NURS 611|NURS611 PATHO EXAM 3 QUESTIONS AND CORRECT VERIFIED ANSWERS AND RATIONAL
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1. Explain the pathophysiolo- Is the result of an autoimmune mediated specific loss of beta cells
gy associate with Type 1 in the pancreatic islet. One of the basic patho of type 2 DM is the
and Type 2 DM development of insulin resistant tissue cells.
2. Explain what occurs in pan- Panhypopituitarism is the term correctly associated with the lack of
hypopituitarism. all anterior pituitary hormones.
3. List the clinical manifesta- The individual develops a low basal metabolic rate, cold intolerance,
tions of hypothyroidism. lethargy, tiredness, and slightly lower basal body temperature.
4. Differentiate diabetes in- DM: is not a single disease but a group of clinical heterogeneous
sipidus, diabetes mellitus disorders that have glucose intolerance in common.
and SIADH.
DI: is an insufficiency of ADH, leading to polyuria and polydipsia.
SIADH: is characterized by high levels of ADH in the absence of
normal physiologic stimuli for its release.
The symptom common to all these conditions is thirst.
5. What causes the microvas- Microvascular complications are a result of capillary basement
cular complications of DM. membranes thickening and endothelial cell hyperplasia.
6. What is the cause of dia- Inability of the kidney to increase permeability of water. This causes
betes insipidus. excretions of large volumes of dilute urine, leading to increase in
plasma osmolality.
7. Describe the pathophysio- Addison disease is a result of hyposecretion of adrenal cortex hor-
logical changes associated mones.
with Addison's Disease.
8. Describe the pathophysio- The most common cause of hyperparathyroidism is damage caused
logical changes associated during thyroid surgery. In hypothyroidism a lack of circulating PTH
with hypoparathyroidism. causes a depressed serum calcium level resulting in the sympto-
matology mentioned in the stem.
, Maryville Nurs611 - Patho Exam 3
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9. What are the caus- In a state of relative insulin deficiency there is an increase in insulin
es and pathophysiological counter regulating hormones including catecholamine's, cortisol,
changes associate with ke- glucagon, and GH. Catecholamine's, cortisol, glucagon and GH
toacidosis? antagonize insulin by increasing glucose production. In addition,
these hormones decrease use of glucose. Profound insulin defi-
ciency results in decrease glucose uptake, increase fat mobilization
with release if fatty acids, and accelerated gluconeogenesis and
ketogenesis. Ordinarily, ketones are used by tissues as an energy
source to regenerate bicarbonate. Hyperkalemia is a result of a
compensatory mechanism directed at eliminating metabolic acido-
sis.
10. What is acromegaly? Acromegaly is a term for adults who have been exposed to contin-
uously high levels of GH, whereas the term gigantism is reserved
for children and adolescents.
11. Differentiate hypothy- One of the cause's hypothyroidism is a deficiency of endemic io-
roidism and Graves' dis- dine. Hypothyroidism are the lower levels of thyroid hormone, with-
ease out the negative feedback of TH in the pituitary, there is an increase
secretion of TSH that may lead to goiter. As a result in decreased en-
ergy metabolism resulting in constipation, regulatory mechanisms
are overridden by abnormal immunologic mechanisms that result
in the stimulation of excessive TH. The systemic symptoms of thy-
rotoxic crisis include hyperthermia and tachycardia; the remaining
options are not associated with this disorder.
12. Describe the pathophysiol- A number of serious complications are associated with any type of
ogy related to chronic DM DM and include microvascular (retinopathy, nephropathy, and neu-
ropathy) and macrovascular (CAD, CVA, PVD) disease and infection.
13. What happens during hy- A person with type 1 DM experiences hunger, lightheadedness,
poglycemia? tachycardia, pallor, HA and confusion. The most likely cause of these
, Maryville Nurs611 - Patho Exam 3
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symptoms is hypoglycemia, which is often caused by a lack of
systemic glucose resulting from muscular activity.
14. What is the metabolic syn- It also has been called the insulin resistance syndrome or syndrome
drome? X. It is a clustering of clinical traits occurring together that increase
the risk for accelerated cardiovascular disease and type 2 DM. Com-
bination of medical disorders that increase the risk of developing
cardiovascular disease and DM.
15. Describe how DM causes It is a form of "dying back" neuropathy, in which the distal portions
peripheral neuropathy of the neurons are initially and eventually more severely affected.
The earliest morphologist change in both the peripheral nerves
and CNS is axonal degeneration that preferentially involves sensory
nerve fibers, particularly the smaller polymodal unmyelinated pe-
ripheral C fibers and the larger myelinated A delta fibers.
16. Trace the electrical activity Normally electrical impulses arise in the SA nose, which is often
of the heart. called the pacemaker of the heart.
The SA node is located at the junction of the right atrium and
superior vena cava, just above the tricuspid valve.
Numerous automatic nerve endings are
within the node.
The SA node is heavily innervated by both sympathetic and
parasympathetic nerve fibers.
The SA node P cells, so-called because they are pale and primitive
appearance, are assumed to be the site of impulse formation.
The action potential is transmitted from the atrial to the ventricular
myocardium through fibers of the conduction system, traveling first
, Maryville Nurs611 - Patho Exam 3
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to the AV node then the bundle of his and finally through the bundle
branches of the interventricular septum to Purkinje fibers of the
heart wall.
17. Identify the location of the Sympathetic neural stimulation of the myocardium and coronary
neurotransmitters in the vessels depends on the presence of adrenergic receptors, which
heart. bind specifically with neurotransmitters of the sympathetic nervous
system.
18. Define adrenergic recep- Sympathetic neural stimulation of the myocardium and coronary
tors. vessels depends on the presence of adrenergic receptors, which
bind specifically with neurotransmitters of the sympathetic nervous
system.
19. Discuss left-ventricular This is a concept expressed in Frank Starling law, cardiac muscle,
end diastolic pressure. like other muscle, increases its strength of contraction when it's
stretched.
20. Define Frank-Starling law As stated in Frank-Starling law, the volume of blood in the heart at
the end of diastole (the length of its muscle fibers) is directly related
to the force (strength) of contraction during the next systole.
21. Discuss the effect of an- Angiotensin II is a powerful vasoconstrictor and stimulates the se-
giotensin II on the heart. cretion of aldosterone from the adrenal gland. Angiotensin II is also
growth promoter in cardiovascular tissues, resulting in monocyte
and vascular hypertrophy and progression of hypertension. Neural
effects of angiotensin II include stimulation of thirst, release of ADH,
and increases in sympathetic nervous system output. Angiotensin
II also causes structural changes in blood vessels (remodeling)
that contribute to permanent increases in peripheral resistance
and make vessels more vulnerable to endothelial dysfunction and
platelet aggregation.
ALREADY Maryville Nurs611
A GRADED WITH - Patho
EXPERT Exam
FEEDBACK 3
VERSION (MARYVILLE)
Study online at https://quizlet.com/_5c7hwd
1. Explain the pathophysiolo- Is the result of an autoimmune mediated specific loss of beta cells
gy associate with Type 1 in the pancreatic islet. One of the basic patho of type 2 DM is the
and Type 2 DM development of insulin resistant tissue cells.
2. Explain what occurs in pan- Panhypopituitarism is the term correctly associated with the lack of
hypopituitarism. all anterior pituitary hormones.
3. List the clinical manifesta- The individual develops a low basal metabolic rate, cold intolerance,
tions of hypothyroidism. lethargy, tiredness, and slightly lower basal body temperature.
4. Differentiate diabetes in- DM: is not a single disease but a group of clinical heterogeneous
sipidus, diabetes mellitus disorders that have glucose intolerance in common.
and SIADH.
DI: is an insufficiency of ADH, leading to polyuria and polydipsia.
SIADH: is characterized by high levels of ADH in the absence of
normal physiologic stimuli for its release.
The symptom common to all these conditions is thirst.
5. What causes the microvas- Microvascular complications are a result of capillary basement
cular complications of DM. membranes thickening and endothelial cell hyperplasia.
6. What is the cause of dia- Inability of the kidney to increase permeability of water. This causes
betes insipidus. excretions of large volumes of dilute urine, leading to increase in
plasma osmolality.
7. Describe the pathophysio- Addison disease is a result of hyposecretion of adrenal cortex hor-
logical changes associated mones.
with Addison's Disease.
8. Describe the pathophysio- The most common cause of hyperparathyroidism is damage caused
logical changes associated during thyroid surgery. In hypothyroidism a lack of circulating PTH
with hypoparathyroidism. causes a depressed serum calcium level resulting in the sympto-
matology mentioned in the stem.
, Maryville Nurs611 - Patho Exam 3
Study online at https://quizlet.com/_5c7hwd
9. What are the caus- In a state of relative insulin deficiency there is an increase in insulin
es and pathophysiological counter regulating hormones including catecholamine's, cortisol,
changes associate with ke- glucagon, and GH. Catecholamine's, cortisol, glucagon and GH
toacidosis? antagonize insulin by increasing glucose production. In addition,
these hormones decrease use of glucose. Profound insulin defi-
ciency results in decrease glucose uptake, increase fat mobilization
with release if fatty acids, and accelerated gluconeogenesis and
ketogenesis. Ordinarily, ketones are used by tissues as an energy
source to regenerate bicarbonate. Hyperkalemia is a result of a
compensatory mechanism directed at eliminating metabolic acido-
sis.
10. What is acromegaly? Acromegaly is a term for adults who have been exposed to contin-
uously high levels of GH, whereas the term gigantism is reserved
for children and adolescents.
11. Differentiate hypothy- One of the cause's hypothyroidism is a deficiency of endemic io-
roidism and Graves' dis- dine. Hypothyroidism are the lower levels of thyroid hormone, with-
ease out the negative feedback of TH in the pituitary, there is an increase
secretion of TSH that may lead to goiter. As a result in decreased en-
ergy metabolism resulting in constipation, regulatory mechanisms
are overridden by abnormal immunologic mechanisms that result
in the stimulation of excessive TH. The systemic symptoms of thy-
rotoxic crisis include hyperthermia and tachycardia; the remaining
options are not associated with this disorder.
12. Describe the pathophysiol- A number of serious complications are associated with any type of
ogy related to chronic DM DM and include microvascular (retinopathy, nephropathy, and neu-
ropathy) and macrovascular (CAD, CVA, PVD) disease and infection.
13. What happens during hy- A person with type 1 DM experiences hunger, lightheadedness,
poglycemia? tachycardia, pallor, HA and confusion. The most likely cause of these
, Maryville Nurs611 - Patho Exam 3
Study online at https://quizlet.com/_5c7hwd
symptoms is hypoglycemia, which is often caused by a lack of
systemic glucose resulting from muscular activity.
14. What is the metabolic syn- It also has been called the insulin resistance syndrome or syndrome
drome? X. It is a clustering of clinical traits occurring together that increase
the risk for accelerated cardiovascular disease and type 2 DM. Com-
bination of medical disorders that increase the risk of developing
cardiovascular disease and DM.
15. Describe how DM causes It is a form of "dying back" neuropathy, in which the distal portions
peripheral neuropathy of the neurons are initially and eventually more severely affected.
The earliest morphologist change in both the peripheral nerves
and CNS is axonal degeneration that preferentially involves sensory
nerve fibers, particularly the smaller polymodal unmyelinated pe-
ripheral C fibers and the larger myelinated A delta fibers.
16. Trace the electrical activity Normally electrical impulses arise in the SA nose, which is often
of the heart. called the pacemaker of the heart.
The SA node is located at the junction of the right atrium and
superior vena cava, just above the tricuspid valve.
Numerous automatic nerve endings are
within the node.
The SA node is heavily innervated by both sympathetic and
parasympathetic nerve fibers.
The SA node P cells, so-called because they are pale and primitive
appearance, are assumed to be the site of impulse formation.
The action potential is transmitted from the atrial to the ventricular
myocardium through fibers of the conduction system, traveling first
, Maryville Nurs611 - Patho Exam 3
Study online at https://quizlet.com/_5c7hwd
to the AV node then the bundle of his and finally through the bundle
branches of the interventricular septum to Purkinje fibers of the
heart wall.
17. Identify the location of the Sympathetic neural stimulation of the myocardium and coronary
neurotransmitters in the vessels depends on the presence of adrenergic receptors, which
heart. bind specifically with neurotransmitters of the sympathetic nervous
system.
18. Define adrenergic recep- Sympathetic neural stimulation of the myocardium and coronary
tors. vessels depends on the presence of adrenergic receptors, which
bind specifically with neurotransmitters of the sympathetic nervous
system.
19. Discuss left-ventricular This is a concept expressed in Frank Starling law, cardiac muscle,
end diastolic pressure. like other muscle, increases its strength of contraction when it's
stretched.
20. Define Frank-Starling law As stated in Frank-Starling law, the volume of blood in the heart at
the end of diastole (the length of its muscle fibers) is directly related
to the force (strength) of contraction during the next systole.
21. Discuss the effect of an- Angiotensin II is a powerful vasoconstrictor and stimulates the se-
giotensin II on the heart. cretion of aldosterone from the adrenal gland. Angiotensin II is also
growth promoter in cardiovascular tissues, resulting in monocyte
and vascular hypertrophy and progression of hypertension. Neural
effects of angiotensin II include stimulation of thirst, release of ADH,
and increases in sympathetic nervous system output. Angiotensin
II also causes structural changes in blood vessels (remodeling)
that contribute to permanent increases in peripheral resistance
and make vessels more vulnerable to endothelial dysfunction and
platelet aggregation.
