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Type 2 Diabetes - Coggle Diagram
Type 2 Diabetes
Diagnosis/ Testing
Basic Metabolic Panel
Na: 144 mEq/L (high normal) - indicates hydrations status and potential dietary imbalance
high sodium levels can be caused by high sodium intake, dehydration and reduced kidney function
The kidneys play a big role in regulating sodium and water balance so impaired kidney function can lead to the inability to excrete sodium, resulting in elevated levels
K: 3.3 mEq/L (low) - suggests hypokalemia, possibly related to diuretic use (hydrochlorothiazide, lasix)
cause low potassium (hypokalemia) because they increase urine production, which leads to the loss of potassium through urine
Cl: 109 mEq/L - reflects electrolyte imbalance
many factors can cause chloride levels to be elevated such as dehydration, kidney problems, medications, and metabolic acidosis
CO2: 20 mEq/L - reflects mild acidosis or chronic metabolic issues
Mild acidosis or chronic metabolic issues can cause CO2 (bicarbonate) levels to be low because the body tries to compensate for the acidosis by retaining bicarbonate to neutralize the excess acid. However, in chronic conditions, the kidneys may not be able to keep up with this compensation, leading to lower levels of bicarbonate in the blood.
BUN/ Creatinine Ratio: elevated - indicates potential kidney function compromise
kidney function compromise causes elevated BUN (Blood Urea Nitrogen) and creatinine levels because the kidneys are responsible for filtering waste products from the blood and excreting them in urine. When kidney function is impaired, these waste products (urea and creatinine) accumulate in the blood, leading to higher levels of BUN and creatinine
Glucose
Current: 148 mg/dL (elevated) - poor glycemic control consistent with the DM II
Poor wound healing, more prone to ulcers
HGA1C: 8.0% (significantly elevated) - reflects long-term hyperglycemia and risk for complications
Complications: DKA, HHS, and damage to organs such as the kidneys, eyes, and nerves
Complete Blood Count
WBC: 4.2 (low normal) - could indicate chronic inflammation or suppressed immunity
chronic inflammation can cause low WBC count due to several mechanisms including, bone marrow suppression, increased consumption and immune dysregulations
bone marrow suppression occurs when chronic inflammation suppresses the its function reducing production of WBCs
increased consumption is when persistent inflammation can lead to the increased consumption of WBCs as they are constantly going to the site of inflammation
Chronic inflammation can disrupt normal immune regulation, leading to decreased production or increased destruction of WBCs
RBC/Hgb/Hct (mildly low) - consistent with anemia of chronic disease or nutritional deficiencies
Anemia results in a reduced number of RBCs, leading to lower Hgb and Hct levels. Anemia can be caused by various factors, including chronic diseases and nutritional deficiencies
Chronic inflammation and diseases can affect the body's ability to produce and maintain healthy RBCs. Inflammation can interfere with iron metabolism, reducing the availability of iron needed for RBC production
Deficiencies in essential nutrients like iron, vitamin B12, and folate can impair RBC production and function. Iron-deficiency anemia is the most common type, but deficiencies in other nutrients can also contribute to low RBC, Hgb, and Hct levels
Plt: 120 (low) - risk for bleeding or delayed wound healing
Platelets play a crucial role in the blood clotting process. When you get a cut or injury, platelets gather at the site and form a plug to stop the bleeding. If platelet count is low, the blood can't clot effectively, leading to an increased risk of bleeding
Platelets release growth factors and other substances that help in the wound healing process by promoting tissue repair and regeneration. Low platelet count can hinder this process, causing wounds to heal more slowly
Urinalysis
Protein (positive), Glucose (positive), Ketones (positive) - suggests poor diabetes management and potential diabetic nephropathy
Diabetic Nephropathy
Proteinuria is a hallmark of kidney damage caused by diabetes
Persistent protein leakage can lead to a decline in glomerular filtration rate, progressing to chronic kidney disease (CKD) or end stage renal disease
Damage to the nephrons (functional kidney units) from the disease or injury leads to reduce filtration capacity
Remaining Nephrons work harder to filter blood, leading to further damage
Chronic Inflammation, fibrosis, and scarring reduce kidney size and functional capacity over time
Reduced excretion or urea, creatinine, and electrolytes causes imbalances and toxin buildup (uremia)
Fatigue, yellow skin, headaches, shortness of breath, rapid heart rate, brittle or spoon shaped nails, cold extremities, loss of appetite
May lead to fluid retention and worsening hypertension
Fluid Retention
Kidney Dysfunction: Decreased GFR impairs the kidneys ability to excrete sodium and water; sodium retention creates an osmotic gradient that pulls water back into circulation, leading to volume expansion
BUN 32 mg/dl (high) and albumin 2.4 g/dl (low)
Heart Failure: reduced cardiac output decreases kidney perfusion, triggering RAAS activation
Shortness of breath, fatigue, swelling in arms and legs, nausea and vomiting, abdominal pain, lightheadedness, tachycardia, hypotension, cool extremities, weak pulses, chest pain, low urine output
Liver Dysfunction: hypoalbuminemia reduces oncotic pressure, leading to fluid leakage into interstitial spaces
Medications- Swelling/Edema/ Fluid overload
Hydrochlorothiazide 12.5 mg Po Q day Lasix 20 mg PO Q daily
Pain, numbness, sensitivity, weakness, balance problems, ulcers, infections, dizziness, digestive issues, double vision
Specific Gravity: 1.028 - concentrated urine indicating dehydration
Urine Osmolality: 1200 mOsm/kg - reflects concentrated urine
Vitamin and Protein Status
Albumin: 2.4 d/dL (low) - indicates malnutrition or chronic illness
Vitamin B12: undetectable in recent labs - may contribute to cognitive issues and nephropathy
Long term Metformin use impairs the ability of calcium to carry out its role leading to Vitamin B12 deficiency
Insulin Resistance
when cells in muscle, fats, and liver don't respond normally to insulin and can't use glucose from your blood for energy.
Causing the pancreas to produce more insulin
Eventually leading to blood sugars rising
Polyuria, excessive thirst, fatigue, dry mouth, weight loss, blurry vision
Also affecting the signaling of insulin in the blood vessels
Endothelial dysfunction
a drop in nitric oxide causes blood vessels to constrict or narrow
Increased risk of: cardiovascular disease, blood clots, diabetic neuropathy, stroke, HTN, kidney failure
Headaches, pallor, numbness, tingling, leg and chest pain, muscle weakness
Impaired insulin signaling- insulin binds to the insulin receptor on the cell surface
Reduced glucose uptake and utilization- the translocation of GLUT4 transporters is impaired, leading to reduced glucose uptake and utilization by cells.
Increased hepatic glucose production- hepatic glucose production is not adequately suppressed, leading to increased glucose output into the bloodstream causing high blood sugar
B Cell Response
The beta-cell (B-cell) response to insulin resistance is central to the progression of type 2 diabetes mellitus (T2DM). When insulin resistance develops in peripheral tissues (e.g., muscle, liver, adipose tissue), beta cells initially compensate by increasing insulin production. However, over time, this compensatory mechanism fails, leading to hyperglycemia and the development of symptoms and complications
Peripheral tissues become resistant to insulin due to factors like obesity, chronic inflammation, and lipid accumulation.
The resistance is marked by
Decreased glucose uptake in muscle.
Increased hepatic gluconeogenesis.
Enhanced lipolysis in adipose tissue, raising free fatty acids
To overcome insulin resistance, pancreatic beta cells increase insulin secretion
Beta cells hypertrophy (increase in size) and hyperplasia (increase in number)
Elevated plasma insulin levels (hyperinsulinemia) maintain normoglycemia for a time
Chronic insulin resistance leads to excessive demand on beta cells, eventually causing beta-cell failure that leads to glucotoxicity, lipotoxicity, inflammation and ER stress
Insulin secretion becomes inadequate to overcome resistance, causing persistent hyperglycemia
Symptoms include: polyurina, polydipsia, pholyphagia, fatigue, and blurred vision
1 more item...
Labs:
HgA1C of 8.0
Lipid Panel
Increased triglyceride levels, decreased HDL, and changes in the composition of LDL cholesterol.
Fasting glucose or oral glucose testing
Medications: Metformin, Thiazolidinediones, GLP-1 Receptor agonists, SGLT-2 Inhibitors, Alpha- glucosidase inhibitors, statins, Insulin
Non-pharmacological- Lifestyle changes like weight loss, exercise, healthy diet (reduce carbs and unhealthy fats), getting enough sleep, smoking cessation, and stress management
High importance especially for older adults so they can have a better quality of life, prevent complications, and maintain ADLs
These medications work to increase insulin sensitivity, slow blood sugar spikes, reduce glucose production, increase feelings of fullness, block hormones (in digestive system), and remove glucose from the blood
Medications work in different ways and have different side effects so it is important to talk to the doctor about which medication would be best for the patient
Hyperglycemia
Insulin as treatment for hyperglycemia
Production and Function: Insulin is a hormone produced by the pancreas that helps regulate blood sugar levels by allowing cells to absorb glucose for energy
In those with DM II, the body either is not producing enough or becomes resistant to insulin's effect
Types of Insulin Therapy: There are many ways with which to treat hyperglycemia, these include rapid acting, short acting, intermediate acting, and long acting insulin
Depending on the patient's needs, the use of insulin will vary
Short-Acting Insulin (regular): begins working within 30 minutes and hits its peak in about 2-3 hours with effects lasting about 3-6 hours
Usually taken before meals to help control sugar spikes that occur after eating
Long Acting Insulin: begins to work several hours after injection, has no peak and last up to 24 hours or more
Usually taken once or twice a day to maintain baseline blood sugar levels to help manage glucose production by the liver
Intermediate Acting Insulin
Inject once or twice per day, starts working in 1-2 hours, and lasts 11-12 hours
Rapid Acting Insulin: begins working in 15 minutes and hits its peak about 1-2 hours after injection, lasting 2-4 hours
usually taken just before or right after meals to help control spikes that occur after eating
Insulin Administration: Can be administered through injections or insulin pump, proper administration techniques and timing are important to ensure effective control of blood sugar
Check glucose levels before meals, at bedtime, and in the morning
With poorly controlled diabetes a patient may need more or less glucose checks
Glucose checks can be done by self-testing-like fingerstick testing or continuous glucose monitoring.
Often Combined with other treatments
When the body is under stress, more insulin is needed
Medication- Diabetes Control
Lantaprost 1 drop each eye Qdaily: prevent eye complications like glaucoma from diabetes
Metformin 500 mg PO BID
Inhibition of Hepatic Glucogenesis
Causes include: poor diet, lack of physical activity, illness, stress or missed diabetes medications
Symptoms: increased thirst, frequent urination, blurred vision, fatigue, headaches
Complications: can lead to serious heath issues such as DKA, HHS, and damage to organs such as the kidneys, eyes, and nerves
Management: involves lifestyle changes that include adjusting diet, increasing physical activity, and monitoring sugar levels regularly Insulin therapy therapy may be necessarys