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DM2 Pathopaper 4 Reflection Journal

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Running head: TYPE II DIABETES REFLECTION JOURNAL
Type II Diabetes Mellitus Reflection Journal:
Pathophysiology Paper #4
Kevin Famighetti
Montana State University Billings City College
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Type II Diabetes Mellitus Pathophysiology Description
One definition of Type II diabetes mellitus (DM2) is the inability of the body to produce
or respond to insulin, resulting in abnormal carbohydrate metabolism and increased levels of
blood glucose (BG) and urine glucose. DM2 is indicated when cellular glucose peripheral uptake
decreases as a result of diminished response to insulin (insulin resistance) as well as increased
hepatic glucose production to the point where blood glucose is no longer adequately controlled
(loss of glucose homeostasis - hyperglycemia).
The number 1 contributing factor toward developing or not developing DM2 is lifestyle.
Eating healthy, daily exercise (active lifestyle), maintaining healthy body weight, not drinking
alcohol in excess, not smoking, and not using drugs lower the chances of developing DM2.
Hypertension (HTN), racial genetic predisposition, familial genetic predisposition, age, and
abnormal cholesterol/triglyceride levels are etiological factors associated with DM2. For women,
add gestational diabetes, and polycystic ovary syndrome to the list (Hubert and VanMeter, 2018).
In the early stages of DM2, healthy insulin levels are produced by β-cells, which reside in
clusters of pancreatic cells called islets of Langerhans cells or islet cells (Marieb and Hoehn,
2019). Normal β-cell insulin production and insulin resistance during Pre-DM2 or early DM2 is
important as this pathology distinguishes DM2 From DM1. Later in the disease, insulin
production decreases due to the following process: Chronic or permanent hyperglycemia results
from the previously mentioned diminished response to insulin (the original cause of DM2).
Permanent hyperglycemia causes glucotoxicity, lipotoxicity, and oxidative stress, which, in turn,
causes pancreatic β-cell damage, followed by apoptosis. Once these insulin-producing cells are
gone, they are gone forever (Marieb and Hoehn, 2019). Progressive insulin secretory failure
ensues and, if left unchecked, can lead to total β-cell destruction. This process occurs over time
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and maybe avoided altogether by most DM2 diabetics if glucose levels are controlled early by
adhering to proper diet/exercise, and strict adherence to medication/insulin regimens. One
exception to this chronology may exist with patients who are genetically predisposed with β-cellglucose-homeostasis-variation-hypersensitivity. The small number of patients with this
hypersensitivity experience both increased insulin resistance and decreased β -cell insulin
production early in the disease process. Decreased insulin production results from damage or
destroyed pancreatic β -cells (Marieb and Hoehn, 2019).
Once an absolute insulin deficiency exists, the patient not only carries a diagnosis for
DM2 but one of DM1 as well. They are now totally insulin-dependent even if they drastically
reduce their insulin resistance via significant positive lifestyle changes, such as losing weight,
eating healthy, minimizing salt intake, and exercising regularly. At this point, the fact that DM1
developed via a different pathological route than the traditional route of idiopathic autoimmune
β-cell destruction is irrelevant. Diabetic ketoacidosis (DKA) becomes a genuine possibility with
these DM2/DM1 patients. Absolute or relative insulin deficiency reduces cellular glucose uptake
to the extent that the cells have very little glucose to metabolize for fuel. The cellular glucose
needed to produce ATP is simply not there. When cells are starved for fuel, the liver frantically
breaks down fats into ketone bodies to cover the fuel-gap. Excessive ketone production by the
liver leads to ketone build-up in the blood and urine and drops serum pH to dangerous,
sometimes fatal levels. Insulin does much more than stimulate skeletal and cardiac muscle
glucose uptake. Insulin indirectly reduces cellular lipolysis and proteolysis. In the liver, insulin
promotes glycogenesis, protein, and lipid synthesis (fats to storage when liver glucose levels
exceed amounts needed for energy and glycogen storage). Hepatic insulin simultaneously
inhibits glycogenolysis, ketogenesis (fats to acids), and gluconeogenesis (proteins to glucose).
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Insulin also plays a crucial role in controlling cholesterol levels by suppressing hepatic very-lowdensity-lipoprotein (VLDL) production (Ignatavicius, Workman, and Rebar, 2018). With all of
this in mind, it becomes clear why an absence of insulin results in run-away DKA. Simply
reverse everything just mentioned dramatically - the result is DKA.
As illustrated by its destructive effect on β-cells, the dangers of DM2 are dominated by
chronic hyperglycemia. For reasons we do not yet fully understand, sustained hyperglycemia
causes macrovascular and microvascular changes. These changes lead to numerous
complications stemming from poor tissue perfusion and cell ischemia. Primary among these
pathologic changes are vascular thickening and chronic high blood pressure AKA HTN.
DM2 induced macrovascular changes lead to Congestive Heart Failure (CHF),
Cardiovascular Disease (CVD), and Peripheral Vascular Disease (PVD). CVD of the arteries
supplying the brain leads to Cerebrovascular Disease and Cerebrovascular Accident (CVA),
AKA stroke. All of these involve HTN. C-reactive protein (CRP) levels among diabetics are
often elevated. CRP is an inflammatory marker associated with a higher risk for cardiovascular
inflammation and death (Ignatavicius, Workman, and Rebar, 2018).
The organ systems most susceptible to chronic hyperglycemia caused microvascular
abnormalities are the renal system, CNS, and the eyes. Kidney failure (nephropathy), nerve
dysfunction (neuropathy), and vision problems (retinopathy) are common microvascular
complications.
Hyperglycemic producing microvascular changes are often more destructive than
macrovascular changes because they not only occur systemically in gas/nutrient/waste
exchanging capillaries but create risk factors related to the premature onset of every pathology
related to macrovascular changes. Large blood vessels have TWO things working against them:
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chronic hyperglycemia AND the adverse effects caused by microvascular complications. DM2
induced microvascular structural and functional changes, such as basement membrane
thickening, defective cell integrity, connective tissue hypoxia, and micro-ischemia, result in
damage to ALL organ systems, albeit to varying degrees (Ignatavicius, Workman, and Rebar,
2018).
Perhaps the most devastating effect of vessel thickening on microcirculation is capillary
bed to tissue nutrient filtration degradation combined with inadequate tissue waste to capillary
reabsorption. While DM2 associated pathological thickening of blood vessels serves to lower the
porosity of capillary beds, the opposite is true of the renal glomerular capillaries of the
glomerulus. Microvascular changes of the glomerular capillaries, especially in the presents of
HTN, lead to excess kidney tissue perfusion, which leads to leaky glomerular capillaries, which
in turn leads to high levels of protein (mostly albumin) in the urine (proteinuria) and decreased
GFR. These proteins form deposits in kidney blood vessels. The vessels narrow and O2 perfusion
diminishes to hypoxia-causing levels. The surrounding renal cells become hypoxic and
eventually die. As these processes worsen over time, scar tissue develops in and on glomerular
capillaries, urine filtration diminishes, and CKD results (Ignatavicius, Workman, and Rebar,
2018). Notice how DM2 caused chronic hyperglycemia leads to microvascular changes, which
have now caused HTN and how exacerbated HTN leads to further renal damage. This insidiously
destructive positive feedback loop (snowball effect) is the hallmark of DM2.
Let us back up to when the glomerular capillaries were still leaky. Excess protein and
glucose in the filtrate cause high filtrate osmotic pressure. Under these conditions, dehydration
can set in rapidly. This is what happened to my patient even though he already has CKD. When
the body is dehydrated, the blood thickens, and cells become hypoxic due to hypovolemia.
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Hypoxic cells, which are already operating at a glucose deficit, will continue to do whatever they
can to produce ATP (energy). Because of deficient cellular oxygenation r/t dehydration, the
aerobic ATP producing pathways (Citric acid cycle and electron transport chain & oxidative
phosphorylation) are cut off to the cells. Hypoxic cells turn to glycolysis (if they have any
glucose), which produces lactic acid in the absence of available O2. The excess lactic acid in the
blood causes decreased serum pH and can lead to anion-gap metabolic acidosis (Ignatavicius,
Workman, and Rebar, 2018).
The amount of damage that can be caused by the body’s inability to produce insulin, or
the inability to respond to insulin is astonishing.
What I learned
My biggest take-away from writing this paper is that diabetes is no joke and should not
be taken lightly. Writing this paper reinforced the importance of early detection. Honestly, I did
not know DM2 to manifest into DM1. I knew they were similar regarding insulin and how those
who suffer from either type I or type II suffered from some form of insulin deficiency. Until my
Adult sims day, writing this paper, and then delving further into DM2 in my clinical work, I’ve
always had the old school definitions in my head: DM1 = insulin-dependent – early-onset
diabetes. DM2 = insulin-resistant - late-onset diabetes - the one you can avoid if you don’t eat
like s***, exercise, and don’t let yourself get fatter than a house. While those definitions are
correct, they are not complete by any means. I learned that racial genetic predisposition plays a
more active role than I previously knew. I had no idea that an A1C value correlated to an average
BG. I’ll have to find that table or equation. I like that you wrote what my patient’s A1C of 13
(13.0 = Avg. BG of 326) meant in the feedback of my lab values assignment. When comparing a
BG of 326 to his admit BG (588), I'm able to make a few assumptions: 1) If those numbers were
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extrapolated into a steady incline (no way of knowing), then my patient’s DM2 onset was far
faster than I'd previously suspected; 2) He has indeed been suffering from chronic hyperglycemia
due to slow-onset DM2 and something happened to spike his BG drastically. Again, there's no
way of knowing. But, knowing what I know now, I would show this data to him and ask him if
he can recall any recent dietary changes regarding his sugar intake i.e., eat an entire cake just for
fun.
The idea that many people have undiagnosed DM2 makes a lot more sense to me now. I
always figured people would just know when they developed DM2 because they’d get sick and
go to the doctor. I now realize that many people have numerous comorbidities and have become
accustomed to feeling terrible all the time. When comorbidities and overall poor health is
combined with the slow and insidious onset of DM2, why people hold out so long before getting
checked out becomes understandable. It is not good, but it is understandable. They probably
already think they know what the doctor will say, “Eat better, lose weight, take your meds,
exercise, blah blah.” Most people know what to do to get into better shape; they just do not want
to or do not value "being in better shape" enough to do anything about it. That is not meant as a
dig; it's just the truth. Change sucks, and sometimes comfortable misery is just that, comfortable.
I suspect many do not like the feeling that comes from someone in a white coat telling them
things they already know but which they just have not been able to accomplish. That feeling of
being belittled, whether real or perceived, is something most people try to avoid; hence, avoiding
the doctor's office unless they are really sick (or their spouse drags them in under threat of being
kicked out of the big bed). I would wager there are very few people in this country who honestly
do not know that smoking, drinking to excess, eating three fast-food meals a day, being obese,
and never doing anything more strenuous than tying their shoes is not healthy. For this reason, I
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will always keep the patient’s dignity firmly in the forefront of my thoughts while providing
nurse-to-patient education.
From an educational standpoint, I am glad my patient had multiple serious comorbid
medical diagnoses. Because of this, I had to think about cause and effect. Writing this paper
served as substantial reinforcement of the “everything is connected” concept.
A mechanic sits next to a doctor at the bar. The mechanic tells the doctor, “I don’t
understand why you get paid so much more than me. We both understand complex machines, we
both have to diagnose the problem, and we both have to either fix the faulty part or change it out
for a new one." The doctor nods in agreement with this. The mechanic then says, "If you find
someone with a bad blood vessel, you go in and either fix it or bypass it, right?" Doc nods. “I do
the same thing, and I change 100 times as many hoses as you do and get paid 1/8th of what you
get paid. So tell me, what makes you so special?” The doctor thinks about that for a minute and
replies, “The next time you dive into an engine to diagnose the problem, and they fix what needs
fixing, do me a favor, leave the engine running." The story may be silly, but it illustrates the fact
that we cannot shut a human off to hyperfocus on a single problem or illness. We must always
take into account what consequences our actions may cause.
How and where can I expect to apply what I have learned?
The rubric says, "… how could…?” For me, this is not a question of “could” but a
question of “will." I did not spend all this time and effort learning about this so that I might use
this knowledge . I will use this knowledge in every aspect of my nursing career as well as at
home or in my social life (community). My mother and grandma taught me the value of having
nurses around. Meaning they did not stop being nurses once they left work. Although sometimes,
when I watch my mom pick my brother's cystic back acne, I wish she would. Yuck! While
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remaining cognizant of the fact that nurses are highly respected and that somebody may base
their medical care on something I say, I feel that letting someone know what I see regarding their
S&S followed by, “I’m not a doctor, so go see one ASAP and tell them X, Y, & Z and ask them
A, B, & C” will become a sort of duty once I earn my RN. That doesn’t mean I’ll go around
pricking fingers, shining my penlight in random strangers' eyes, or scrutinizing everyone's
jugular for distension. I mean, if someone I know asks me about their diabetes, I’ll be able to
answer them, ask a few pertinent questions of my own, and be able to direct them to someone
who can better assist them. I have a feeling that my go-to questions will be, “So how good is
your BG control?”, “When was the last time you saw your doctor?” and "what did your last A1C
look like?"
What I learned will have the most significant impact in the clinical/hospital setting. A
few of my classmates told me I was nuts for choosing COPD and DM2 as pathopaper topics. I
hindsight, they may have been somewhat correct in that assertion. Both of these topics are
absolute beasts. When I chose COPD, I do not, for the life of me, know how I forgot that
essentially I would be writing about three very different diseases that happen to have many of the
same manifestations. I know you think 21 pages is a lot for these papers, and it is. But I had a
tough time keeping that one under 30. I chose DM2 because we not only covered it in Adult sims
but because my 3F Med Surge patient’s primary Dx was DM2. I immediately found this guy's
situation, if a bit tragic, extremely interesting. Here is a guy who has had horrible health for
years, multiple serious comorbidities, then at 60, he gets hit with DM2 manifested by literally not
being able to stand or see straight. If his situation were not so serious, it would be comical. My
point, yes, I do have one, is that the more I learn about DM2, the more I realize that my patient’s
story, while being a bit dramatic, is very normal: A man or woman entering their later years
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gradually allows their health to slide, they feel a bit under the weather, but because they do not
have a temp, cough, phlegm, fever, severe muscle aches, or any of the cardinal S&S of the flu
and since they can still function, they put it off and wait to heal up. Then boom! Something along
the same lines that happened to my patient occurs, and they wind up in the hospital with chronic
hyperglycemia and possible organ damage. Because this scenario is so common, and because
DM2 is so common, I feel learning about it sooner rather than later will help me become a good
nurse sooner than later. The same can be said for learning about COPD.
I have an entire year left in school, yet I feel confident that I would be able to properly assess a
patient with newly diagnosed DM2. My biggest obstacle is translating what I have learned in the
"classroom" setting to the "clinical" setting. Nevertheless, that will come with practice and
experience.
What would I change?
As I stated in my Abnormal Labs assignment, I have come to recognize a colossal
connection I missed while writing my DM2 paper. I knew that CKD, HTN, CHF, PVD,
cerebrovascular disease, CVA, neuropathy, retinopathy, and many other vasculature associated
pathologies went hand in hand with DM2. Yet I knew very little as to why DM2 is so intimately
linked to so many disease processes until I did my Abnormal Labs assignment – macrovascular
and especially microvascular changes caused by DM2. So I lengthily incorporated these
concepts into my revised pathophysiology description of DM2 (section 1 of this paper)
Interestingly, I had written a paragraph about how permanent hyperglycemia caused by
DM2 could cause enough pancreatic β-cell damage to effectively earn a patient the diagnosis of
DM1 as well. I even had a blurb about DKA written in. However, because I could not find any
source that explicitly stated, "DM2 can cause total cessation of insulin secretion; therefore,
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causing DM1,” I took it out in the final draft. I knew I was on the right track, but I was not
totally sure if “causes DM1” was actually true, and I did not want to look like I was just making
stuff up – which is exactly what I was doing. Having a better understanding of the damage
caused by chronic hyperglycemia, as well as your comment stating that yes, this can happen, and
yes, DKA becomes a very real threat, has connected the dots enough for me to include that in the
revised pathophysiology section.
Lastly, while I did understand the importance of educating the patient on how to selfmonitor his BG, how to draw up insulin, how to store insulin, how and where to inject insulin,
how to dispose of needles, what to do if BG becomes too low (hypoglycemia) and what S&S of
hypoglycemia to watch for, I totally forgot to add most of that into the paper. I think it was one
of those things that was so obvious that I assumed I had already added it in. If I were to write a
final final draft of my DM2 pathopaper, I would definitely add all of this in. I did add this vital
info to my Abnormal Labs assignment and my concept map.
How have I changed my nursing practice since writing this paper?
Perhaps “changed" is not the best term considering I do not even have a basis of nursing
practice from which to change. Unfortunately, I have not had the opportunity to practice any
nursing, let alone change anything. In the spirit of being thorough (I am nothing if not thorough
), I will tell you what I will do in my nursing practice in light of what I have learned.
I will be diligent in assessing the patient’s readiness to learn. I would not expect someone
who only hours ago went blind and crippled to welcome an onslaught of new information. I
would give him some to adjust to his new situation. With that said, I would immediately ensure
the patient’s safety and assess his VS and his pain level. I would tailor pain reduction
interventions specific to my patient. Then I would perform a thorough head-to-toe assessment.
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Many patients may not require a full head-to-toe. The sheer volume of comorbidities of this
patient warrants a full head-to-toe. Depending on the patients’ mood and level of consciousness,
I feel a recap of his 911 incident, as well as a psychosocial assessment, are in order. Having the
patient describe his series of events while still fresh in his mind would be beneficial. While doing
all of this, I would pay close attention to his physical, mental, and emotional state. I would not
press him at this juncture. I would be cognizant of his dignity and of the fact he just went through
something traumatic. Social queues, body language, facial expressions, openness, and a myriad
other factors play into my judgment of whether or not he is ready to talk.
Once the patient is stable and showing improvement (as he was the morning of the 16th), I
would, of course, continue to fulfill the doctors' orders, such as taking VS, ensuring the 125
mg/hr. ½ NS KCl infusion was going continuously, administering meds on time, taking his BG
15 mins before meals, and reporting the results to Dr. McClave via telephone and administering
his insulin right at mealtime. I would also ask him questions regarding when he may have begun
noticing symptoms of DM2. I would describe what S&S are common among this with
hyperglycemia and give him time to think them over and answer when he is ready. I would avoid
asking him questions while he was eating, if possible.
As his stay lengthens and he recovers (he better, as I will be assessing for that). I would
assess his understanding of his current situation and, using therapeutic communication, either
reaffirm those understandings or challenge them. I have said it before; we must meet the patient
where they are and not where we think they should be or where we think we would be if we were
in their position. Education is paramount in this situation. There are life-changing and life-saving
habits he must develop (mentioned in the last section). I would impress upon him the importance
of these, and after a few hours, I would assess his understanding and tell him we are going to
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come up with a plan. He gets to choose the time to make this plan (within reason). I would strive
to get his family involved. This is where a good psychosocial assessment comes in handy.
Inviting someone, he cannot stand simply because they were listed as NOK would be a grievous
error. I feel the key to this education and home care plan creation is to be just assertive enough
for him to understand the importance and severity of his situation, but not so much as to make
him feel like he has no say in the matter. That would be the worst outcome as he will ultimately
be the one responsible for self-testing and insulin administration once he is discharged.
Hypothetical day four scenario - fluid and electrolyte balance are close to back to normal
levels, his GFR continues to steadily increase, while BUN and serum creatinine are steadily
declining, CBCs are stabilizing back to normal levels, ketones are down to just above the target
range, proteinuria is 0, and BGs are consistently in the upper 100’s to lower 200’s before meals.
What I have come to appreciate the most from studying this patient is the fact that even though
he may be recovering, his preexisting comorbidities of HTN, MS, CKD, BPH, MDD, Back pain
r/t spinal stenosis and herniated nucleus pulposus w/myelopathy, balance problems, and
abnormal gait have not disappeared. It would be easy to focus on DM2 and CKD in this
situation. However, I feel keeping the patient in perspective as a whole will not only enable me
to provide him with better care but will serve to keep the patient grounded. Meaning, if I never
mentioned anything other than how great he was doing based on his recovering from extreme
chronic hypoglycemia, I may be sending the message of dealing with his kidneys and DM2 are
the only important aspect of his current situation. I would not want this patient to be unprepared
for discharge and his return home because we all had DM2 tunnel-vision for seven days in a row.
Recovery and therapeutic responses to treatment are great, and they will get their due accolades
for sure. However, they are not our only goal. Setting realistic, attainable goals with
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contingencies in the event those goals are not met are also essential. All parties involved must
understand that our patient has a lot of hard work ahead of him. We must all be realistic about
the possibility that he may not reach his health goals. Perhaps even more important than reaching
his goals is knowing what to do and whom to call if he does not.
These are just a sample of the nursing practices I would implement based on what I have
learned from this experience and research. Although I regret our clinicals being cut short, I feel
these five and a half hours have been the most important hours of my schooling thus far.
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References
Ignatavicius, D. D., Workman, L. M., and Rebar, C. R. (2018). Medical-surgical nursing:
concepts for international collaborative care (9th ed.). St. Louis, MO: Elsevier.
Hubert R. J. and VanMeter K. C. (2017). Goulds's Pathophysiology for the health professions
(6th ed.). Saint Louis, MO: Saunders.
Marieb, E. N., and Hoehn, K. (2019). Human Anatomy and Physiology (11th ed.). Hoboken, NJ:
Pearson Education.
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