The purpose of this course is to give students interested in health care professions a solid, general background in pathophysiology. This course will focus on understanding abnormal function in diseased states in association with the body’s healing responses.

Pathophysiology will examine what happens when the body is not working the way it is supposed to. We will cover various physiological systems of the body in an integrated fashion and examine general mechanisms of disease within each system as well as selected diseases. For each category of pathology covered, we will examine its causes, effects, symptoms, diagnosis, and treatment(s). In the case of treatments, if this is covered, minor attention will be given to the pharmacological basis of the drug’s actions or procedural treatments. This course focuses on the theoretical aspects of medicine, not the clinical ones.

Required Text: “Pathophysiology: Introductory Concepts and Clinical Perspectives”, 3rd edition, Capriotti and Frizzell, F.A. Davis Publishers, ISBN-13: 978-1-7196-4859-2.

Computer/Internet: This course emphasizes proficiency with computers, word processing, the internet, email, working with .pdf files, and especially SUU’s Canvas System. Assignments will be submitted, and quizzes/tests MAY be taken via Canvas if necessary. Students are expected to utilize personal computers or student computer labs on campus to complete assignments. Planning is essential and “computer problems” is not an acceptable excuse for not completing an assignment by the due date.

Pre-Requisites: Minimum grades of “C” earned in BIOL 1610, BIOL 2320/2325 and BIOL 2420/2425. 

There are many factors that will affect your grade in this class. The most important things are:

Early exams will only be given for SUU-sanctioned events or documented emergencies. If you miss an exam, quiz, or final without an approved excuse, you may earn a zero. Excused absences require a letter from a coach/instructor prior to the absence or documentation from a certified medical professional within one day of return. Make-ups must occur within three school days.

A= 92.45–100% 
A-= 89.45–92.44% 
B+= 86.45–89.44% 
B= 82.45–86.44% 
B-= 79.45–82.44% 
C+= 76.45–79.44% 
C= 72.45–76.44%
C-= 69.45–72.44%
D+= 66.45–69.44%
D= 62.45–66.44%
D-= 59.45–62.44%
F= less than 59.45%

If you miss an exam, quiz, or final exam, there are no provisions for make ups. If there is a documentable excuse for missing a graded activity, you must contact me as soon as possible regarding the absence. Contacting me about it does not guarantee that accommodations will or can be made for you. The only type of excused absence is one sanctioned by university activities such as sports or academic field trips. Excused absences require a letter from a coach/instructor prior to the absence.

Make-ups must be within 3 school days. If an emergency arises and you miss an exam, a certificate signed by a certified medical professional with diagnostic AND prescriptive powers (M.D., D.O., N.P., P.A.) or a documented family emergency provided within one day of return to campus are the only acceptable excuses for missing a lab/graded activity unless prior arrangements are made. A note from an employer, friend, or family member is not valid unless that person saw you in a professional, diagnostic capacity. Students that miss lecture due to an SUU sponsored event will be dealt with on a case-by-case basis.

If you are in the military and have an official exercise that may cause you to miss class, please see me immediately as this is a vital and valid reason for missing class also. See me if you fall into any of these categories.

Vacation, a honeymoon, or leaving town early before the semester is over is not an acceptable excuse for missing an exam, quiz, or class.

Additional Information:

Academic Dishonesty Policy: Scholastic dishonesty will not be tolerated. You are expected to have read and understand the current issue of the Student Handbook (published by Student Affairs) regarding student responsibilities and rights, and for the intellectual property policy, information about procedures, and what constitutes acceptable behavior. You should also be familiar with SUU’s Academic Integrity Policy #6.33. If you are found guilty of any form of Academic dishonesty, I will fully prosecute you according to SUU’s policy.

You must be logged in and visible on Zoom for every graded activity that may be conducted online or you will earn a zero for it.

I will treat emergencies on a case-by-case basis: As this semester progresses, if you must miss class, please contact me so that we can arrange for you to deal with what you have missed because of your absence if possible. If you have any issue at all, please contact me so that we can discuss how to best proceed and succeed in this course. I will do everything in my power for your experience in this class to be a fair, equitable, and rewarding one. Please note, however, I will never allow you to do anything that would give you a distinct advantage for a better grade over the other students enrolled in my courses. My goal here is to keep this as simple, fair, and honest as possible.
You are responsible for any information missed due to absence. An absence from a class does not excuse you from the class work that you missed, or from an exam. You will not get a good grade if you miss class or aren’t actively engaged while here. It is your responsibility to get the information you missed from a classmate.

The PowerPoints that are used during lecture class are not lecture notes. The slides are an outline to use to organize topics in your notebook, get proper spelling of terms, etc. Just writing down the words on the slides will not give you adequate information to pass this class.

After exam grades are released, students will have until the day of the next exam to review their test during office hours. After the next exam occurs, old tests are destroyed. You will not have the opportunity to review the old exam once the new one has taken place. I highly encourage all of you to review your tests and to get feedback on them with me after receiving your grade. Everyone should pick up their exam paper and check the grades on the paper with what is in Canvas.

You are expected to write and speak in standard English for all classroom related activities. 

DO NOT USE YOUR COMPUTERS AND PHONES TO MESS AROUND AND NOT PAY ATTENTION. You are here to learn. Staying focused on the lecture will enhance the likelihood that you will earn a grade you will be happy with. Staying focused on the live instruction will also enhance your sense of connectedness and community with me and your peers that are enrolled in this course with you. I WILL call you out in class if you are sleeping, talking, or not paying attention. When this happens it will be an awkward and intimidating event for all of us, me included. Avoid it.

Tentative Course Schedule – Fall 2025 Semester:
The information listed here is subject to change at the discretion of the instructor.

A more detailed schedule is available on Canvas. The dates for readings, quizzes, and assignments will be assigned as we maneuver through the course. This course has a discussion component to it so the speed at which we move through our material will depend on our discussions, Q and A sessions, etc…

Pay attention to all course announcements and emails for final dates and information regarding this course.

Chapter 1: The Cell in Health and illness
Chapter 2: Cellular Injury, Adaptations, and Maladaptive Changes
Cardiovascular Pathophysiology: Selected sections of Chapters 14-19, other selections in the book
Chapter 7 Fluid and Electrolyte Imbalances
Chapter 8 Acid-Base Imbalances

Readings from our required textbook and other primary research papers will be assigned throughout the semester and will be used to learn the information covered in lecture in more depth. Consider these readings part of our course content/course schedule. Most of these readings are already posted, and their due dates will be announced well before you are tested on them. Your quizzes and exams will contain information from these readings. Consider these readings part of our course content/course schedule. 

We will be using a discussion-based approach to this class. Based on the questions you have, and the experience you already have in the medical field, we will loop in other systems and pathologies to hi-light how these foundational concepts and systems are intertwined  and interdependent on one another within the human body in health and disease.  

Final Exam: Thursday December 11: 11:00-12:50 pm, SC 016

Textbook Readings: These readings will be assigned this semester based on how fast we move through our lecture material. Assigned readings will be announced in class.

Selected Readings to reinforce learning material: Unit 1

Pgs. 164-166: Tissue Repair and Wound Healing, Normal Wound Healing
• Be able to state the stages and types of wound healing and tissue repair.
• Be able to relate this to the process of “fibrosis”.
• Can you relate this process to the different types of cells in the body?
• Labile vs. Stable vs. Permanent?
• What types of tissues are featured in this reading passage? WHY are these tissues featured based on the type of cells (see the above bullet point) from which they are built?
• Please pay attention to the bolded words in this section. Be sure that you can define/describe/explain them.

Pgs. 581-583: Basic concepts of Endocrine Control
• Please pay attention to the bolded words in this section. Be sure that you can define/describe/explain them.
• Be able to explain the basic anatomy and physiology of the hypothalamus and pituitary gland as it is described in this reading section.
• Be able to state the hormones released by the anterior and posterior pituitary, as described in this reading section.
• Specific feedback loops are described in this reading passage (under “The Feedback System), as well as regulation of these hormones released by the pituitary.
• Prednisone is a powerful glucocorticoid drug that is often prescribed to patients to reduce inflammation in several different types of pathologies, and to suppress the immune system also.

Examples of conditions that are commonly treated with Prednisone or a similar drug include:
• hormonal disorders.
• skin diseases and rashes.
• autoimmune pathologies such as arthritis, lupus, and allergic conditions.
• digestive pathologies such as ulcerative colitis and Crohn's disease.
• lung diseases such as asthma, bronchitis, tuberculosis, and pneumonia.
• CNS swelling from a brain tumor or injury.
• Under “Regulation of Endocrine Receptors,” be able to explain the difference between “upregulation” and “downregulation” and how a patient’s ACTH/pituitary feedback loop will be affected if that patient has been taking prednisone for a long period of time (a week or more).

Pgs. 723-740: Select Gastrointestinal disorders
• Pgs. 723-724: Epidemiology of GERD, PUD, gastroenteritis.
• 724-725: Basic concepts of esophageal, stomach, and small intestine function: This is a review of the concepts you learned in physiology.
• SKIP TO pg. 731: Gastroesophageal Reflux Disease: Read up to Clinical Presentations (stop before you get to this).
• SKIP TO pg. 738: Peptic Ulcer Disease:  After reading through the etiology (can you define this word?), pathophysiology, clinical presentation, diagnosis, treatment, and complications of this pathology, can you list the different diagnostic methods used to determine whether a patient has PUD and identify and explain which of those uses a pathognomonic change to diagnose the presence or absence of PUD?

Pgs. 522-523: Environmental Lung Disorders: Coal Worker’s Pneumoconiosis, Asbestosis, Silicosis
• Describe the causes and manifestations (what does a victim of each pathology have in terms of their signs and symptoms?) of these pathologies.
• Which one of the three is the best example of a pathognomonic change occurring?
• Which increases the likelihood of tuberculosis infection?
• Which increases the likelihood of mesothelioma?
• What IS mesothelioma?
• Why is mesothelioma considered an adaptation of cells trying to adapt?
• Be able to state what types of people are more likely to develop these pathologies.?

Pgs. 781-803: Chapter 31: Infection, Inflammation, and Cirrhosis of the liver
• 781-785: Epidemiology and basic functions of the liver.
• Be able to name and describe 7 important functions of the liver.
• 786-787: Hyperbilirubinemia and Jaundice, Hepatocyte Inflammation and Infection, Non-Alcoholic Fatty Liver Disease.
• Be able to define what hyperbilirubinemia is, where bilirubin comes from, and how this causes jaundice.
• Be able to define what the GENERAL term “hepatitis” is.
• Be able to explain the different causes of hepatitis.
• You should SKIP Bile duct obstruction completely (787-789).
• 789-803: Select Pathophysiological disorders of the Liver: Stop at Biliary Cirrhosis, you don’t need to do that one.
• For all the Hepatitis viruses, you only need to know the introductory paragraphs below each of them. Don’t go any further than that.
• For Nonalcoholic Fatty Liver Disease, you only need to read the Pathophysiology of it. Stop at Clinical Presentation.
• Same for Alcoholic Liver Disease. Stop at Clinical Presentation.
• Same for Cirrhosis and end stage liver disease. Stop at Clinical Presentation on pg. 803.

Pgs. 335-339: Pathophysiology of Arterial Disorders
• Hyperlipidemia: stop at “Treatment” on pg. 339.

Pgs. 475-481: Basic Physiological and Pathophysiological Concepts of Respiratory Function
• Review the basic physiological concepts of respiratory function that you learned in your physiology and anatomy courses (475-479).
• Be able to explain what Dyspnea, Cough, Hemoptysis, Atelectasis, and Hypoxia is (479-481).

Pgs. 498-501: Review of Basic Concepts of Pulmonary Structure and Function and Chronic Hypoxia
• Review the basic concepts of pulmonary structure and function that you learned in your physiology and anatomy courses (498-500).
• Describe what Chronic Hypoxia is, as outlined on pg. 501.

Pg 1172-1174: Free Radical Accumulation theory and aging
• Describe the basic concepts of physiological aging.
• Describe what free radicals do to collagen fibers.
• Describe the effect of free radicals on muscles, skin, cartilage, and arteries.
• Describe the overall effect of accumulated damage from free radicals on the body.
 
Pg 1050: the Etiology of Cancer
• All carcinogens have ROS.
• Be able to name several carcinogenic substances/events.
• Be able to explain how ROS damages cells/organelles and causes cancer.

Pgs. 833-843: Basic Pathophysiological Concepts of Cerebrovascular Disorders:
• If you feel that you need to review the anatomy and physiology of the brain, please read the beginning of this chapter (pg. 833-838).
• Be able to explain how each concept that is described causes “scary flow chart” in the brain. (pgs. 839-843).
• Ischemic Stroke: Cerebral Arteriosclerosis, Atrial Fibrillation, Carotid Stenosis, Ischemia and Ischemic Penumbra, Glutamate Toxicity, Transient Ischemic Attack.
• Hemorrhagic Stroke.
• Pay particular attention to the bolded words in each section.

Pg 382-384: Reperfusion Injury in MIs
• Be able to explain what a MI is.
• Be able to explain how it may cause reperfusion injury and how that injures cardiac muscle tissue.
• Be able to explain what “myocardial stunning” is.

Pg 1160-1164: Hearing loss in older adults
• If you need to review/learn the basic anatomy and physiology of the ear, please review this from pgs.1160-1162.
• Be able to explain how natural hearing loss in older adults is an example of a physical injury to cells, and how it can happen in younger people in their day to day lives.

1177-1178: How aging effects, the Gastrointestinal System
• What is gastric atrophy?
• Explain how gastrointestinal changes because of aging can be linked to the development of anemia, dementia, paresthesias (do you know what this word means?), and gait disturbances (do you know what this means?).

Pg 1131: Hypertrophic Scarring
• What is a keloid and how do they often form (most common cause for their formation)?
• Be able to name and explain 3 therapies/treatments to slow down/stop their formation.

Pgs. 452-453: Hypertrophic Cardiomyopathy
• Please review the anatomy of the heart.
• What is HCM?
• How and why does HCM differ from ventricular hypertrophy that is caused by hypertension?
• Name 3 types of meds and 4 invasive surgical treatments for this pathology.
• Based on what we have covered in lecture, can you explain why the invasive surgical treatments for this pathology only work because they kill cardiac tissue?

Pg 593-594: Goiter
• What is the difference between common goiter formation and non-toxic goiter formation?
• What cellular adaptation occurs when goiters form?

Pg 731: Gastrointestinal Reflux Disease
• What are 2 potential causes of reflux disease?
• Be able to define gastroparesis, Barrett’s esophagus, and dyspepsia.
• Why is diagnosis of this category of pathology considered a pathognomonic change?

Pg 1068-1069: Cervical Cancer
• Etiology: what are the two most common/significant causes of this pathology?
• Pathophysiology: define the term “squamous intraepithelial lesions.”
• CIN ratings? Which rating has the best prognosis? Which has the poorest? Can you relate this to what we discussed in lecture about these  cellular changes/adaptations?

Pg 1050-1052: Cancer, some of this was assigned earlier in the semester, but some is new.
• Etiology: How is ROS considered a major cause of cancers?
• Please review the cell cycle.
• Cancer Genetics: What is the TP53 gene? Why is it so important? Why is it called “the guardian of the genome?”
• What does a defective TP53 gene do to cells that have it?
• Explain how cellular proliferation and apoptosis must be balanced within a tissue to prevent neoplasias.

Pg 1172-1173: Programmed aging of the cell, some of this was assigned earlier, but some is new
• Be able to explain the following words, and how they relate to what we have discussed in lecture: apoptosis, telomeres, telomerase.
• How could/does telomerase affect apoptosis?

Pg 871-873 Parkinson’s disease
• Which cells go through uncontrolled excessive apoptosis when this pathology develops?
• In addition to the loss of cells described above, can you explain what accumulates in brain tissue when this pathology develops?

Below is a link to a research article. While some of the things discussed in this article are not relevant to what we do in our lecture, this is an excellent resource for review and “tying the concepts together” in terms of apoptosis and necrosis. Please either go to this article using the link below or download/read it from our Canvas page. A pdf of it can be found in a module on our Canvas page.

https://portlandpress.com/bioscirep/article/39/1/BSR20180992/191/Apoptosis-and-apoptotic-body-disease-message-and

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Selected Readings to reinforce learning material for Cardiovascular lectures: Unit 2
As you are going through these readings, pay particular attention to other systems and organs that are profoundly affected by cardiovascular pathologies, or that could cause disease in the cardiovascular system due to pathologies in themselves. The reason that we are using the cardiovascular system as an anchor point for this class is because every system/organ/tissue/cell is dependent on the proper functioning of this system for its own normal physiology. When there is an issue with the heart and vasculature in the body, it will predispose a patient to other pathologies, and vice versa.

Pgs. 329-335: Review of anatomy/physiology of blood vessels
• Be able to define/explain the following terms:
    • Arteries
    • Endothelium
    • Arteriosclerosis
    • Atherosclerosis
    • Tunica intima, Tunica media, Tunica externa
    • Nitric oxide, Endothelin, VEGF
    • Cardiac output (CO or Q)
    • Explain how blood flow is regulated
    • Laminar blood flow vs. turbulent blood flow
    • HTN and changes to blood vessel walls as a result
    • Distension
    • Compliance
    • Blood Pressure Regulation
    • Systole
    • Diastole
    • Stroke Volume
    • The ONLY equation you need to be responsible for explaining in detail is Q=HRxSV
    • Baroreceptors
    • RAAS
    • Natriuresis (we will cover this in more detail in the last 1/3 of the semester)
    • The effects of Blood composition on Arteries
    • Lipids: Cholesterol, LDL, HDL
    • Glucose, glycosylation
    • Free radicals

Pgs. 335-337: Hyperlipidemia
• How does the liver make cholesterol?
• How does the body transport it, deposit it, and return it to the liver if necessary?
• What is “reverse cholesterol transport?”
• Stop at “Clinical Presentation” on pg. 337.

Pgs. 348-351: Atherosclerosis
• All of it, stop at “Manifestations” on pg. 351.

Pgs. 339-348: Hypertension, a major risk factor for CAD and other types of cardiovascular pathologies
• Primary HTN vs. Secondary HTN: what’s the difference, which is more common?
• Risk factors for HTN: you should be able to see how the risk factors for this are heavily intertwined with the risk factors for other serious cardiovascular pathologies.
• Pathophysiology of HTN.
• Complications of HTN. Again, be able to see how the complications of HTN are heavily intertwined with other serious cardiovascular pathologies.

Pgs. 356-359: Aneurysm and Aortic dissection
• Be able to describe the etiology, risk factors, pathophysiology of aneurysms, the types of aneurysms. Stop at “Clinical Presentations,” pg. 357.
• Aortic Dissection: same as aneurysms. Stop at “Clinical Presentations,” pg. 358.

Pgs. 370-374/75: Review of heart anatomy and physiology
• Everything described in these pages is material learned in pre-requisite physiology courses and is essential to understanding cardiac pathologies.

Pgs. 375-378: Selected Pathophysiological Disorders of the heart
• What is “Acute Coronary Syndrome?”
• Be able to describe what chronic stable angina is, and what unstable angina is. Chronic stable angina is also discussed briefly in a paragraph on pg. 382.
• Based on what you learned in physiology, how does angina relate to the Law of Projection and Referred Pain? Looking at figure 16-13 on pg. 378 should be helpful for this.
• What are “anginal equivalents” and why is it so important to recognize them?
• As usual, stop at “Clinical Presentations” on pg. 377.
• State the 5 different pathophysiological processes by which cardiac muscle cells can suffer ischemia and lack of sufficient oxygen, leading to UA, pg. 377.

Pgs. 382-386: Acute Myocardial Infarction
• In addition to all the text (including clinical presentationdiagnosis), pay particular attention to the “diagnosis” section that explains how elevated cardiac enzymes occur because of an MI?
• Stop at “Treatment” on pg. 386.

Chapter 17: Heart Failure
• Pgs. 400-403: review of cardiac physiology
• Be able to explain/define these terms:
    • Q (CO)
    • HR
    • SV
    • The Frank-Starling Law
    • Afterload
    • Preload
    • Cardiac Contractility
• Stop at “Inotropic vs, Chronotropic Function of the Heart” on pg. 403.

Pgs. 406-408: Review of Cardiovascular Regulatory Mechanisms
• All of these were discussed in your physiology course, or here. You are responsible for understanding how each affects the physiology of the heart.
• RAAS and all its components
• Natriuretic Peptides (we will also cover these in more detail in the last 1/3 of this course)
• Neprilysin
• Endothelin
• TNF-alpha
• NO
• ADH
• ANS regulation

Pgs. 408-413: Basic Pathophysiological concepts of Heart Failure
• There are 4 basic changes to the heart that will lead to the development of heart failure.
• There are 7 etiological conditions that can cause heart failure. Be able to define and explain each of them.

Pg 413: Acute vs. Chronic Heart failure: describe the differences between these pathologies.

Pgs. 414-423: Left Ventricular Heart Failure vs. Right Ventricular Heart Failure: describe these pathologies and how they differ from each other in terms of signs and symptoms
• Stop at “Diagnosis” on page 423.
• Be sure to include Box 17-8 as a nice, condensed study chart of the differences in signs/symptoms of LVF and RVF.

Pgs. 432-433: Making the Connections Chart
• This is another nice, condensed study chart to use when learning the backward and forward effects of LVF and RVF.

Pgs. 389-394: Cardiac Inflammation and Infection
• Pg 389-909 Infective Endocarditis: Be able to explain what this is, based on the first paragraph that describes it.
• Etiology: You do NOT have to know all the distinct types of IE, just be able to explain the most common causes of IE, and the very general different categories of NE because this explains the most common types of patients that present with IE.
• Be able to explain the pathophysiology of IE, paying particular attention to these concepts/terms that are associated with it:
• How do bacterial infections cause inflammation?
• What is “vegetation?”
• What are “septic emboli?”
• Stop at “Clinical Presentations” on pg. 390

Pg 392: Myocarditis: describe what this pathology is, as well as the etiology and pathophysiology of it.

Pgs. 393-394: Pericarditis: Be able to explain what this is. You may skip the epidemiology section.
• Pay particular attention to everything else including the following:
• The pericardial membrane
• The epicardium
• Serous fluid
• Pericardial effusion
• Pulsus paradoxus
• Box 16-7
• Cardiac Tamponade

Pg 119: Sequestered Fluids
• This short paragraph reviews and redefines the concepts of the subcavities found in the ventral body cavities, and the serous membranes/fluids that form these subcavities. You learned this in Anatomy.
    • Be able to define such basic anatomical terms as:
    • Parietal serous membrane
    • Visceral serous membrane
    • Space that is filled with serous fluid (the cavity)
    • Pericardial Cavity
    • Pleural Cavity
    • Peritoneal Cavity
    • Be able to describe the updated terms related to these cavities, as described in this paragraph on pg. 119.
    • Third Space (Third Spacing)
    • Transudate
    • Exudate
    • Effusion

Pgs. 1195-1195: Cardiogenic shock: basic definition
• Shock caused by an acute MI.
• Shock caused by Cardiac Tamponade.

______________________

Chapter 7-8 Textbook readings: Unit 3

Pgs. 801-802: Cirrhosis: discusses decreased albumin synthesis. Can you explain how that affects blood volumes?

pg. 592-593, 1062: SIADH: definition and explanation of what “Syndrome of inappropriate ADH secretion is” and how it affects blood composition and volumes.

Pg 1062; paraneoplastic syndrome and lung cancer, SIADH, box 40-3.

Pgs.  589-590: Diabetes Insipidus: definition? Causes? How does this pathology cause a sodium imbalance in bodily fluids?

Pgs. 594-596, “Alert” box on pg. 596: Severe Hypothyroidism: how does this pathology cause a sodium imbalance in bodily fluids?

Pgs. 523-525: Chapter 22: Renal disorders: basic review of anatomy and physiology of the kidney.

Pgs. 533-536: Basic Pathophysiological concepts of renal disorders; be able to define what these are:
• Pre-Renal pathologies.
• Intra-Renal pathologies.
• Post-Renal pathologies.
Pgs. 536-557: Renal Disorders; be able to define and explain what they are (and nothing more), and if possible classify them as pre-renal, intra-renal, or post- renal.
Pgs. 558-561: Making Connections Chart: at the end of the Chapter: this is an EXCELLENT place to get the info for the above learning objectives. The blue bar that defines each disorder is a great resource for all that you need to learn about these disorders. As you are learning these, can you classify them as pre-renal, intra-renal, or post- renal?

Chapter 25: Diabetes Mellitus and the Metabolic Syndrome: basic definitions of the classifications of Diabetes Mellitus (table 25-1 pg. 613), box 25-2 pg. 620, what is metabolic syndrome?
Pgs. 624-627: Short term acute complications of type-1 diabetes; can you relate these to what we have already covered all semester and what we’re doing now?
        • Polydipsia
        • Polyuria
        • Dehydration from hyperglycemia
        • Electrolyte imbalances
        • Polyphagia
        • Diabetic ketoacidosis
Pgs. 627-629: Short term acute complications of type-2 diabetes; can you relate these to what we have already covered all semester and what we’re doing now?
        • Hyperosmolar Hypoglycemic Syndrome

Pgs. 630-631: Table 25.3 Long term complications of Diabetes Mellitus: