Diabetes, Metabolic Syndrome, PAD Flashcards
How many people in the US are diagnosed with pre-diabetes?
96 million or 38% of the US population
How does Type I & Type II DM differ?
DM: Chronic metabolic disorder characterized by high blood glucose (“hyperglycemia”)
TYPE 1:
-beta cells of pancreas (produce insulin) are destroyed
-insulin dependence –> need supplemental
-commonly dx before age 30
TYPE II
1) insulin resistance - insulin action is abnormal and cells become resistant to insulin (abnormal uptake of blood glucose)
2) pancreas continues to produce more insulin to counteract insulin resistance–> over time B cells burn out –> insulin production decreases –> need supplemental insulin (insulin dependence)
-commonly dx after 40 years
-effects >90% of DM population
Can someone with Type II DM require insulin? Why?
-yes, transition from insulin resistance to insulin dependence
-diabetes is a combination of macrovascular and microvascular complications
Common precautions of hypoglycemia for DM population. Why are these important?
DEFINITION: BG <60 mg/dL
EXERCISE:
-exercise increases the risk of hypoglycemia bc it accelerates glucose uptake into peripheral tissues
-monitor blood glucose before, during, and after exercise
NOCTURNAL:
-can happen at night too
-know/compare timing of tube feeding and insulin dosing
What types of cells release glucagon?
pancreatic alpha cells
-glucagon stimulates gluconeogenesis and glycogenolysis in liver and release of glucose to plasma (more glucose in the blood stream)
** primary target organ for glucagon is the liver (because liver can help to breakdown the glycogen that it stores)
What cell types are highly responsive to insulin (glucose uptake)?
liver, fat, muscle
Explain how insulin and glucagon are “counter regulatory” hormones to each other.
Insulin increases blood glucose uptake into cells
Glucagon increases release of blood glucose into blood steam (stimulates hepatic glucose production)
What are the common diagnostic tests for DM? What information is derived from each?
Fasting Plasma Glucose Test:
-cheap, fast
-normal: 70-100 mg/dL
-100-125 mg/dL- prediabetes
-> 125 mg/dl - diabetes
Glycosylated Hemoglobin tests: (Hb A1c)
-normal <5.7% of total Hb
-tells you your 90 day history of glucose levels in blood
-if you leave RBC in a sugary solution it will add glucose to its structure –> measure this
-how elevated has glucose been over the lifetime of the RBC (90 days)
Oral Glucose Tolerance Test (OGTT)
-tested 2 hours after glucose-rich drink
-140-199 mg/dl signals pre-diabetes
-> 200 mg/dl signals diabetes
Criteria for the Diagnosis of Diabetes
Fasting plasma glucose (FPG) ≥126 mg/dL (7.0 mmol/L)
OR
2-h plasma glucose ≥200 mg/dL (11.1 mmol/L) during an OGTT
OR
A1C ≥6.5%
(5.7-6.5% is pre-diabetic)
OR
Classic diabetes symptoms + random plasma glucose ≥200 mg/dL (11.1 mmol/L)
Clinical Manifestations of heart disease in patients with diabetes:
CAD:
-late dx atypical symptoms: silent ischemia or silent MI
-angina equivalents: SOB/DOE; GI symptoms
Heart Disease risk in patients with DM vs without:
-increased atherosclerosis throughout coronary arteries
-increased HTN, CHF, and CVA risk
-increased incidence of dysrhythmias post MI (lack of blood flow to conduction system)
** assume a patient with DM has heart disease until proven otherwise
What are the common complications of DM?
-atherosclerosis
-hyperglycemia
-hypertension
-retinopathy: multiple fragile micro-aneurysms
-nephropathy
-neuropathy (DPN, CAN)
-diabetic ketoacidosis
-peripheral vascular disease/peripheral arterial occlusive disease
-osteopathy
-immune dysfunction (increased infection risk–> poor blood flow and lack of sensation)
WORST: blindness (caused by retinopathy), renal failure, CAD, MI, HF, amputation, CVA
a. Why is the patient with DM at a greater risk of CV disease? CV-related mortality?
-greater risk for atherosclerosis and HTN
-oxidative stress
-microvascular and macrovascular changes
-poor glycemic control can cause vascular changes
What are the multiple factors that increase the risk of wound development in the DM population?
-lack of sensation
-poor blood flow (occluded blood vessels)
-innate immunity is impaired –> decreased function of macrophages
-infections more rapidly enter the body
-hyperglycemia –> increased bacterial growth and proliferation glucose feeds the infection)
What is DKA? Who is at risk of developing DKA? What are the medical consequences of DKA?
Definition:
- very high levels of blood glucose
-lack of insulin and increased glucagon (more glucose in blood)
-increased release of glucose by liver (gluconeogenesis and glycogenolysis)
Etiology:
-more in DM I > DM II
-release of free fatty acids from adipose tissue lipolysis) –> converted by liver into ketone bodies (ketogenesis)
-ketones lead to acidosis –> respiratory compensation (kussmaul breathing)
** OCCURS BECAUSE LACK OF INSULIN PREVENTS GLUCOSE FROM GETTING INTO CELLS FOR USE AS ENERGY SOURCE
Medical Consequences:
-acidosis –> respiratory compromise
–with a lot of glucose in the urine–> water follows urine –> increased urine output (9-10 L/hr)
-osmotic diuresis: blood volume and blood pressure decrease; loss of H2O and electrolytes; because serum glucose exceeds reabsorption capability of the kidneys
-if severe: hemodynamic compromise= medical emergency
What is DKA commonly precipitated by?
acute illness (infection, pneumonia); MI, CVA, drug abuse (cocaine); poor DM management
Signs and symptoms of DKA:
N/V
abdominal pain
polydipsia- excessive thirst
polyuria
-dehydration (hypotension)
What are the benefits of tight glucose management in the DM population?
-decreases risk of medical complications associated with DM