Week 1 & 2 - Diabetes Flashcards by Ebby K

Describe Diabetes Mellitus

A group of metabolic diseases characterized by:

(Causes):
- Decreased insulin secretion / Insulin deficiency
- Insulin resistance

Which leads to hyperglycemia (high blood sugar levels)

Prolonged hyperglycemia affects nearly all body tissue, and it’s associated with various complications

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LECTURE OBJECTIVE - Differentiate the (3) types of Diabetes

Type 1 Diabetes Mellitus (insulin dependent):
- Typically occurs in younger people
- Cause unknown; may result from autoimmune process
- Pharmacologic intervention is NECESSARY

Type 2 Diabetes Mellitus (non-insulin dependent):
- Defects in insulin release and use + insulin resistance
- Often due to unhealthy lifestyle choices (obesity, poor diet, no exercise)
- Common in diabetic patients
- Early T2DM = Insulin resistance → β-cells still functional but overworked
- Late T2DM = β-cell failure → Reduced insulin production

Gestational Diabetes Mellitus
- Glucose intolerance of any degree during pregnancy

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LECTURE OBJECTIVE (Differentiating Types of Diabetes)

Type 1 Diabetes Mellitus Pathophysiology

Patho
Effect on Kidneys
Effect on Energy Production

Pathophysiology:
- Destruction of (Beta) islet cells in pancreas leads to insufficient insulin and excess glucagon
- Hyperglycemia (high blood sugar) occurs

Kidneys:
- Hyperglycemic blood going to kidneys causes glycosuria (excess glucose in urine) and osmotic diuresis (excess urine production d/t excess glucose holding onto water)

Energy:
- Body can’t use carbs, instead uses fats and proteins for energy which = ketosis & weight loss
- Results in: polyphagia (insatiable hunger) and fatigue

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LECTURE OBJECTIVE (Differentiating Types of Diabetes)

Pathophysiology: Type 2 Diabetes Mellitus

Normally, insulin binds to cell receptors and causes reaction for glucose metabolism
But in T2DM, these intracellular reactions are diminished which = insulin less effective at causing glucose uptake and regulating gluconeogenesis by liver
If beta cells cannot keep up, blood glucose rises and T2DM develops

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LECTURE OBJECTIVE (Differentiating Types of Diabetes)

Pathophysiology: Gestational Diabetes Mellitus

Anti-Insulin hormones are secreted during pregnancy: Human placental lactogen (hPL), progesterone, cortisol, prolactin

Placental hormones cause insulin resistance which = development of hyperglycemia & increase amount of insulin needed

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What are the hormones and enzymes produced by the pancreas?

Hormones:
Beta cells - Insulin
Alpha cells - Glucagon
Somatostatin - Delta Cells

Enzymes:
Amylase
Lipase

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Describe insulin action

Insulin = “Use the ‘free’ glucose, and hang on to all the stored energy”

Glucose

Increase Glycogenesis; insulin stimulates liver and muscles to store excess glucose as glycogen

Fats
- Increased lipogenesis; glucose transport into adipose cells for storage
- Inhibits lipolysis: breakdown of fat

Liver
- Inhibits glycogenolysis: conversion of stored glycogen to glucose
- Inhibits gluconeogenesis: production of new glucose

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What is insulin release normally stimulated by?

Stimulated:
-Parasympathetic stimulation: (“Rest and digest = Insulin helps STORE energy and nutrients; glucose gets turned into glycogen, fat and protein synthesis”)

-Elevated serum glucose: (Glucose intake, then needs to be stored)
-Increased GI hormones:
-Increased serum potassium:

Inhibited:
- Sympathetic

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Effects of insulin on:
Glucose
Fats
Liver
Protein
Potassium

Glucose - Mobilizes to be used as energy
- Increased glycogenesis - transport of glucose into cells, resulting in increased glycogen synthesis
(antagonist to glucagon)

Fats:
- Increases lipogenesis - glucose transport into adipose cells for storage
- Inhibits lipolysis - Breakdown of fat

Liver:
- Inhibits glycogenolysis - conversion of stored glycogen to glucose

Protein:
- Facilitates transport of amino acids into cells

Potassium:
- Facilitates intracellular transport of potassium

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Glucagon:

Function
Stimulation for release/

Acts to keep blood glucose elevated
(antagonist to insulin)

Stimulated by:
- Sympathetic stimulation
- Decreased serum glucose
- Secretion of growth hormone

Decreased stimulation by:
- Increased glucose levels

Functions:
- Stimulates glycogenolysis (breakdown glycogen into glucose)
- Stimulates gluconeogenesis (make new glucose)
- Enhances lipolysis (breakdown fats)

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Somatostatin:

Function

Inhibits release of glucagon, insulin, growth hormone & thyroid hormone
Exerts a hypoglycemic feeling in the patient

“Growth hormone stimulates the liver to produce glucose, as well as the release of glucagon, which also increases blood glucose. Somatostatin inhibits the release of GH, insulin and glucagon. This lowers the amount of blood glucose and reduces the amount of glucose taken up by the body cells, creating a drastic hypoglycemic feeling in the patient.”

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What are “The 3 P’s” of Type 1 Diabetes?

“The 3 P’s”
- Polyuria - Frequent urinating
- Polydipsia - Frequent drinking
- Polyphagia - Frequent eating

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Explain the relationship between diet and glycemic control; how to avoid spikes?

How fast the blood sugar rises after eating something

Goal for diabetes patients:
- Prevent “rollercoaster” of blood sugar spikes

High GI may also lead to sugar crash, low GI helps provide steady energy

Tips:
- Combine starch with protein and fat
- Raw/whole forms of foods > cooked or chopped
- Whole fruit > fruit juice

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What are exercise recommendations for pts with diabetes?

Exercise 3x a week
Exercise at the same time of day
Proper footwear (“If something is hurting pts feet, they might not feel it”)
Inspect feet daily after exercise
Keep simple CHO (carbohydrate) on hand

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What is the relationship of Diabetes Patients and Alcohol Consumption?

Patients can have in moderation
BUT, liver gets busy breaking down alcohol
Liver then can’t produce glucose, which leads to hypoglycemia
Can result in DKA in Type 1

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Explain the relationship between exercise and glycemic control/diabetes

Patients should exercise at the same time, preferably whenever blood sugar is highest

Lowers blood glucose
Lower cardiovascular risk
Weight loss

Pt with diabetes lack physical sensation, make sure they have good shoes

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Exercise precautions for diabetes patients

Avoid exercise if:
- Blodo sugar >250 mg/dl
- Ketones in urine

If pt is on insulin:
- Eat 15g CHO prior to exercise
- Monitor for delayed hypogylcemia

Pt should inform others of their diabetes
Pt should get cardiac clearance

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What is Glycemic Index?

How fast the blood sugar rises after eating something

Goal for diabetes patients:
- Prevent “rollercoaster” of blood sugar spikes

High GI may also lead to sugar crash, low GI helps provide steady energy

Prior to antidiabetic meds, what should be the first line for diabetes patients?

When are oral antidiabetic meds indicated?

What is the main side effect?

First line: Diet and exercise
Indication: Patients who do not respond to medical nutrition therapy and exercise alone
Major side effect: Hypoglycemia

Describe oral antidiabetic meds used to manage blood glucose, including insulin and oral antidiabetic agents:

Glucophage (metformin)

Only for pt with Type 2
Biguanides

Mechanism of action:
- Inhibits production of glucose by liver
- Increases tissue sensitivity to insulin + increases insulin uptake
- Decreases hepatic synthesis of cholesterol

Beneficial features:
- Improved glycemic control in most patients
- Effective as monotherapy

Side effects:
- GI side effects
- Lactic acidosis

Contraindications:
- Renal dysfunction
- Liver dysfunction
- Alcoholism

Major side effect of all is hypoglycemia (drug does their job too well)

Dipeptidyl Peptidase-4

Januvia (sitagliptin)

Mechanism of Action:
- Prolongs the action of incretin
- Results in improved glucose control

Side effects:
- Frequent URIs
- Headache
-GI Side effects
- Hypoglycemia if combined with sulfonylurea

Trulicity (dulaglutide)

Mechanism of action:
- Enhances glucose dependent insulin secretion
- Incretin mimetic

Side effects:
- Pancreatitis
- Weight loss
- GI effects

Ozempic (semaglutide)

Glucagonlike Peptide-1 Agonist

Not recommended as firsty line in patients with poor glycemic control
Side effects:
- Pancreatitis
- Gi symptoms
- Weight loss

Mounjaro (tirezepatide)

Adjunct to improve glycemic control

Side effects:
- Pancreatitis
- GI symptoms
- Weight loss
- Hypoglycemia

Contraindicated for patients w/ hx of thyroid cancer

Glucotrol (glipizide) Diabeta (glyburide) Amaryl (glimepiride) -ide's

2nd Gen Sulfonylureas Mechanism: - Stimulate beta cells to secrete insulin - May improve insulin sensitivity Side effects: - Hypoglycemia - GI symptoms - Weight gain Contraindications/Implications: - Alcohol use - Sulfa allergy

LECTURE OBJECTIVE - Complications of Diabetes Hypoglycemia: What is it? What causes it? Timing

Blood glucose = <70 mg/dl Causes: - Too much insulin - Result of oral hypoglycemic agents - Excessive physical activity Timing: - Can occur day or night - Often occurs just before meals or if meals are delayed - Can occur when insulin levels are peaking

LECTURE OBJECTIVE - Complications of Diabetes MILD Hypoglycemia: Cause s/s

Cause: sympathetic nervous stimulation s/s: - sweating - tremors - tachycardia - palpitations

LECTURE OBJECTIVE - Complications of Diabetes MODERATE Hypoglycemia: Cause s/s

Cause: - Central Nervous System stimulation s/s: -trouble concentrating -headache -memory lapses -confusion -slurred speech

LECTURE OBJECTIVE - Complications of Diabetes Severe hypoglycemia: s/s

- Impaired CNS function - Disorientation - Seizures - Loss of consciousness - Can be fatal

Management of Mild Hypoglycemia

Give 15-20g of fasting acting Carb Retest blood glucose in 15 minutes; retreat if <70 mg/dl

Management of Moderate Hypoglycemia

If awake and alert = give 15g CHO by mouth If drowsy = give glucagon IM or D50 IV

Management of Severe hypoglycemia

Parenteral glucagon IV glucagon commonly leads to vomiting If pt is unconscious: - Glucagon 1mg subQ or IM - 25-50mL of D50 IV

LECTURE OBJECTIVE - Complications of Diabetes Diabetic KetoAcidosis (DKA): Pathophysiology Clinical manifestation

More common in Type 1 Diabetes Mellitus; caused by insulin deficit Patho: - Insulin deficit - Gluconeogenesis leads to hyperglycemia - Kidneys attempt to eliminate glucose --> osmotic diuresis --> dehydration, electrolyte loss - Lipolysis results in production of ketone bodies (which are acidic) Clinical features aka "What to look for": - Hyperglycemia - Dehydration, electrolyte losses - Acidosis s/s: - Ketonemia, ketonuria - Fruity ordor - Dry mucus membranes - Hypotension, tachycardia - Blurred vision, weakness, headache - Kussmaul respirations

LECTURE OBJECTIVE - IDENTIFY DIAGNOSTIC STUDIES What are some Labs/Diagnostic Findings for Diabetic Ketoacidosis?

DKA Diagnostic Findings: - Blood Glucose levels 250 - 800 mg/dl - Metabolic acidosis: low pH, low serum HCO3, low PCO2 - Ketone bodies in blood and urine - Evidence of dehydration: elevated Hct, BUN, creatinine - Sodium and potassium abnormalities

LECTURE OBJECTIVE - Complications of Diabetes Hyperglycemic Hyperosmolar Syndrome (HHS)

Usually in Type 2 Diabetes Mortality rate: 5-16% Pathophysiology - Hyperglycemia --> hyperosmolarity (very concentrate) --> osmotic diuresis (increased urination d/t substances in kidney fluid) --> dehydration, electrolyte imbalances --> intracellular to extracellular shifts "Too much glucose in the blood makes it highly concentrated (hyperosmolar). Excess glucose spills into kidney fluid, pulling water with it (osmotic diuresis), leading to excessive urination (polyuria). This causes dehydration and electrolyte imbalances." Causes: - Relative insulin deficiency secondary to increased demands - Physiologic stress - Dialysis - Medications Clinical manifestations: - Hypotension, tachycardia - Profound dehydration - Altered level of consciousness, seizures

LECTURE OBJECTIVE - IDENTIFY DIAGNOSTIC STUDIES What are Diagnostic Findings for Hyperglycemic Hyperosmolar Syndrome (HHS)?

Diagnostic findings: - Blood Glucose >600mg/dl - Osmolality >320 mOsm/kg - Elevated BUN, creatinine - Mental status changes secondary to cerebral dehydration - No ketosis, normal pH

LECTURE OBJECTIVE - TREATMENT/MANAGEMENT What is the treatment for Hyperglycemic Hyperosmolar Syndrome (HHS)?

- Fluid Replacement - Correction of electrolyte imbalances - Insulin administration Nursing implications: Monitor for signs of fluid overload, fluid + electrolyte status

LECTURE OBJECTIVE - DIFFERENTIATE TYPES OF DIABETES Gestational Diabetes What is it? When does it resolve? Treatment?

Any degree of glucose intolerance with onset during pregnancy - Usually diagnosed in 2nd or 3rd trimesters; often resolves after birth of fetus - Treated with insulin

LECTURE OBJECTIVE - DIFFERENTIATE TYPES OF DIABETES Latent Autoimmune Diabetes of Adults (LADA)

Subtype of Diabetes; autoimmune in nature Clinical manifestations: Similar to Type 1 or Type 2 Diabetes

LECTURE OBJECTIVE - DIFFERENTIATE TYPES OF DIABETES Prediabetes

Impaired glucose tolerance or impaired fasting glucose - Blood glucose values higher than normal, but lower than classified diabetes - Often leads to diagnosis of diabetes

LECTURE OBJECTIVE - DESCRIBE POTENTIAL COMPLICATIONS Long Term Complications prevention: **Macrovascular** Categories and Management/Prevention

Categories: - Atherosclerotic changes - Coronary artery disease - Cerebrovascular disease - Peripheral vascular Management/Prevention: - Risk factor modification - Diet, exercise, smoking cessation - Glycemic control

LECTURE OBJECTIVE - DESCRIBE POTENTIAL COMPLICATIONS Long term complications prevention: Microvascular Retinopathy & Nephropathy

1) Retinopathy - Vessel damage of retinal vessels - Diagnosed via ophthalmoscopy Management: - Glycemic control, smoking cessation, BP Control - Laser surgery

LECTURE OBJECTIVE - DESCRIBE POTENTIAL COMPLICATIONS Long term complications: Microvascular Nephropathy

Nephropathy - Kidney disease secondary to diabetic microvascular changes - May lead to insulin catabolism --> hypoglycemia Management: - Glycemic control, BP Control, avoid nephrotoxic agents, low sodium, low protein diet - Annual kidney function tests - ESRD: Dialysis or transplant

LECTURE OBJECTIVE - DESCRIBE POTENTIAL COMPLICATIONS Long Term Complications prevention: Neuropathy: Peripheral vs. Autonomic What is it Management of neuropathy

Peripheral neuropathy - Affects distal portion of nerves - Paresthesia, burning --> Numbness Management: - Glycemic control, pain meds prn Autonomic neuropathy: - Autonomic (fight or flight) nervous system - GI, Cardiac, Renal - Hypoglycemic Unawareness - Sexual Dysfunction Management: - Specific to symptoms