Northeastern University
2350 Integrated Pathophysiology and Pharmacology
Final Exam Study Guide
Overview: The Final Exam will cover both NEW and Cumulative content. The focus of this study guide is an overview of
the NEW content only. For a review of cumulative content, please reference your study guides prepared for Exams 1, 2
and 3.
New Content Overview: Modules covered include 9, 10 and 11
Test Composition: 75 questions, multiple choice, select all that apply
Note: New content will be covered in 45 questions, cumulative content will be covered in the remaining 30 questions.
Study Tips:
How to study Pathophysiology
● There are many different diseases, illnesses and syndromes you will be learning about this semester. When you look
at these different diseases a helpful structure to review is to consider the following for each disease process:
o Pathophysiology: What normal process of the body is being disrupted and how? What is the course of the
disease, acute vs. Chronic, etc.? Other things to consider: prognosis, morbidity and mortality.
o Manifestations: What will I see/what will a person with this disease experience? Signs/symptoms
o Treatments: Can this be treated? Possible medications reviewed for treatment and other nonpharm treatments.
How to study Pharmacology
● There are many different drugs and drug classes that are covered throughout this semester. It can be challenging to
determine what is need to know versus what is nice to know. When you review different drugs and drug classes
consider the following information:
o Mechanism of action: how does it work
o Therapeutic use: what is it used to treat
o Nursing Process: What information do you need to safely give the drug? What information do you need to
know if the drug is working?
o Adverse Effects: What is common and what is high risk?
o Off label: what else might this drug be used for?
● Note on drug names: NCLEX testing will include drug names. Drugs will be listed by generic name only. Knowing
generic names is important as this is the universal language of drug therapy.
o Specific drugs names will be highlighted as prototypes/examples of drugs. You are expected to know these
names.
o Other names might be included on an exam. If this happens, you will see the drug class (broader category)
included in the question prompt.
▪ Drug classes in some cases may be identifiable by naming norms often in the form of a common
suffix. Keep an eye out for this to easily identify drugs as part of drug class.
o Key takeaway: know example/prototype/gold standard drugs, be able to identify drug classes as the broader
identifier in pharmacology.
,Module 9: Endocrine
Module Objectives:
● Describe the role of the endocrine system
● Distinguish between negative and positive feedback:
o Negative feedback – maintains homeostasis. System responds to reduce the effect of the initial
stimulus. Self-regulating
▪ Example:
● Body temp –
o Stimulus: increase in body temp.
o Response: sweating and vasodilation reduce temp back to normal.
● Glucose –
o Stimulus: elevated blood glucose after meal.
o Response: insulin release lowers blood glucose
o Positive feedback – amplifies the change in a system. Pushes the system to further from baseline or
normal. Requires an external interruption
▪ Example:
● Childbirth –
o Stimulus: stretching of cervix during labor.
o Response: releases oxytocin increases uterine contractions, further stretching
cervix.
o Cycle: intensifies until delivery, then feedback loop stops
● Blood clot –
o Stimulus: a tear in blood vessel.
o Response: platelets are activated & release chemicals that attract more
platelets to the site.
o Cycle: continues until clot is formed and bleeding stops
● Examine the pathophysiology of the pituitary gland, the thyroid gland, the pancreas, and the adrenal gland
o Pituitary gland: Master gland – controls other endocrine glands through hormone secretion
▪ Pathophysiology:
● Hyperfunction:
o Acromegaly (excess growth hormone after puberty): Overgrowth of bones
and soft tissues.
o Cushing's Disease: Overproduction of ACTH, leading to excess cortisol.
o Hyperprolactinemia: Excess prolactin causes menstrual irregularities or
infertility.
● Hypofunction:
o Hypopituitarism: Deficiency in one or more pituitary hormones leads to
stunted growth, adrenal insufficiency, or hypothyroidism.
o Diabetes Insipidus: Deficiency of antidiuretic hormone (ADH) causing
polyuria and dehydration.
o Thyroid gland: regulates metabolism through T3 and T4 hormones, controlled by thyroid-
stimulating hormone (TSH) from pituitary
▪ Pathophysiology:
● Hyperthyroidism (Grave’s disease):
, o Overproduction of thyroid hormones leads to increased metabolism,
tachycardia, heat intolerance, weight loss
o Causes goiter & exophthalmos (protruding eyes)
● Hypothyroidism (Hashimoto’s Thyroiditis):
o Autoimmune destruction reduces thyroid hormone levels, causing lethargy,
weight gain, cold intolerance, and bradycardia.
o Myxedema in severe cases: life-threatening hypothyroidism.
o Pancreas gland: has endocrine & exocrine glands. It’s islets of Langerhans secrete hormones
▪ Beta cells – insulin (lowers glucose)
▪ Alpha cells – glucagon (raises glucose)
▪ Pathophysiology:
● DM Type 1 (3 P’s)
o Autoimmune destruction of beta cells = insulin deficiency = hyperglycemia,
polyuria, polydipsia, polyphagia
● DM Type 2
o Insulin resistance in tissue = chronic hyperglycemia, weight gain, long-term
complications (neuropathy, nephropathy, retinopathy)
● Pancreatitis
o Inflammation impairs insulin production = secondary diabetes
● Hypoglycemia
o Excess insulin secretion = dangerously low blood sugar
o Adrenal gland:
▪ Cortex: cortisol (stress hormone), aldosterone (regulates NA+/K+), androgens
▪ Medulla: epinephrine & norepinephrine for fight or flight response
▪ Pathophysiology:
● Adrenal insufficiency (Addison’s Disease)
o Autoimmune destruction of the cortex causes cortisol and aldosterone
deficiency
o Symptoms: HypoTN, hyperkalemia, hyponatremia, fatigue, weight loss,
hyperpigmentation
● Hyperfunction
o Cushing’s Syndrome
▪ Excess cortisol = moon face, truncal obesity, hyperglycemia, striae
● Describe the medications used to treat diabetes mellitus (DM), thyroid disorders, alterations in antidiuretic
hormone (ADH), and adrenal disorders including mechanisms of action and key nursing consideration
o Diabetes Mellitus (DM)
▪ Medications for Type 1 DM:
● Insulin (e.g., rapid-acting, short-acting, intermediate-acting, long-acting):
● MOA: Replaces endogenous insulin to regulate blood glucose levels by promoting
glucose uptake into cells.
● Nursing Considerations:
o Monitor blood glucose levels before administration.
o Teach proper injection technique and rotation of injection sites.
o Watch for signs of hypoglycemia (e.g., sweating, confusion).
▪ Type 2 DM
● Biguanides (e.g., Metformin):
● MOA: Decreases hepatic glucose production and increases insulin sensitivity in
tissues.
, ● Nursing Considerations:
o Monitor for GI upset and lactic acidosis (rare but serious).
o Avoid in patients with renal impairment.
o Thyroid Disorders
▪ Hypothyroidism:
● Levothyroxine (Synthroid)
● MOA: Synthetic form of T4, converted to T3 in the body, normalizing thyroid
hormone levels.
● Nursing Considerations:
o Take on an empty stomach, 30–60 minutes before breakfast.
o Monitor TSH levels regularly.
o Teach the patient to report symptoms of hyperthyroidism (e.g., palpitations,
anxiety).
▪ Hyperthyroidism:
● Methimazole (Tapazole) or Propylthiouracil (PTU):
● MOA: Inhibits thyroid hormone synthesis.
● Nursing Considerations:
o Monitor for agranulocytosis (e.g., fever, sore throat).
o PTU is preferred during pregnancy.
▪ Beta-Blockers (e.g., Propranolol):
● MOA: Reduces adrenergic symptoms (e.g., tachycardia, anxiety).
● Nursing Considerations:
o Monitor heart rate and blood pressure.
o ADH – Alterations in antidiuretic hormone (ADH)
▪ Diabetes Insipidus (ADH Deficiency):
● Desmopressin (DDAVP)
o Mechanism of Action: Synthetic ADH; reduces urine output by increasing
water reabsorption in the kidneys.
o Nursing Considerations:
▪ Monitor for water intoxication (e.g., headache, confusion).
▪ Assess daily weights and urine output.
▪ SIADH (ADH Excess):
● Demeclocycline
● MOA: Reduces kidney sensitivity to ADH, increasing urine output.
● Nursing Considerations:
o Monitor for nephrotoxicity.
o Ensure adequate hydration.
o Adrenal Disorders
▪ Adrenal Insufficiency (Addison’s Disease):
● Hydrocortisone, Prednisone:
● MOA: Replace cortisol to manage stress and maintain glucose metabolism.
● Nursing Considerations:
o Take with food to reduce GI upset.
o Do not stop abruptly; taper to avoid adrenal crisis.
2350 Integrated Pathophysiology and Pharmacology
Final Exam Study Guide
Overview: The Final Exam will cover both NEW and Cumulative content. The focus of this study guide is an overview of
the NEW content only. For a review of cumulative content, please reference your study guides prepared for Exams 1, 2
and 3.
New Content Overview: Modules covered include 9, 10 and 11
Test Composition: 75 questions, multiple choice, select all that apply
Note: New content will be covered in 45 questions, cumulative content will be covered in the remaining 30 questions.
Study Tips:
How to study Pathophysiology
● There are many different diseases, illnesses and syndromes you will be learning about this semester. When you look
at these different diseases a helpful structure to review is to consider the following for each disease process:
o Pathophysiology: What normal process of the body is being disrupted and how? What is the course of the
disease, acute vs. Chronic, etc.? Other things to consider: prognosis, morbidity and mortality.
o Manifestations: What will I see/what will a person with this disease experience? Signs/symptoms
o Treatments: Can this be treated? Possible medications reviewed for treatment and other nonpharm treatments.
How to study Pharmacology
● There are many different drugs and drug classes that are covered throughout this semester. It can be challenging to
determine what is need to know versus what is nice to know. When you review different drugs and drug classes
consider the following information:
o Mechanism of action: how does it work
o Therapeutic use: what is it used to treat
o Nursing Process: What information do you need to safely give the drug? What information do you need to
know if the drug is working?
o Adverse Effects: What is common and what is high risk?
o Off label: what else might this drug be used for?
● Note on drug names: NCLEX testing will include drug names. Drugs will be listed by generic name only. Knowing
generic names is important as this is the universal language of drug therapy.
o Specific drugs names will be highlighted as prototypes/examples of drugs. You are expected to know these
names.
o Other names might be included on an exam. If this happens, you will see the drug class (broader category)
included in the question prompt.
▪ Drug classes in some cases may be identifiable by naming norms often in the form of a common
suffix. Keep an eye out for this to easily identify drugs as part of drug class.
o Key takeaway: know example/prototype/gold standard drugs, be able to identify drug classes as the broader
identifier in pharmacology.
,Module 9: Endocrine
Module Objectives:
● Describe the role of the endocrine system
● Distinguish between negative and positive feedback:
o Negative feedback – maintains homeostasis. System responds to reduce the effect of the initial
stimulus. Self-regulating
▪ Example:
● Body temp –
o Stimulus: increase in body temp.
o Response: sweating and vasodilation reduce temp back to normal.
● Glucose –
o Stimulus: elevated blood glucose after meal.
o Response: insulin release lowers blood glucose
o Positive feedback – amplifies the change in a system. Pushes the system to further from baseline or
normal. Requires an external interruption
▪ Example:
● Childbirth –
o Stimulus: stretching of cervix during labor.
o Response: releases oxytocin increases uterine contractions, further stretching
cervix.
o Cycle: intensifies until delivery, then feedback loop stops
● Blood clot –
o Stimulus: a tear in blood vessel.
o Response: platelets are activated & release chemicals that attract more
platelets to the site.
o Cycle: continues until clot is formed and bleeding stops
● Examine the pathophysiology of the pituitary gland, the thyroid gland, the pancreas, and the adrenal gland
o Pituitary gland: Master gland – controls other endocrine glands through hormone secretion
▪ Pathophysiology:
● Hyperfunction:
o Acromegaly (excess growth hormone after puberty): Overgrowth of bones
and soft tissues.
o Cushing's Disease: Overproduction of ACTH, leading to excess cortisol.
o Hyperprolactinemia: Excess prolactin causes menstrual irregularities or
infertility.
● Hypofunction:
o Hypopituitarism: Deficiency in one or more pituitary hormones leads to
stunted growth, adrenal insufficiency, or hypothyroidism.
o Diabetes Insipidus: Deficiency of antidiuretic hormone (ADH) causing
polyuria and dehydration.
o Thyroid gland: regulates metabolism through T3 and T4 hormones, controlled by thyroid-
stimulating hormone (TSH) from pituitary
▪ Pathophysiology:
● Hyperthyroidism (Grave’s disease):
, o Overproduction of thyroid hormones leads to increased metabolism,
tachycardia, heat intolerance, weight loss
o Causes goiter & exophthalmos (protruding eyes)
● Hypothyroidism (Hashimoto’s Thyroiditis):
o Autoimmune destruction reduces thyroid hormone levels, causing lethargy,
weight gain, cold intolerance, and bradycardia.
o Myxedema in severe cases: life-threatening hypothyroidism.
o Pancreas gland: has endocrine & exocrine glands. It’s islets of Langerhans secrete hormones
▪ Beta cells – insulin (lowers glucose)
▪ Alpha cells – glucagon (raises glucose)
▪ Pathophysiology:
● DM Type 1 (3 P’s)
o Autoimmune destruction of beta cells = insulin deficiency = hyperglycemia,
polyuria, polydipsia, polyphagia
● DM Type 2
o Insulin resistance in tissue = chronic hyperglycemia, weight gain, long-term
complications (neuropathy, nephropathy, retinopathy)
● Pancreatitis
o Inflammation impairs insulin production = secondary diabetes
● Hypoglycemia
o Excess insulin secretion = dangerously low blood sugar
o Adrenal gland:
▪ Cortex: cortisol (stress hormone), aldosterone (regulates NA+/K+), androgens
▪ Medulla: epinephrine & norepinephrine for fight or flight response
▪ Pathophysiology:
● Adrenal insufficiency (Addison’s Disease)
o Autoimmune destruction of the cortex causes cortisol and aldosterone
deficiency
o Symptoms: HypoTN, hyperkalemia, hyponatremia, fatigue, weight loss,
hyperpigmentation
● Hyperfunction
o Cushing’s Syndrome
▪ Excess cortisol = moon face, truncal obesity, hyperglycemia, striae
● Describe the medications used to treat diabetes mellitus (DM), thyroid disorders, alterations in antidiuretic
hormone (ADH), and adrenal disorders including mechanisms of action and key nursing consideration
o Diabetes Mellitus (DM)
▪ Medications for Type 1 DM:
● Insulin (e.g., rapid-acting, short-acting, intermediate-acting, long-acting):
● MOA: Replaces endogenous insulin to regulate blood glucose levels by promoting
glucose uptake into cells.
● Nursing Considerations:
o Monitor blood glucose levels before administration.
o Teach proper injection technique and rotation of injection sites.
o Watch for signs of hypoglycemia (e.g., sweating, confusion).
▪ Type 2 DM
● Biguanides (e.g., Metformin):
● MOA: Decreases hepatic glucose production and increases insulin sensitivity in
tissues.
, ● Nursing Considerations:
o Monitor for GI upset and lactic acidosis (rare but serious).
o Avoid in patients with renal impairment.
o Thyroid Disorders
▪ Hypothyroidism:
● Levothyroxine (Synthroid)
● MOA: Synthetic form of T4, converted to T3 in the body, normalizing thyroid
hormone levels.
● Nursing Considerations:
o Take on an empty stomach, 30–60 minutes before breakfast.
o Monitor TSH levels regularly.
o Teach the patient to report symptoms of hyperthyroidism (e.g., palpitations,
anxiety).
▪ Hyperthyroidism:
● Methimazole (Tapazole) or Propylthiouracil (PTU):
● MOA: Inhibits thyroid hormone synthesis.
● Nursing Considerations:
o Monitor for agranulocytosis (e.g., fever, sore throat).
o PTU is preferred during pregnancy.
▪ Beta-Blockers (e.g., Propranolol):
● MOA: Reduces adrenergic symptoms (e.g., tachycardia, anxiety).
● Nursing Considerations:
o Monitor heart rate and blood pressure.
o ADH – Alterations in antidiuretic hormone (ADH)
▪ Diabetes Insipidus (ADH Deficiency):
● Desmopressin (DDAVP)
o Mechanism of Action: Synthetic ADH; reduces urine output by increasing
water reabsorption in the kidneys.
o Nursing Considerations:
▪ Monitor for water intoxication (e.g., headache, confusion).
▪ Assess daily weights and urine output.
▪ SIADH (ADH Excess):
● Demeclocycline
● MOA: Reduces kidney sensitivity to ADH, increasing urine output.
● Nursing Considerations:
o Monitor for nephrotoxicity.
o Ensure adequate hydration.
o Adrenal Disorders
▪ Adrenal Insufficiency (Addison’s Disease):
● Hydrocortisone, Prednisone:
● MOA: Replace cortisol to manage stress and maintain glucose metabolism.
● Nursing Considerations:
o Take with food to reduce GI upset.
o Do not stop abruptly; taper to avoid adrenal crisis.
