is a protein coat surrounding viral genetic material
  2. it is the lipid envelope of the virus
  3. it never contains antigenic proteins
  4. it is made of host cell material
25
Q

Most DNA viruses replicate:

  1. in the host cell nucleus
  2. in the host cell cytoplasm
  3. in the capsid
  4. none of the above
A

Most DNA viruses replicate:

  1. in the host cell nucleus
  2. in the host cell cytoplasm
  3. in the capsid
  4. none of the above
26
Q

Nucleoside reverse transcriptase inhibitors (NRTIs) inhibit viral replication without impacting host cell division because:

  1. mammalian cells do not use reverse transcriptase
  2. mammalian cells possess efflux pumps to remove NRTIs
  3. viral cells replicate more quickly than mammalian cells
  4. none of the above.
A

Nucleoside reverse transcriptase inhibitors (NRTIs) inhibit viral replication without impacting host cell division because:

  1. mammalian cells do not use reverse transcriptase
  2. mammalian cells possess efflux pumps to remove NRTIs
  3. viral cells replicate more quickly than mammalian cells
  4. none of the above.
27
Q

The Pfizer and Moderna COVID-19 vaccines are mRNA vaccines. They contain a small amount of viral mRNA that encodes for a spike protein located on the viral capsid.

Based on your knowledge of the viral life cycle, what happens to the viral mRNA once injected into a host?

  1. the host recognizes and destroys viral mRNA
  2. viral mRNA is converted into protein in the host cytoplasm
  3. viral mRNA is converted into protein in the host nucleus
  4. viral mRNA integrates into the host genome
A

The Pfizer and Moderna COVID-19 vaccines are mRNA vaccines. They contain a small amount of viral mRNA that encodes for a spike protein located on the viral capsid.

Based on your knowledge of the viral life cycle, what happens to the viral mRNA once injected into a host?

  1. the host recognizes and destroys viral mRNA
  2. viral mRNA is converted into protein in the host cytoplasm
  3. viral mRNA is converted into protein in the host nucleus
  4. viral mRNA integrates into the host genome
28
Q
A