NSG 533 ADVANCED PATHOPHYSIOLOGY
EXAM WITH QUESTIONS AND ANSWERS||
GUARANTEED PASS|| ALREADY GRADED A+||
LATEST VERSION 2026
Describe apoptosis- Inducing Factor (AIF) - ANSWER-1. Neurons, and perhaps
other cells, have another way to self-destruct that- unlike the two paths
described- does not use caspases
2. Apoptosis inducing factor (AIF) is a protein that is normally located in the
intermembrane space of the mitochondria
3. When the cell receives a signal telling it that it is time to die, AIF
- is released from the mitochondria
-migrated into the nucleus
-binds to DNA which
-triggers the destruction of the DNA and cell death
Why are thyroid replacement drugs considered to have a narrow therapeutic
index ( NTI )and what does that mean clinically? - ANSWER-The therapeutic
index (TI) is the range of doses at which a medication is effective without
unacceptable adverse events. Drugs with a narrow TI (NTIs) have a narrow
window between their effective doses and those at which they produce adverse
toxic effects. Oral Bioavailability: (erratic) 40-80%brand vs generic Highly
protein bound (99%)Half-lifeEuthyroid = 6-7 daysHypothyroid = 9-10
daysSteady State: @ 6 weeks or 4-5 t1/2 's ... this is the bases for monitoring @
six weeks from start or changes!
,Consider changes such as brand to generic, different generics manufactures,
different pharmacies, etcAny such change will require repeat lab monitoring @
~ 6 weeks to confirm the same clinical response
What are some drug-drug, drug-food interactions associated with thyroid
replacement - ANSWER-drug binding interactions, di-valent cations,
amiodarone, certain antibiotics
RECOMMENDATION 13 Methimazole should be used in virtually every
patient who chooses antithyroid drug therapy for GD, except during the first
trimester of pregnancy when propylthiouracil is preferred, in the treatment of
thyroid storm (inhibition of peripheral conversion), and in patients with minor
reactions to methimazole who refuse radioactive iodine therapy or
surgeryDelayed onset - ANSWER-
Beta-blockers role in therapy? - ANSWER-So .. beta blockers are used for
Symptomatic relief of hyperthyroidism until more definative therapy is
instituted and thyroid levels retun to normal or near normal..
Reduction of peripheral manifestations
Tachycardia, sweating, severe tremor, nervousness
Inhibition of peripheral conversion of thyroid hormones at higher doses
(propranolol ONLY)
Small therapeutic effect in magnitude
thyrotoxicosis
Why does amiodarone pose a unique concern to thyroid disorders - ANSWER-
"Amiodarone-normal thyroid autoregulation is lost because of the relatively
high iodine content" .. this fact can lead to a situation where amiodarone can
cauase BOTH hyper- and hypo- thyroidism, depending on the patient, through
several process
blocking thyroid peroxidase
blocking proteolysis of Tg and thyroid hormone
,altering organification, etc
What would you recommend if a patient is taking Nexium and Plavix together?
- ANSWER-As we have seen through our discussions, there is a lot of
information (including an FDA issued statement in the package insert)
describing the drug interaction and reduced efficacy of clopidogrel if used with
a PPI (primarily omeprazole) (or in patients who are genetically slow CYP2C19
metabolizers); however there is also evidence based information indicating the
interaction is not as significant as originally thought. Bottom line: Despite
pharmacokinetic evidence that omeprazole interferes with clopidogrel
metabolism, COGENT trial found addition of omeprazole to clopidogrel
reduced gastrointestinal events without increasing cardiovascular events.
Describe the relationship of apoptosis to cancer - ANSWER-1. Some viruses
associated with cancers use tricks to prevent apoptosis of the cells they have
transformed.
e.g., HPV virus that causes cervical cancer produces protein E6 that binds and
inactivates the apoptosis promoter p53
2. Cancer cells produced without the participation of viruses may have trick to
avoid apoptosis
e.g., Some B-cell leukemias and lymphomas express high levels of Bcl-2, thus
blocking apoptotic signals they may receive.
- Melanoma cells avoid apoptosis by inhibiting the expression of the gene
coding Apaf-1
-Some cancer cells secrete elevated levels of a soluble "decoy" molecule that
binds to FasL, plugging it up so it cannot bind Fas, Thus, cytotoxic T cells
(CTL) cannot kill the cancer cells.
, -other cancer cells express high levels of FasL and can kill any cytotoxic T cell
(CTL) that try to kill them because CTL also express Fas (but are protected
from their own FasL)
Describe the relationship of apoptosis and organ transplantation - ANSWER-
The anterior chamber of the eye and the testes express high levels of FasL at all
times. Thus antigen-reactive T-cells, which express Fas, would be killed when
they enter these sites.
This finding raises the possibility of a new way of preventing graft rejection.
If at least some of the cells on a transplanted kidney, liver, heart etc. could be
made to express high levels of FasL, that might protect the graft from attack by
the T cells of the host's cell mediated immune system. If so, then the present
need for treatment with immunosuppressive drugs for the rest of the transplant
recipient's life would be reduced or eliminated.
Describe physiologic atrophy and give an example - ANSWER-Physiological
atrophy occurs with early development. For example, the thymus gland
undergoes physiological atrophy during childhood.
Describe pathological atrophy and give an example - ANSWER-pathological
atrophy occurs as a result of decreases in workload, use, pressure, blood supply,
nutrition, hormonal stimulation, and nervous stimulation. For example,
individuals immobilized in bed for a prolonged time exhibit a type of skeletal
muscle atrophy called disuse atrophy.
Is the result caused by increased demand, stimulation by hormones and growth
factors? Give example. - ANSWER-Physiological hypertrophy
For example, physiological hypertrophy in skeletal muscle occurs in response to
heavy work. Pregnancy is also an example of physiological hypertrophy and
hormone induced uterine enlargement.
EXAM WITH QUESTIONS AND ANSWERS||
GUARANTEED PASS|| ALREADY GRADED A+||
LATEST VERSION 2026
Describe apoptosis- Inducing Factor (AIF) - ANSWER-1. Neurons, and perhaps
other cells, have another way to self-destruct that- unlike the two paths
described- does not use caspases
2. Apoptosis inducing factor (AIF) is a protein that is normally located in the
intermembrane space of the mitochondria
3. When the cell receives a signal telling it that it is time to die, AIF
- is released from the mitochondria
-migrated into the nucleus
-binds to DNA which
-triggers the destruction of the DNA and cell death
Why are thyroid replacement drugs considered to have a narrow therapeutic
index ( NTI )and what does that mean clinically? - ANSWER-The therapeutic
index (TI) is the range of doses at which a medication is effective without
unacceptable adverse events. Drugs with a narrow TI (NTIs) have a narrow
window between their effective doses and those at which they produce adverse
toxic effects. Oral Bioavailability: (erratic) 40-80%brand vs generic Highly
protein bound (99%)Half-lifeEuthyroid = 6-7 daysHypothyroid = 9-10
daysSteady State: @ 6 weeks or 4-5 t1/2 's ... this is the bases for monitoring @
six weeks from start or changes!
,Consider changes such as brand to generic, different generics manufactures,
different pharmacies, etcAny such change will require repeat lab monitoring @
~ 6 weeks to confirm the same clinical response
What are some drug-drug, drug-food interactions associated with thyroid
replacement - ANSWER-drug binding interactions, di-valent cations,
amiodarone, certain antibiotics
RECOMMENDATION 13 Methimazole should be used in virtually every
patient who chooses antithyroid drug therapy for GD, except during the first
trimester of pregnancy when propylthiouracil is preferred, in the treatment of
thyroid storm (inhibition of peripheral conversion), and in patients with minor
reactions to methimazole who refuse radioactive iodine therapy or
surgeryDelayed onset - ANSWER-
Beta-blockers role in therapy? - ANSWER-So .. beta blockers are used for
Symptomatic relief of hyperthyroidism until more definative therapy is
instituted and thyroid levels retun to normal or near normal..
Reduction of peripheral manifestations
Tachycardia, sweating, severe tremor, nervousness
Inhibition of peripheral conversion of thyroid hormones at higher doses
(propranolol ONLY)
Small therapeutic effect in magnitude
thyrotoxicosis
Why does amiodarone pose a unique concern to thyroid disorders - ANSWER-
"Amiodarone-normal thyroid autoregulation is lost because of the relatively
high iodine content" .. this fact can lead to a situation where amiodarone can
cauase BOTH hyper- and hypo- thyroidism, depending on the patient, through
several process
blocking thyroid peroxidase
blocking proteolysis of Tg and thyroid hormone
,altering organification, etc
What would you recommend if a patient is taking Nexium and Plavix together?
- ANSWER-As we have seen through our discussions, there is a lot of
information (including an FDA issued statement in the package insert)
describing the drug interaction and reduced efficacy of clopidogrel if used with
a PPI (primarily omeprazole) (or in patients who are genetically slow CYP2C19
metabolizers); however there is also evidence based information indicating the
interaction is not as significant as originally thought. Bottom line: Despite
pharmacokinetic evidence that omeprazole interferes with clopidogrel
metabolism, COGENT trial found addition of omeprazole to clopidogrel
reduced gastrointestinal events without increasing cardiovascular events.
Describe the relationship of apoptosis to cancer - ANSWER-1. Some viruses
associated with cancers use tricks to prevent apoptosis of the cells they have
transformed.
e.g., HPV virus that causes cervical cancer produces protein E6 that binds and
inactivates the apoptosis promoter p53
2. Cancer cells produced without the participation of viruses may have trick to
avoid apoptosis
e.g., Some B-cell leukemias and lymphomas express high levels of Bcl-2, thus
blocking apoptotic signals they may receive.
- Melanoma cells avoid apoptosis by inhibiting the expression of the gene
coding Apaf-1
-Some cancer cells secrete elevated levels of a soluble "decoy" molecule that
binds to FasL, plugging it up so it cannot bind Fas, Thus, cytotoxic T cells
(CTL) cannot kill the cancer cells.
, -other cancer cells express high levels of FasL and can kill any cytotoxic T cell
(CTL) that try to kill them because CTL also express Fas (but are protected
from their own FasL)
Describe the relationship of apoptosis and organ transplantation - ANSWER-
The anterior chamber of the eye and the testes express high levels of FasL at all
times. Thus antigen-reactive T-cells, which express Fas, would be killed when
they enter these sites.
This finding raises the possibility of a new way of preventing graft rejection.
If at least some of the cells on a transplanted kidney, liver, heart etc. could be
made to express high levels of FasL, that might protect the graft from attack by
the T cells of the host's cell mediated immune system. If so, then the present
need for treatment with immunosuppressive drugs for the rest of the transplant
recipient's life would be reduced or eliminated.
Describe physiologic atrophy and give an example - ANSWER-Physiological
atrophy occurs with early development. For example, the thymus gland
undergoes physiological atrophy during childhood.
Describe pathological atrophy and give an example - ANSWER-pathological
atrophy occurs as a result of decreases in workload, use, pressure, blood supply,
nutrition, hormonal stimulation, and nervous stimulation. For example,
individuals immobilized in bed for a prolonged time exhibit a type of skeletal
muscle atrophy called disuse atrophy.
Is the result caused by increased demand, stimulation by hormones and growth
factors? Give example. - ANSWER-Physiological hypertrophy
For example, physiological hypertrophy in skeletal muscle occurs in response to
heavy work. Pregnancy is also an example of physiological hypertrophy and
hormone induced uterine enlargement.
