NURS 5315 Exam 3 UTA 2026 Actual
Exam Test Bank | Advanced
Pathophysiology | Complete 300 Q&A
with Verified Answers | Graded A+
Thyroid hormones - answer- T3, T4 and calcitonin
Pancreas hormones - answer- Insulin and glucagon
Adrenal Glands hormones - answer- Made up of the cortex which secretes steroids
such as cortisone and aldosterone and the medulla which secretes catecholamines
such as epi and norepi
Primary thyroid disorders - answer- result in alterations of thyroid hormone (TH) levels
with secondary feedback effects on pituitary thyroid stimulating hormone (TSH)
Subclinical Thyroid disease - answer- Thyroid disease that presents with minimal to no
symptoms but with abnormal lab values
Secondary Thyroid disorders - answer- conditions that results from the dysfunction of
the pituitary gland TSH production
Thyrotoxicosis - answer- (hyperthyroidism) a condition that results from any cause of
increased TH levels. Will how low TSH levels and high T4 level. S&S: increased
metabolic rate, heat intolerance, goiter, menstrual irrregularities, weight loss,
diaphoresis, fine tremor, tachycardia, frequent bowel movements, restlessness, short
attention span, hair loss, anorexia, exophthalmos, pretibial edema, and heart failure.
Thyrotoxic Crisis(thyroid storm) - answer- worsening hyperthyroid state triggered by an
igniting even such as infection, trauma, cardiopulmonary disorder, burns, seizures
surgery, or spontaneously. S&S: extreme restlessness and agitation, delirium, seizures,
coma, severe tachycardia, heart failure, hyperthermia, delirium, volume depletion, NVD
and death if not treated.
Grave's disease - answer- Most common cause of hyperthyroidism and is an
autoimmune disorder. Antibodies attach to the thyroid cells and mimic the function of
TSH which results in an increased secretion of T3 and T4 and overrides the negative
feedback mechanisms which regulate TSH secretion. The stimulation of the receptors
by the antibodies results in the development of goiter. May also experience
, exophthalmos, periorbital edema, and extraocular muscle weakness leading to
strabismus and diplopia
Hyperthyroidism from nodular thyroid disease - answer- Follicular hypertrophy of the
thyroid cells is responsible for the formation of the thyroid nodules which secrete extra
hormones. Nodules develop bc of normal changes during pregnancy or puberty or as a
result of an autoimmune issue, viral infection or genetic influence. Symptoms develop
slowly and will not display exophthalmos or pretibial myxedema
Primary hypothyroidism - answer- Defect is in the thyroid gland itself which causes
insufficient amounts of thyroid hormone. Causes include congenital defects,
thyroidectomy, thyroid radiation, iodine deficiency, anti-thyroid medications, or
impairment in thyroid hormone synthesis
Secondary hypothyroidism - answer- Malfunction in the pituitary or hypothalamus
glands which leads to a lack of TSH. Most common cause is pituitary tumors. Other
causes include TBI, subarachnoid hemorrhage, or pituitary infarction
Subclinical hypothyroidism - answer- mild thyroid failure. defined by elevated TSH level
with normal TH level.
Hypothyroid S&S - answer- confusion, syncope, slow speech and thinking, anemia,
bradycardia, reduced stroke volume and cardiac output, dyspnea, hypoventilation,
decreased appetite, weight gain, dry hair, cold intolerant, constipation, hyperlipidemia,
periorbital edema, peripheral edema, myxedema(puffy face), increased total body
water, hyponatremia, reduced renal blood flow
Myxedema coma - answer- thyroid emergency which has the opposite effect of thyroid
storm. Results in decreased LOC and is usually precipitated by an event such as
infection, discontinuation of thyroid medications, narcotic or sedative use. other S&S
hypotension, hypoventilation, shivering, hypothermia, lactic acidosis, coma, and
hypoglycemia.
Type 1 DM - answer- 3 types: 1A is autoimmune, 1B is idiopathic and 3c is associated
with chronic pancreatitis. in 1A: autoimmune response destroys the beta cells in the
pancreas which leads to apoptosis. Beta cell destruction is what causes a lack of insulin
to be produced.
Type 1 clinical manifestations - answer- polydipsia, polyuria, polyphagia, weight loss
and fatigue.
Typer 2 DM - answer- pathlogical defect is insulin resistance. A decrease in number of
insulin cell receptors or insufficient amounts of insulin secretion to meet metabolic
needs are characteristic of DM 2.
Exam Test Bank | Advanced
Pathophysiology | Complete 300 Q&A
with Verified Answers | Graded A+
Thyroid hormones - answer- T3, T4 and calcitonin
Pancreas hormones - answer- Insulin and glucagon
Adrenal Glands hormones - answer- Made up of the cortex which secretes steroids
such as cortisone and aldosterone and the medulla which secretes catecholamines
such as epi and norepi
Primary thyroid disorders - answer- result in alterations of thyroid hormone (TH) levels
with secondary feedback effects on pituitary thyroid stimulating hormone (TSH)
Subclinical Thyroid disease - answer- Thyroid disease that presents with minimal to no
symptoms but with abnormal lab values
Secondary Thyroid disorders - answer- conditions that results from the dysfunction of
the pituitary gland TSH production
Thyrotoxicosis - answer- (hyperthyroidism) a condition that results from any cause of
increased TH levels. Will how low TSH levels and high T4 level. S&S: increased
metabolic rate, heat intolerance, goiter, menstrual irrregularities, weight loss,
diaphoresis, fine tremor, tachycardia, frequent bowel movements, restlessness, short
attention span, hair loss, anorexia, exophthalmos, pretibial edema, and heart failure.
Thyrotoxic Crisis(thyroid storm) - answer- worsening hyperthyroid state triggered by an
igniting even such as infection, trauma, cardiopulmonary disorder, burns, seizures
surgery, or spontaneously. S&S: extreme restlessness and agitation, delirium, seizures,
coma, severe tachycardia, heart failure, hyperthermia, delirium, volume depletion, NVD
and death if not treated.
Grave's disease - answer- Most common cause of hyperthyroidism and is an
autoimmune disorder. Antibodies attach to the thyroid cells and mimic the function of
TSH which results in an increased secretion of T3 and T4 and overrides the negative
feedback mechanisms which regulate TSH secretion. The stimulation of the receptors
by the antibodies results in the development of goiter. May also experience
, exophthalmos, periorbital edema, and extraocular muscle weakness leading to
strabismus and diplopia
Hyperthyroidism from nodular thyroid disease - answer- Follicular hypertrophy of the
thyroid cells is responsible for the formation of the thyroid nodules which secrete extra
hormones. Nodules develop bc of normal changes during pregnancy or puberty or as a
result of an autoimmune issue, viral infection or genetic influence. Symptoms develop
slowly and will not display exophthalmos or pretibial myxedema
Primary hypothyroidism - answer- Defect is in the thyroid gland itself which causes
insufficient amounts of thyroid hormone. Causes include congenital defects,
thyroidectomy, thyroid radiation, iodine deficiency, anti-thyroid medications, or
impairment in thyroid hormone synthesis
Secondary hypothyroidism - answer- Malfunction in the pituitary or hypothalamus
glands which leads to a lack of TSH. Most common cause is pituitary tumors. Other
causes include TBI, subarachnoid hemorrhage, or pituitary infarction
Subclinical hypothyroidism - answer- mild thyroid failure. defined by elevated TSH level
with normal TH level.
Hypothyroid S&S - answer- confusion, syncope, slow speech and thinking, anemia,
bradycardia, reduced stroke volume and cardiac output, dyspnea, hypoventilation,
decreased appetite, weight gain, dry hair, cold intolerant, constipation, hyperlipidemia,
periorbital edema, peripheral edema, myxedema(puffy face), increased total body
water, hyponatremia, reduced renal blood flow
Myxedema coma - answer- thyroid emergency which has the opposite effect of thyroid
storm. Results in decreased LOC and is usually precipitated by an event such as
infection, discontinuation of thyroid medications, narcotic or sedative use. other S&S
hypotension, hypoventilation, shivering, hypothermia, lactic acidosis, coma, and
hypoglycemia.
Type 1 DM - answer- 3 types: 1A is autoimmune, 1B is idiopathic and 3c is associated
with chronic pancreatitis. in 1A: autoimmune response destroys the beta cells in the
pancreas which leads to apoptosis. Beta cell destruction is what causes a lack of insulin
to be produced.
Type 1 clinical manifestations - answer- polydipsia, polyuria, polyphagia, weight loss
and fatigue.
Typer 2 DM - answer- pathlogical defect is insulin resistance. A decrease in number of
insulin cell receptors or insufficient amounts of insulin secretion to meet metabolic
needs are characteristic of DM 2.
