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NURS 5663 EXAM 3 REVIEW QUESTIONS WITH VERIFIED SOLUTIONS LATEST UPDATE 2026

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NURS 5663 EXAM 3 REVIEW QUESTIONS WITH VERIFIED SOLUTIONS LATEST UPDATE 2026 Steps involved in the synthesis of thyroid hormones - Answers (1) iodide (I-) trapped by the thyroid follicular cells; (2) diffusion of iodide to the apex of the cells; (3) transport of iodide into the colloid; (4) oxidation of inorganic iodide to iodine and incorporation of iodine into tyrosine residues within thyroglobulin molecules in the colloid; (5) combination of two DIT molecules to form tetraiodothyronine (T4) or of MIT with DIT to form T3; (6) uptake of thyroglobulin from the colloid into the follicular cell by endocytosis, fusion of the thyroglobulin with a lysosome, and proteolysis and release of T4, T3, DIT, and MIT; (7) release of T4 and T3 into the circulation; and (8) deiodination of DIT and MIT to yield tyrosine. T3 is also formed from monodeiodination of T4 in the thyroid and in peripheral tissues. Insulin Definition - Answers the storage and anabolic hormone of the body General characteristics of Insulin - Answers - small protein that contains 51 amino acids arranged in 2 chains (A & B) linked by disulfide bridges. - stored in beta cells of pancreas in form of hexameric crystals 1. Entire human pancreas stores up to 8mg (200 units) of insulin. - Insulin is released from pancreatic beta cells at a low BASAL rate -- plus with stimulation releases at a much higher rate Insulin synthesis - Answers Insulin is synthesized as preproinsulin and processed to proinsulin. Proinsulin is then converted to insulin and C-peptide and stored in secretary granules awaiting release on demand. Insulin synthesis is regulated at both the transcriptional and translational level. insulin Stimulates release - Answers glucose, sugars (eg. Mannose), amino acids (esp. glyconeogenic amino acids like leucine, arginine), hormones like glucagon-like polypeptide 1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), glucagon, cholecystokinin, high concentrations of fatty acids, and B-adrenergic sympathetic activity Stimulatory drugs of insulin - Answers sulfonylureas, meglitinides, D-phenylalanine derivatives, isoproterenol, and acetylcholine Insulin Inhibitory hormones: - Answers insulin, islet amyloid polypeptide, somatostatin, and leptin; alpha-adrenergic sympathetic activity; chronically elevated glucose; low concentrations of fatty acids Insulin Inhibitory drugs: - Answers diazoxide, phenytoin, vinblastine, clonidine, verapamil, and colchicine One mechanism of stimulated insulin release - Answers 1. in resting cell: normal (low) ATP levels→ K+ diffuses down its concentration gradient through ATP-gated K+ channels, maintaining the intracellular potential @fully polarized, negative level→ insulin release is minimal 2. if glucose concentration rises → ATP production increases → K+ channels close -- depolarization results → in muscle/nerve voltage-gated Ca2+ channels open in response to depolarization -- allows more Ca2+ to enter cell -- increased intracellular Ca2+ results in increased insulin secretion → insulin secretagugues close the ATP-dependent K+ channel→ depolarizes membrane→ increased insulin release by same mechanism Effects of insulin - Answers - Promotes the storage of fat as well as glucose (both sources of energy) within specialized target cells & influences cell growth and the metabolic functions of a wide range of tissues -Promotes synthesis and storage of glycogen, triglycerides, and protein in its major target tissues: liver, fat, and muscle. Release of insulin from pancreas is stimulated by increased blood glucose, incretins, vagal nerve stimulation, and other factors. Endocrine Effects of Insulin - Answers LIVER: -Reversal of Catabolic features of insulin deficiency: 1. inhibits glycogenolysis 2. inhibits conversion of fatty acids & amino acids to keto acids 3. inhibits conversion of amino acids to glucose -Anabolic action: 1. promotes glucose storage as glycogen (induces glucokinase & glycogen synthase, inhibits phosphorylase) 2. increases triglyceride synthesis & very-low-density lipoprotein formation MUSCLE: - Increased protein synthesis 1. increases amino acid transport 2. Increases ribosomal protein synthesis - Increased glycogen synthesis 1. increases glucose transport 2. induces glycogen synthase & inhibits phosphorylase ADIPOSE TISSUE: - Increased triglyceride storage 1. Lipoprotein lipase is induced & activated by insulin to hydrolyze triglycerides from lipoproteins 2. Glucose transport into cell provides glycerol phosphate to permit esterification of fatty acids supplied by lipoprotein transport 3. Intracellular lipase is inhibited by insulin glucagon definition - Answers the hyperglycemic factor that mobilizes glycogen stores Glucagon synthesis - Answers in the alpha cells of the pancreatic islets of Langerhans Glucagon characteristics - Answers -Peptide (identical in ALL mammals) consisting of single chain of 29 amino acids - Degraded in the liver and kidney as well as in plasma and at its tissue receptor -half-life is between 3-6 months Effects of Glucagon - Answers 1. 1st six amino acids at the amino terminal of glucagon molecule bind to Gs protein-coupled receptors on liver cells --leads to increase in cAMP -- facilitates catabolism of stored glycogen -- increases gluconeogenesis and ketogenesis 2. Immediate pharmacological result of glucagon infusion --raise blood glucose by using stored hepatic glycogen 3. NO effect on skeletal muscle glycogen because of lack of receptors 4. Pharmacological amounts of glucagon cause release of insulin from normal pancreatic beta cells, catecholamines from pheochromocytoma, and calcitonin from medullary carcinoma cells 5. Has potent inotropic and chronotropic effect on heart, mediated by the cAMP mechanism → produces effect similar to B-adrenergic agonists without requiring functioning B-receptors 6. LARGE doses of glucagon produce profound relaxation of the intestine Uses of Glucagon - Answers 1. Emergency treatment of severe hypoglycemic reactions due to insulin therapy when pt is unable to self-administer oral glucose and IV glucose treatment is not possible 2. IV, IM, sub Q, or nasal powder 3. Main adverse effect is nausea/vomiting so place unconscious pt on side after administration 4. Beta blocker overdose to increase cAMP 5. In endoscopic procedure to relax sphincter of Oddi Contraindications of Glucagon - Answers a. Pheochromocytoma → can cause release of catecholamines and increase BP b. Patients with insulinoma→ can cause rebound hypoglycemia Different types of insulin - Answers Short-acting: Regular insulin and rapidly acting insulin analog Long-Acting Insulin: NPH, Insulin Glargine, Insulin Detemir, insulin degludec, and mixture insulin Short-Acting insulin - Answers 1. Regular: short-acting, soluble crystalline zinc insulin. Hypoglycemic effect appears within 30 mins after SubQ injection -Peak @ 2hrs -Duration: 5-7hrs - If inpatient needing infusion: regular is used for diabetic ketoacidosis and during perioperative glucose management 2. Rapidly acting insulin analogs: (1)Insulin lispro (Humalog), (2)Insulin aspart (Novolog, Admelog, FiAsp), (3) Glulisine (Apidra) - Peak @ around 1 hr - Duration: 3-4hrs - Optimal times for administration: Rapid - 15 mins before meal; Regular - 45 mins after meal -Uses: Rapidly acting insulin is choice for insulin pumps Long-Acting insulin - Answers 1. NPH (Neutral protamine Hagedorn, or isophane): Humulin N, Novolin N Intermediate-acting -Onset: 2-4hrs - Peak @ 6-7hrs - Duration: 10-20hrs -Its usually mixed with regular, lispro, aspart, or glulisine insulin - Given 2-4 times a day - Smaller doses have lower, earlier peaks and short duration of action vs. larger doses (converse) 2. Insulin Glargine: soluble "peakless"; long-acting: Lantus, Toujeo, Sanofi Avents; Basaglar, Lilly - Low, continuous level of circulating insulin - Onset: slow (0.5 - 1hr) - Duration: 24hrs - Given once daily - Formulation is high acidic (pH 4) so can't mix with other insulins 3. Insulin Detemir: Levemir - Duration: 17hrs - Once or twice a day for stable basal coverage 4. Insulin Degludec: Tresiba - half-life: 25hrs - Onset: 30-90 mins - Duration: 42hrs - Once or twice a day to achieve stable basal coverage Mixture Insulin - Answers Since NPH requires several hrs to reach therapeutic levels, it usually requires supplements of rapid/short-acting insulin before meals - Mixed in same syringe -Clear before cloudy -Premixed available: 70/30 regular Pituitary hormone - Answers -master gland of the body -Anterior and posterior pituitary secretes many hormones that influence all cells and physiologic processes - Individual cells within the anterior pituitary only secrete a SINGLE hormone for the most part so, for ex, cells that secrete TSH don't also secrete growth hormone Pituitary hormone: Anterior - Answers - Growth hormone: Targets liver and adipose tissue to promote growth (indirectly), control of protein, lipid and carb metabolism - Thyroid-stimulating hormone: targets thyroid gland to stimulate secretion of thyroid hormones - Adrennocorticotropic hormone: targets adrenal gland (cortex) to stimulate secretion of glucocorticoids - Prolactin: Targets mammary gland for milk production - Luteinizing hormone: Targets ovary and testis to control reproductive function - Follicle-stimulating hormone: Targets ovary and testis to control reproductive function Pituitary hormone: Posterior - Answers - Antidiuretic hormone: Targets kidney to conserve body water - Oxytocin: Targets ovary and testis to stimulate milk ejection and uterine contractions Hypothalamus hormone - Answers is the "power" behind the pituitary; releasing and inhibiting hormones - Secretes hormones that strictly control secretion of pituitary hormones - The hormones travel to pituitary via the hypothalamic-hypophyseal portal veins Hypothalamus hormone: Releasing hormones - Answers - Feedback inhibitory regulation: 1. Thyrotropin-releasing hormone controls TSH release Inhibited by two thyroid hormones: Thyroxine and Triiodothyronine 2. Gonadotropin-releasing hormone controls LH and FSH release Inhibited in women by estrogen and progesterone Inhibited in men by testosterone and other androgens 3. Corticotropin-releasing hormone controls ACTH release Inhibited by cortisol 4. Growth-hormone-releasing hormone stimulates GH production Inhibiting hormones: * Somatostatin (SST) inhibits GH production * Dopamine inhibits prolactin production Adverse Effects of Glucocorticoids: Musculoskeletal effects - Answers - Induced osteoporosis with long-term use: up to 40% of pts on long-term use develop bone loss -- fractures - Steroid induced myopathy: reversible, painless myopathy; direct result of muscle breakdown usually with high-dose long-term use - Osteonecrosis: Pts with Lupus and children at highest risk; long term use more than 20mg daily; knees and hips are more common Adverse Effects of Glucocorticoids: Metabolic and endocrine effects - Answers - Systemic steroid cause dose-dependent increase in fasting glucose levels, esp post-prandial - Development of cushingoid features: redistribution of body fat; truncal, buffalo hump, and moon face Weight gain: Suppression of hypothalamic-pituitary-adrenal (HPA) axis decreasing cotricotropin-releasing hormone (CRH) from the hypothalamus, adrenocorticotropic hormone (ACTH) from anterior pituitary and endrogenous cortisol Prolonged ACTH suppression causes atrophy of adrenal gland -- abrupt glucocorticoid cessation causes symptoms of adrenal insufficiency Adrenal suppression is most common cause of adrenal insufficiency in children. Children with adrenal crisis secondary to adrenal suppression present with hypotension, shock, decreased consciousness, lethargy, unexplained hypoglycemia, seizures, and even death Impairment of growth and delay in puberty in children when used for chronic illnesses like nephrotic syndrome or asthma Adverse Effects of Glucocorticoids: Infections - Answers - D/t immune suppression Adverse Effects of Glucocorticoids: Cardiovascular - Answers - Usually seen with cortisol and cortisone - Fluid retention, edema, wt gain, HTN, and arrhythmias bc of increased renal excretion of K, Ca, and phosphate - HTN usually only in high doses - Long term moderate doses -- premature atherosclerosis Adverse Effects of Glucocorticoids: Dermatologic - Answers - Ecchymosis, skin thinning and atrophy, acnes, mild hirsutism, facial erythema, stria, impaired wound healing, thinning of hair, and perioral dermatitis Adverse Effects of Glucocorticoids: Ophthalmologic - Answers - High risk of cataracts with daily use of 10mg of prednisone for 1 year - Increased intraocular pressure (glaucoma) - Chorioretinopathy: Retinal detachment in central macular region Adverse Effects of Glucocorticoids: GI - Answers - Gastric, gastric ulcer formation, and GI bleeding - 4 fold risk if concurrent use of NSAIDS - Pancreatitis, visceral perforation, and hepatic steatosis (fatty liver) Adverse Effects of Glucocorticoids: Neuropsychiatric - Answers - Mild euphoria or anxiety initially - Depression is greater in pts on longstanding therapy -Psychosis can occur at 20mg daily - Sleep disturbance - Akathisia (motor restlessness) Menstrual Cycle - Answers - Starts at puberty; 30-40 year of cyclic function - Average of 28 days - Hormone secretion begins in hypothalamus where gonadotropin-releasing hormone (GnRH) is secreted in increased, pulsatile fashion once puberty starts GnRH is then transported to anterior pituitary where it activates its 7-transmembrane G-Protein receptor -- signals anterior pituitary to secrete stimulating FSH and LH -- provides input to ovaries * Within ovarian follicile there are 2 cell types: Theca and granulosa 1. LH stimulates theca cells to produce progesterone and androstenedione by activating the enzyme, cholesterol desolase -- once androstenedione is secreted, the hormone diffuses to nearby granulosa cells 2. FSH stimulates granulosa cells to convert androstenedione to testerone then 17-beta-estradiol by activating enzyme Aromatasea as 17=beta-estradiol or progesterone levels increase there is negative feedback to anterior pituitary to lower levels of FSH and LH

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NURS 5663 EXAM 3 REVIEW QUESTIONS WITH VERIFIED SOLUTIONS
LATEST UPDATE 2026


Steps involved in the synthesis of thyroid hormones - Answers (1) iodide (I-) trapped
by the thyroid follicular cells;
(2) diffusion of iodide to the apex of the cells;
(3) transport of iodide into the colloid;
(4) oxidation of inorganic iodide to iodine and incorporation of iodine into tyrosine
residues within thyroglobulin molecules in the colloid;
(5) combination of two DIT molecules to form tetraiodothyronine (T4) or of MIT
with DIT to form T3;
(6) uptake of thyroglobulin from the colloid into the follicular cell by endocytosis,
fusion of the thyroglobulin with a lysosome, and proteolysis and release of T4, T3,
DIT, and MIT;
(7) release of T4 and T3 into the circulation; and
(8) deiodination of DIT and MIT to yield tyrosine. T3 is also formed from
monodeiodination of T4 in the thyroid and in peripheral tissues.
Insulin Definition - Answers the storage and anabolic hormone of the body
General characteristics of Insulin - Answers - small protein that contains 51 amino
acids arranged in 2 chains (A & B) linked by disulfide bridges.
- stored in beta cells of pancreas in form of hexameric crystals
1. Entire human pancreas stores up to 8mg (200 units) of insulin.
- Insulin is released from pancreatic beta cells at a low BASAL rate --> plus with
stimulation releases at a much higher rate
Insulin synthesis - Answers Insulin is synthesized as preproinsulin and processed to
proinsulin. Proinsulin is then converted to insulin and C-peptide and stored in
secretary granules awaiting release on demand. Insulin synthesis is regulated at both
the transcriptional and translational level.
insulin Stimulates release - Answers glucose, sugars (eg. Mannose), amino acids
(esp. glyconeogenic amino acids like leucine, arginine), hormones like glucagon-like
polypeptide 1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP),
glucagon, cholecystokinin, high concentrations of fatty acids, and B-adrenergic
sympathetic activity
Stimulatory drugs of insulin - Answers sulfonylureas, meglitinides, D-phenylalanine
derivatives, isoproterenol, and acetylcholine
Insulin Inhibitory hormones: - Answers insulin, islet amyloid polypeptide,
somatostatin, and leptin; alpha-adrenergic sympathetic activity; chronically elevated
glucose; low concentrations of fatty acids
Insulin Inhibitory drugs: - Answers diazoxide, phenytoin, vinblastine, clonidine,
verapamil, and colchicine
One mechanism of stimulated insulin release - Answers 1. in resting cell: normal
(low) ATP levels→ K+ diffuses down its concentration gradient through ATP-gated
K+ channels, maintaining the intracellular potential @fully polarized, negative
level→ insulin release is minimal
2. if glucose concentration rises → ATP production increases → K+ channels close --
> depolarization results → in muscle/nerve voltage-gated Ca2+ channels open in
response to depolarization --> allows more Ca2+ to enter cell --> increased
intracellular Ca2+ results in increased insulin secretion → insulin secretagugues close

,the ATP-dependent K+ channel→ depolarizes membrane→ increased insulin release
by same mechanism
Effects of insulin - Answers - Promotes the storage of fat as well as glucose (both
sources of energy) within specialized target cells & influences cell growth and the
metabolic functions of a wide range of tissues
-Promotes synthesis and storage of glycogen, triglycerides, and protein in its major
target tissues: liver, fat, and muscle. Release of insulin from pancreas is stimulated by
increased blood glucose, incretins, vagal nerve stimulation, and other factors.
Endocrine Effects of Insulin - Answers LIVER:
-Reversal of Catabolic features of insulin deficiency:
1. inhibits glycogenolysis
2. inhibits conversion of fatty acids & amino acids to keto acids
3. inhibits conversion of amino acids to glucose
-Anabolic action:
1. promotes glucose storage as glycogen (induces glucokinase & glycogen synthase,
inhibits phosphorylase)
2. increases triglyceride synthesis & very-low-density lipoprotein formation
MUSCLE:
- Increased protein synthesis
1. increases amino acid transport
2. Increases ribosomal protein synthesis
- Increased glycogen synthesis
1. increases glucose transport
2. induces glycogen synthase & inhibits phosphorylase
ADIPOSE TISSUE:
- Increased triglyceride storage
1. Lipoprotein lipase is induced & activated by insulin to hydrolyze triglycerides from
lipoproteins
2. Glucose transport into cell provides glycerol phosphate to permit esterification of
fatty acids supplied by lipoprotein transport
3. Intracellular lipase is inhibited by insulin
glucagon definition - Answers the hyperglycemic factor that mobilizes glycogen
stores
Glucagon synthesis - Answers in the alpha cells of the pancreatic islets of Langerhans
Glucagon characteristics - Answers -Peptide (identical in ALL mammals) consisting
of single chain of 29 amino acids
- Degraded in the liver and kidney as well as in plasma and at its tissue receptor
-half-life is between 3-6 months
Effects of Glucagon - Answers 1. 1st six amino acids at the amino terminal of
glucagon molecule bind to Gs protein-coupled receptors on liver cells -->leads to
increase in cAMP --> facilitates catabolism of stored glycogen --> increases
gluconeogenesis and ketogenesis
2. Immediate pharmacological result of glucagon infusion -->raise blood glucose by
using stored hepatic glycogen
3. NO effect on skeletal muscle glycogen because of lack of receptors
4. Pharmacological amounts of glucagon cause release of insulin from normal
pancreatic beta cells, catecholamines from pheochromocytoma, and calcitonin from
medullary carcinoma cells

, 5. Has potent inotropic and chronotropic effect on heart, mediated by the cAMP
mechanism → produces effect similar to B-adrenergic agonists without requiring
functioning B-receptors
6. LARGE doses of glucagon produce profound relaxation of the intestine
Uses of Glucagon - Answers 1. Emergency treatment of severe hypoglycemic
reactions due to insulin therapy when pt is unable to self-administer oral glucose and
IV glucose treatment is not possible
2. IV, IM, sub Q, or nasal powder
3. Main adverse effect is nausea/vomiting so place unconscious pt on side after
administration
4. Beta blocker overdose to increase cAMP
5. In endoscopic procedure to relax sphincter of Oddi
Contraindications of Glucagon - Answers a. Pheochromocytoma → can cause release
of catecholamines and increase BP
b. Patients with insulinoma→ can cause rebound hypoglycemia
Different types of insulin - Answers Short-acting: Regular insulin and rapidly acting
insulin analog
Long-Acting Insulin: NPH, Insulin Glargine, Insulin Detemir, insulin degludec, and
mixture insulin
Short-Acting insulin - Answers 1. Regular: short-acting, soluble crystalline zinc
insulin. Hypoglycemic effect appears within 30 mins after SubQ injection
-Peak @ 2hrs
-Duration: 5-7hrs
- If inpatient needing infusion: regular is used for diabetic ketoacidosis and during
perioperative glucose management
2. Rapidly acting insulin analogs: (1)Insulin lispro (Humalog), (2)Insulin aspart
(Novolog, Admelog, FiAsp), (3) Glulisine (Apidra)
- Peak @ around 1 hr
- Duration: 3-4hrs
- Optimal times for administration: Rapid - 15 mins before meal; Regular - 45 mins
after meal
-Uses: Rapidly acting insulin is choice for insulin pumps
Long-Acting insulin - Answers 1. NPH (Neutral protamine Hagedorn, or isophane):
Humulin N, Novolin N
Intermediate-acting
-Onset: 2-4hrs
- Peak @ 6-7hrs
- Duration: 10-20hrs
-Its usually mixed with regular, lispro, aspart, or glulisine insulin
- Given 2-4 times a day
- Smaller doses have lower, earlier peaks and short duration of action vs. larger doses
(converse)
2. Insulin Glargine: soluble "peakless"; long-acting: Lantus, Toujeo, Sanofi Avents;
Basaglar, Lilly
- Low, continuous level of circulating insulin
- Onset: slow (0.5 - 1hr)
- Duration: 24hrs
- Given once daily
- Formulation is high acidic (pH 4) so can't mix with other insulins
3. Insulin Detemir: Levemir

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