N333: Diabetes Mellitus & Complications

Types, Pathophysiology, and Complications

____ ____ is a chronic metabolic disorder marked by hyperglycemia caused by insulin deficiency or insulin resistance. It results in insufficient glucose for cellular metabolism, leading to glycogenolysis, lipolysis, and gluconeogenesis

Diabetes mellitus (types include type 1, type 2, gestational, and other causes)

Early symptoms of Diabetes Mellitus include _____, _____, _____, and ____ ____

Polydipsia, polyphagia, polyuria, and blurred vision

____ ____ in diabetes is caused by a lack of insulin or insulin resistance prevents glucose from entering cells. Cells "sense" this because glucose is unavailable for energy production, it triggers the breakdown of fat and muscle for energy (lipolysis and proteolysis)

Cellular starvation (results in hyperglycemia, fat breakdown, and, in some cases, increased ketone production leading to diabetic ketoacidosis (DKA) or other complications)

In Type 1 DM, cellular starvation leads to _____ _____ (ketogenesis) resulting in ketosis and ketoacidosis (DKA) and in Type 2 DM, the body attempts to compensate by _____ insulin production, but cells still remain resistant

Ketone production, increasing

During glucose regulation, in the pancreas, beta cells release ____ and alpha cells release ____. In the liver, glucagon promotes _____ (glucose release) and ____ (glucose production from non-carbs)

Insulin, glucagon, glycogenolysis, gluconeogenesis

_____ is released when glucose levels rise, helping cells use glucose, store it as glycogen, and store fat in adipose tissue

Insulin

____ is released when glucose levels drop, increasing glucose production through glycogenolysis and gluconeogenesis

Glucagon

Glucose can be used for ____, stored as _____, or converted to ____. The brain solely depends on glucose for function, so blood glucose levels should remain stable

Energy, glycogen, fat

Blood Glucose Testing: ____ _____ ____ Normal 70–100 mg/dL | DM ≥126 mg/dL

Fasting Blood Glucose (FBG)

Blood Glucose Testing: ____ ____ ____ Normal <126 mg/dL | DM ≥200 mg/dL

Random Blood Glucose (RBG)

Blood Glucose Testing: ____ ____ _____ ____ Normal <140 mg/dL | DM ≥200 mg/dL

Oral Glucose Tolerance Test (2 Hour)

Blood Glucose Testing: ____ Normal <5.7% | Prediabetes 5.7–6.4% | DM ≥6.5%

A1c (Hemoglobin A1c) (Normal = less than or equal to 5.6, Pre-diabetes = 5.7-6.4, Diabetes is 6.5+)

Blood Glucose Testing: _____ <154 mg/dL ≈ A1c <7%

eAG (Estimated Average Glucose)

Urinalysis (UA) has two findings including ______ where glucose exceeds renal threshold (~180 mg/dL) and ______ which refers to ketosis (fat breakdown)

Glucosuria, Ketonuria

Type 1 Diabetes Mellitus (T1DM) Specific Diagnostic Findings include _____ ____ ____ which is autoimmune β-cell destruction and ______ which decreases endogenous insulin production

Islet Cell Autoantibodies (ICAs), C-peptide

Effects of Diabetes: ____ ____ hyperglycemia leads to endothelial injury and inflammation, ____ ____ endothelial injury causes secretion of endothelin narrowing arterial vessels, and ______ lipid and macrophage deposition forms foam cells, leading to plaque

Chronic inflammation, vascular narrowing, atherosclerosis

___ ___ ____ ____: starts juvenile with complete beta-cell failure, caused by autoimmune destruction of beta cells, resulting in insulin deficiency, requires lifelong insulin replacement. The classic triad of symptoms include polydipsia, polyuria, polyphagia. Common first signs include Diabetic ketoacidosis (DKA). Risk factors include family history, genetic predisposition (HLA genes) and environmental factors (viral infections)

Type 1 Diabetes Mellitus (lack of insulin production due to loss of beta cells so glucose does NOT get into cells)

____ ____ ____ ____ has an adult onset, caused by insulin resistance, leading to beta-cell exhaustion resulting in insulin production that may initially increase but eventually declines as beta cells fail. The classic triad of symptoms include polydipsia, polyuria, polyphagia. Common first signs include how it is often asymptomatic; may present with hyperglycemia or complications like neuropathy. Risk factors include family history, age >45, obesity, inactivity, hypertension, hyperlipidemia, and history of GDM, metabolic syndrome

Type 2 Diabetes Mellitus (cells do NOT accept insulin)

Acute DM Complications include _____ and ______ (DKA in Type 1, HHS in Type 2).

Hypoglycemia, Hyperglycemia

Chronic DM Complications include ______ ASCVD, CAD, MI, CVA, PVD, ______ retinopathy, nephropathy, neuropathy, and ______ poor wound healing, infections and amputations

Macrovascular, microvascular, other

_____ is an emergent issue where blood glucose <70 mg/dL, causes include insulin excess, missed meals, increased activity and illness. Symptoms include confusion, hunger, tachycardia, cool skin, diaphoresis, seizures, coma. Treatment includes fast-acting carbs (15g), IV dextrose if unresponsive and glucagon injection if needed

Hypoglycemia

____ is nocturnal hypoglycemia causes rebound hyperglycemia by morning

Somogyi (adjust insulin or antidiabetic medications, meals, and exercise routines)

____ ____ is elevated morning glucose due to nocturnal growth hormone release

Dawn Phenomenon (adjust insulin or antidiabetic medications, meals, and exercise routines)

_____ (Type 1 Diabetes) and _____ (Type 2 Diabetes) are Acute Hyperglycemic Emergencies. Both are caused by insulin problems leading to hyperglycemia. Both lead to osmotic diuresis leading to dehydration and electrolyte imbalance.

DKA, HHS

The key difference between DKA and HHS is that DKA involves ____ and _____ whereas HHS involves severe ____ and NO ____

Ketosis, acidosis, hyperosmolarity, ketosis

____ ____ is caused by insulin deficiency (usually Type 1 with often new onset). Precipitating factors include stressors (infection, trauma, illness) that increase glucose demand. There is NO insulin so glucose cannot enter cells leading to hyperglycemia so cells “starve” leading to lipolysis, fatty acids, ketones, and metabolic acidosis. Osmotic diuresis leads to dehydration and electrolyte shifts lead to K abnormalities. There is usually a rapid onset (2–3 days)

Diabetic Ketoacidosis (DKA)

Diabetic Ketoacidosis DKA: Signs and Symptoms: ____ = thirst, polyuria, fatigue, _____ = N/V, abdominal pain, and ____ = Kussmaul respirations, fruity breath, altered LOC, tachycardia

Early, progressive, severe

DKA Lab Findings: Blood Glucose _____ mg/dL (glucosuria), ketones are ____ (blood and urine), pH <7.35, HCO₃⁻ <18, anion gap >12, osmolality >310, K normal or ↑ (total body ↓), BUN/Cr ↑

>300, present

Consequences of DKA include ______, _____ _____ (ketones) _____ (osmotic diuresis), and electrolyte imbalance

Hyperglycemia, Metabolic acidosis, Dehydration

The goals of ___ treatment are too correct dehydration, hyperglycemia, acidosis, electrolytes

DKA

To treat DKA, ____ ___ are FIRST (NS 1–2 L then continue), followed by ____ ____ ____ to decrease glucose gradually (≤100 mg/dL/hr), and trransition to SQ when <250 mg/dL

IV fluids, IV insulin infusion

Electrolyte Management in DKA: ____ monitor frequently (at least q2hrs), DO NOT treat mild ____ initially (insulin causes K⁺ shifts INTO cells so rapid decrease in K⁺ requires replacement of K⁺ as levels fall

K+, hyperkalemia

DKA Treatment: Acid–Base (Conditional): _____ ONLY if pH <7.0 (avoid if pH >7.1 as it worsens hypokalemia). Complication Monitoring: watch for cerebral edema risk with rapid correction (early signs include headache, confusion, decreased LOC), monitor I&O, cardiac rhythm, neurological status, manage N/V, abdominal pain. KEY IDEA = ____ correction of glucose and fluids

Bicarbonate, gradual

____ ____ ____ is caused by insulin resistance (Type 2 with some insulin present). Precipitating factors include stressors (infection, trauma, illness). Insulin resistance leads to hyperglycemia, some insulin leads to NO significant ketone production, osmotic diuresis (severe dehydration), and hyperosmolar state (decreased tissue perfusion). The onset is gradual (days to weeks)

Hyperosmolar Hyperglycemia Syndrome (HHS)

HHS Signs and Symptoms: ____ = polyuria, polydipsia, dry mouth, _____ = weakness, confusion, blurred vision and ____ = altered LOC, seizures, coma, hypotension, tachycardia

Early, progressive, severe

HHS Lab Findings include Glucose ____ mg/dL, NO ____ , pH normal, osmolality >350 mOsm/kg (275–295 mOsm/kg), severe dehydration and electrolyte imbalances (Na, K)

>600, ketones,

Consequences of HHS include severe _____, profound ____, _____ leading to decreased perfusion and an increased risk of shock

Hyperglycemia, dehydration, hyperosmolarity

The goal of ____ treatment is to correct dehydration, hyperosmolarity, glucose, electrolytes

HHS

To treat HHS, ____ ____ are FIRST (aggressive) since severe dehydration is primary problem, ____ _____ ____ (LOW dose) to decrease glucose gradually, electrolyte replacement (K⁺, Na⁺)

IV fluids, IV insulin infusion

In HHS, electrolyte management involves monitor ___ closely (insulin causes K⁺ to shift INTO cells leading to a risk of hypokalemia) should replace as needed. Complication monitoring includes cerebral edema risk with rapid correction, decrease glucose and osmolality ____, monitor I&O, cardiac rhythm, and neurological status. KEY IDEA: ____ FIRST, ____ correction

K+, gradually, fluids, slow

____ _____ requires treatment to normalize maternal blood glucose to prevent infant complications. Screening involves a oral glucose tolerance test (OGTT) during the second trimester (24-28 weeks)

Gestational Diabetes (GDM)

Risks of ____ include high maternal glucose leads to fetal insulin production, resulting in macrosomia, fetal defects, and newborn hypoglycemia

GDM

Vascular Damage in DM: Chronic ____ is a major cause of damage to both small and large arterial vessels leading to a condition called ____ which is responsible for many of the long-term complications of DM

Hyperglycemia, angiopathy

_____ Complications: ____ blood sugar (BS) causes damage to the smallest arterial vessels, affecting the endothelial cells that line arterioles and arteries. The key affected areas are ____, ____, and ___ (small blood vessels)

Microvascular, increased, retina, neurons, and nephrons

Diabetic ____ is the leading cause of blindness and diabetic ____ leading to kidney failure

Retinopathy, Nephropathy (Microvascular Complication)

Diabetic _____ has 2 subdivisions. ____ (burning, tingling, lack of sensation in lower limbs) and _____ (affecting sympathetic nervous system responses like unawareness of hypoglycemia)

Neuropathy, peripheral, autonomic

____ Complications: ____ BS causes vascular damage that leads to arteriosclerosis (hardening of arteries). The key affected areas are larger arterial vessels

Macrovascular, increased,

_____ Complications can result in ASCVD (AtheroSclerotic CardioVascular Disease), Myocardial Infarction (Heart Attack), Cerebrovascular Accident (CVA) (Stroke), Peripheral Vascular Disease (PVD), Limb Ischemia (Poor circulation, leading to amputations)

Macrovascular (poor wound healing leads to an increased risk of infection and immunosuppression leads to an increased susceptibility to infections)

DM Management & Prevention: ____ Risk Reduction (Control HTN, Cholesterol, Smoking cessation), ___ & ____ (healthy diet, weight management, exercise, foot care, annual eye exam, kidney screening (urine), _____ (annual influenza and pneumococcal), and ____ ____ (before meals, after meals, bedtime *consider continuous monitoring)

Cardiovascular, Lifestyle, Screening, Immunizations, Glucose Monitoring