128 terms

Diabetes Patho


Terms in this set (...)

Diabetes is a disease in which the
which the body does not produce or properly use insulin
Insulin is produced by
-Beta cells of the islets of Langerhands of the pancreas
What is insulin?
A hormone directly secreted into the blood stream to uptake of glucose
How insulin works to lower blood sugar
Lowers blood sugar by attaching to cells and allowing transport of glucose into cells to be used as a source of energy, or if in excess, to be stored as glycogen.
More Actions of Insulin
-Prevents fat and glycogen breakdown
-Inhibits gluconeogenesis and increases protein synthesis.
-Increases fatty acid transport into adipose cells
-Inhibits adipose cell lipase
-Increases transport of amino acids into cells
Insulin is required for cellular transport of
Glucose into muscle cells and adipose tissue
Insulin is NOT required for cellular uptake of
Glucose into the liver cells, brain, and RBCs
Diabetes Mellitus
Group of metabolic disorders in which there is impaired metabolic functioning affecting carbohydrate, fat and protein metabolism and characterized by hyperglycemia. It results from an imbalance between insulin availability and need.
DM is the
7th leading cause of death of adults in the US
DM is more prevalent in
Native Indians, African-Americans, and Hispanics
Pre diabetes
86 million
All diabetes
29.1 millioin
Significance of DM
-Major risk factor for heart disease and stroke
-Number one cause of blindness
-Number one cause of end-stage renal disease (ESRD)
-Number one cause of non traumatic lower extremity amputations
-Huge contributor of medical expenses, and cause of decreased QOL among many
Complications of DM
-Heart disease
-Neuropathy (amputations)

-Complications take around 5 years (of hyperglycemia) to develop in both types
Factors Contributing to Hyperglycemia
-Impaired secretion of insulin (Pancreas)
-GI absorption of glucose
-Decreased insulin stimulated glucose uptake (Muscles)
-Increased basal hepatic glucose production (Liver)
Mechanisms of Controlling Blood Glucose
-Insulin secretion
-Uptake and utilization of glucose by peripheral tissues
-Glucose Production in the Liver
Other Types of Diabetes
including genetic defects, MODY- (Mature Onset of Diabetes in the Young) is autosomal dominant and linked to Chromosomes 7 and 20,associated with obesity; diseases of the pancreas (pseudocysts); endocrine disorders such as Cushings
Hormones of the pancreas to control glucose regulation

They control the regulation and absorption of glucose, amino acids and fatty acids.
-Glucagon secretion causes transformation of glycogen (stored in the liver) to glucose.
-Low levels of blood glucose stimulate the release of glucagon from the pancreas.
-RAISES blood glucose
-A cells
Glucagon: Clinical Significane
Glucagon (IM/SC) can be given to the person with diabetes who is unconscious, at home, and has low blood sugar in order to cause the release of stored glycogen which then breaks down into glucose for body needs.
-Islet amyloid polypeptide
-Co-secreted with insulin from the beta cells
-Plasma levels increase in response to nutrition stimuli to inhibit gastric emptying and glucagon section.
-May cause degeneration of the beta cells and contribute to development of T2DM
Amylin: Clinical Significane
Given SC before meals as symelin (Pramlintide acetate) in people with T1/T2 to slow the movement of food through the stomach and thereby lower postprandial blood glucose.
-Give before meals to lower blood sugar rise after a person eats
-Released by the Delta cells of the Pancreas (also in the pituitary)
-Inhibits release of both insulin and glucagon
-Decreases gastrointestinal activity after ingestion of food, extends the time during which food is absorbed into the blood.
Somatostatin: Clinical Significance
synthetic forms of hormone not used in diabetes but used in acromegaly and other growth hormone disorders.
-Incretins are intestinal hormones released in response to ingestion of food that, at physiologic levels, increase the insulin response in a glucose-dependent manner.
-Incretin response in T2D is known to be decreased.
-Incretins are GIP and GLP-1 and are degraded by an enzyme, DPP-4
Incretin: Clinical Significance
-Exenatide, a synthetic GLP-1 that is resistant to DPP-4 degradation, is given by injection to potentiate insulin release; A DPP- 4 agent (Januvia) has been synthesized to decrease hyperglycemia
-Original research in the Gila monster
Don't give Incretin to T1DM bc?
They don't have insulin to begin with
Diagnostic Criteria for Diabetes
-A1C>= 6.5% lab needs to be certified and standardized to DCCT assay
-Fasting blood glucose>= 126 mg/dl (7.0 mmol/l. Fasting is no caloric intake for at least 8 hours.
-2 hour plasma glucose>=200 mg (OGTT, 75 g glucose)
-With signs of hyperglycemia, random glucose >=200 mg.
-RBC getting glycolistated with glucose
-Average of the last 3 months of blood glucose levels
Gestational Diabetes GDM
-Develops during pregany
-All women not known to have diabetes undergo a 75 gm OGTT at 24-28 weeks of gestation/

-Diagnostic Criteria: ADA, 2012
Fasting >= 92
1 hour >=180 mg/dl
2 hour >= 153
GDM: Treatment
Glyburide or preferably insulin
-Absolute insulin deficiency
-Results from a severe, absolute lack of insulin caused by a reduction in beta-cell mass
T1DM: Symptoms
-Weight loss

Symptoms are due to an absolute lack of insulin available to cells
Diabetes causes
-Osmotic diuresis which causes polyuria
In diabetes the patient is really thirsty and hungry bc
-Glucose is not being brought into the cells for use (Hungry)
-Osmotic diuresis (peeing off all the water)
T1DM: Most common in
Under age 30
T1DM: Treatment
-Without treatment, progression to Diabetic Ketoacidosis (DKA) leading to coma and death

-Insulin, MNT (medical nutrition therapy), and physical activity
T1DM: Etiology
Type 1 A: Immune mediated (autoimmune destruction of beta cells)
Type 1 B: Idiopathic (unknown etiology)

-Islet destruction: Genetic susceptibility, autoimmunity, and an environmental insult.
People with T1DM always take?
-Must receive exogenous insulin injections or they will die.
T1DM: Genetics
-Long known that diabetes can aggregate in families
-Precise mode of inheritance is unknown
-Concordance rate for twins is 50%
-Only 5-10% of children of first-order relatives develop overt disease
-At least one of the susceptibility genes resides in the genes of chromosome 6 (HLA-D); there may be more
T1DM: Autoimmunity
-CD4+ and CD8+ T lymphocyte cells are frequently found in islets in cases of recent onset
-90% of pts. have circulating islet cell antibodies (ICA) within a year of diagnosis
-Approximately 10% have other organ-specific autoimmune disorders such as Graves Disease, Addison's Disease
T1DM: Environmental Factors
-Viruses are suspected as initiators or the trigger to cause diabetes to begin
-There has probably already been a long latency period of development with subsequent loss of beta cell tissue
-Chemical toxins and ingestion of cow's milk as an infant have also been implicated
Blood Glucose Monitoring
Fasting blood sugar FBS- as needed,
Blood glucose machine- Fingertip, alternative site- 4X daily for T1, 2X for T2, test two hours after meals occasionally
A1C- 3-4 times annually, T1 and T2
Medicare/Medicaid Coverage for costs
When was insulin discovered?
Banting and Best discovered insulin in Canada in a dog in 1921
The patient with type 1 diabetes has lost 8 lbs over the last 3 days. Which of the following must be given/increased in dosage in order to regain homeostasis?
T2DM: Patho
-Insulin resistance
-Diminished tissue responsiveness to insulin at one or more points in the insulin pathway, leading to hyperglycemia and then eventually overt diabetes
-Insulin secretion is INCREASED, NORMAL, or DECREASED
-Inappropriate Hepatic glucose production
-Beta cell dysfunction
Insulin Resistance
-There is impaired attachment of the insulin molecule to the target cell
-Peripheral insulin resistance in muscle and fat
-This results in high circulating blood levels of glucose
Hepatic Glucose Production
-Hepatic glucose production continues even though a person is not eating

-Clinical Significance: In later stages of Type 2 diabetes, despite adherence to diet recommendations, blood glucose levels may be high and uncontrolled; a person with diabetes has no external control over this process and will probably need insulin or an oral agent that diminishes hepatic glucose production e.g. Glucophage (metformin)
Dyslipidemia Metabolic Defects in T2DM
-Eventual decreased beta cell insulin secretion
-Increased triglyceride levels
-Decreased HDL levels
-Increased LDL levels
T2DM: Symptoms
-Acute classical signs of Type 1 RARELY are present
-Blurred vision
-Skin infection
-Foot ulcers
-Vulvovaginitis (yeast)
T2DM: Risk Factors
-Most common over age 40
-Family history of T2D in 1st or 2nd degree relative
-Insulin resistance signs, e.g. acanthosis nigricans, hypertension, dyslipidemia, PCOS (polycystic ovarian syndrome),
-Small for gestational age birth wt, maternal hx of GDM during child's gestation
-History of GDM
-History of Diabetes related complications e.g. neuropathy, retinopathy, nephropathy, gastroparesis
-Presence of insulin resistance; there may be a decrease in insulin receptors associated with obesity
-Genetics: Concordance rate between identical twins is >90%
If baby over 9 lbs
MOM is at high risk for T2DM
If baby low birth weight
BABY is at risk for T2DM
Diagnostic Testing for Asymptomatic Adults
-Asymptomatic Adults of any age who are overweight or obese (BMI > 25 kg/m2 ) and who have one or more additional risk factors for diabetes.
-If no risk factors, then begin testing at age 45,
-Repeat testing every three years if normal.
-ONLY applies to Type 2
-Diagnostic criteria: Impaired glucose tolerance (140-180), impaired fasting glucose (100-125), A1C 5.7-6.4%
Prevention of T2DM
-Referral to an effective ongoing support program targeting 7% total body wt loss and increasing physical activity to at least 150/min/week of moderate activity such as walking.
-Metformin may be used for PREVENTION T2D in those with IGT, IFG, or A1C 5.7-6.5 especially if BMI >35 , age <60, and women with prior GDM
-Individualized Medical Nutrition Therapy (MNT) preferably with a registered dietician familiar with components of Diabetes MNT
T2DM: Children
-The rise of obesity in children has precipitated a huge rise in type 2 in children which was not commonly dx until the last decade.
-Risk Factors:
1. Low levels of exercise; no PE in school
2. High fat levels in foods in school lunches
3. Coke/soda machines in schools
-Treatment/Prevention: Metformin
T2DM Causes Hyperglycemia despite the availability of what?
People with T2DM will start taking what?
-Beta Cell Failure will most likely eventually occur, requiring insulin injections
-Or if patient is sick or in the hospital they may be put on sliding scale insulin
T2DM: Treatment
-Dietary Management: individualized diet plan focusing on mild to moderate weight loss, limitation of fat to <30% fat calories, counting carbohydrate grams, and protein according to recommendations for general public unless person has kidney disease

-Exercise: has been shown to lower BG in persons with Type 2; weight loss if obese

-Oral medications which lower blood glucose, single/multiple; insulin may be needed
The patient with diabetes is complaining about feeling shaky and hungry. The treatment is:
Oral glucose
T2DM: Tests to Monitor and Manage
1.) Glycated or glycosolated hemoglobin (HgA1c or AIC) - 4-6 % is normal; diabetics should have <7 % (Should be done 3-4 X per year)
2.) Self-monitoring of blood glucose (SMBG) (finger stick): Pt. must have a monitor and strips for reading the results; usually done 2-4 X per day unless needed more often for intensive control
3.) Periodic fasting Blood glucose
Effects of Catecholamines on Blood Glucose Levels
-Epinephrine and Norepinephrine raise BG levels during times of stress, e.g. fever, surgery, emotional problems, pain
-Mechanism: Inhibits insulin release and promotes glycogenolysis by stimulating the conversion of muscle and liver glycogen to glucose.
Glucocorticoid Hormones Effects on Blood Glucose
-Raise blood glucose by stimulating liver to break down glycogen to glucose
-Can actually cause diabetes mellitus in some predisposed persons.
-Can also moderately decrease tissue use of glucose.
Glucocorticoid Hormones: Clinical Significance
A sick person with diabetes will have more difficulty maintaining normal glucose levels due to the stressor effects of glucocorticoid hormones
Diabetic Ketoaciosis
-Acute complications of DM
-Usually occurs in type 1 when the lack of insulin leads to breakdown of adipose tissue into fatty acids
-Can occur at the beginning of the disease before diagnosis or later if management is not good
DKA: Patho
-Metabolic acidosis
Major Metabolic Problems in DKA
-Metabolic acidosis
Precipitating Factors
-Newly diagnosed type 1 and some type 2's
-Not taking sufficient insulin
-Too little exercise/too much food/stress/infection for the insulin being taken
-Slow onset over several days unlike hypoglycemia
DKA Labs
-Hyperglycemia > 250mg/dl
-Bicarbonate low (<15 mEq/L)
-Ph low (< 7.3)
-Ketonuria (moderate to large)
-Na level low or normal related to intracellular/extracellular shifts
-K level normal or elevated, actual level is depletion
DKA Symptoms
-Classical S&S of DM related to osmotic effect of glucose-polyuria
-Abdominal pain or tenderness
-Fruity odor to breath,
-Kussmaul's respiration
-Hypotension, tachycardia, (hypovolemia)
-Decreasing level of consciousness;
-Progression to coma, if no intervention;
-Death can result: metabolic acidosis and hypovolemic shock are both critical events
DKA: Treatment
-IV Insulin
-Replacement of electrolytes, Na, K, PO4, Mg as necessary
-Monitoring of electrolytes and glucose q hour
-Admission to ICU is usually necessary
-Identification and Rx of underlying cause
-An acute complication of diabetes
-Previously called "insulin reaction"
-Etiologies: Too much insulin or oral agents, too much exercise, too little food
-Definition- Blood glucose 53 mg/dl or lower
-Requires fast intervention to prevent coma and death (brain must have glucose!)
Hypoglycemia: Symptoms
-Confusion, headache, slurred speech, change in emotional behavior, sleepiness, hunger, hypotension, diaphoresis, pale and cool skin, tachycardia, coma.
-Each person responds in an individual way, and usually the same way each time.
-Hypoglycemia Unawareness may occur- person unable to feel effects of low blood sugar
Hypoglycemia: Patho
lowering of blood glucose means that the cells of the body are lacking glucose needed to perform cellular functions; brain must have glucose. Also, Sympathetic NS activated
Hypoglycemia: Treatment
Administration of 15 gms glucose, e.g candy; follow by a complex carbohydrate; if unconscious, IV 50 % glucose is given; glucagon can be given to Type 1
Hyperglycemic Hyperosmolar State HHS
-Hyperglycemia WITHOUT DKA
-Happens in the eldery
-Hyperglycemia >600 mg/dL (33.3 mmol/L)
-Plasma Osmolarity > 320 mOsm/L
-No Ketoacidosis
-Depressed sensorium (NOT clinical depression!); (limited ability to respond cognitively appropriately)
-Seen most frequently in elderly people with T2D
Complications of HHS
severe potassium loss, seizures, cerebral edema, severe dehydration
A patient age 82 is admitted into the ER with a diagnosis of HHNK. His blood glucose is 1500 mg/dL. Which of the following represents one difference between HHNK and Type 2 diabetes?
BGs are higher in HHNK than in T2DM
The blood glucose level is ________ in hypoglycemia while in DKA it is ______.
DKA: > 250mg/dl
Hypoglycemia: 53 mg/dl or lower
The normal (fasting) blood (or plasma) glucose level is _________.
70-100 mg/dl
Hypoglycemia is usually felt with a glucose level of _______________.
Less than 53 mg/dl
A person with hypoglycemia should receive __________________.
15 gms glucose
A person with DKA should receive ______________________.
IV Insulin
Longterm Chronic Complications
-Major cause of blindness, amputations, need for renal dialysis
-T1DM and T2DM
-Complications affect every symptom
-peripheral neuropathy
-macro-vascular complications
-skin lesions and foot ulcers
Most common cause of of death
Cardiac complications
(CAD resulting in MI)
Chronic Complications: Patho
1. Polyol Pathway: this pathway represents the mechanism for converting (OH) hydroxyl groups on the glucose molecule to sorbitol and then fructose; in the eye lens sorbitol causes swelling and opacity. Kidneys, nerves and blood vessels also use this pathway.
2. Formation of glycoproteins (advanced glycation end products; these are found in the basement membrane and produced structural defects in the eye, kidney, and vascular system.
3. Problems with tissue oxygenation; a defect in the RBC function that interferes with release of oxygen from the hemoglobin molecule
Protein Kinase C
An intracellular signaling molecule that regulates permeability, vasodilatation, endothelial activation, and growth factor signaling. Levels are elevated in diabetes and can cause disorders in mitochrondrial function in response to chronic hyperglycemia.
-Diabetes is the leading cause of new cases of blindness in adults 20-74
-Care: Annual Dilated pupillary exam
-Diabetic Retinopathy
Kidney Disease
-Diabetes is the leading cause of kidney failure
-Annual microalbumenuria exam
Peripheral Neuropathy
-60-70% of people with diabetes have mild to severe nervous system damage
-60% of non-traumatic lower-limb amputations occur in people with diabetes
-Check feet without shoes/ socks every provider visit.
Foot and Leg Neuropathies: Patho
-Thickening of the basement membrane of the walls of the blood vessels supplying the nerves
-Demyelinization process occurs that causes a slowdown in nerve conduction
-Sensory neuropathy leads to loss of pain and pressure sensation; injuries go unnoticed
Foot care for Diabetics
-No shaving calluses
-No open toed shoes
-Do not use alcohol, iodine, etc on any skin breaks
-Once a year podiatrist visit (ADA)
-Inspection of feet by physician at every visit (ADA)
-In hospital, daily inspection and documentation of feet by nurse
-Assessment of level of knowledge re foot care by nurse
Prevention: Peripheral Neuropathy
-Control of Blood Sugar
-Daily inspection of feet with mirrors, look between toes
-Always wear shoes: indoors & outdoors
-Do not use heating pads
-Break in new shoes gradually
-Trim nails carefully - avoid injury
Normal Glucose
< 70-100 (fasting)
100-126 (fasting)
Diabetes glucose
> 126 (fasting)
People with pre-diabetes should
Lose 5-8% of their body weight
DCCT Research Study: Conclusions
-Intensive therapy of patients with insulin-dependent diabetes delays the onset and slow progression of retinopathy
-Intensive therapy reduces risk of albuminuria and microalbuminuria and therefore progression to ESRD
-There is a clear-cut efficacy (benefit) of intensive insulin therapy in reducing long-term complications but risk of hypoglycemia increases three times.
-Significant difference in HgA1C average (P<0.001)
-After 5 yrs there was a 50% difference in incidence of retinopathy
-Nephropathy developed less frequently
-Reduction of incidence of neuropathy by five yrs.
-Intensive therapy reduced develop. of hypercholesterolemia by 34 %
Management of Diabetes in Adults
1. Dietary management
2. Prescription for exercise (150 minutes per week)
3. Hyperglycemic control, insulin, oral agents (not in T1), or both
4. Blood glucose monitoring
5. Blood pressure to < 130/80 (ace inhibitor or ARB), usually two or more agents required.
6. Dyslipidemia management (LDL< 70 or <100; HDL > 50; triglycerides < 150.)
(Lifestyle, increased activity, weight loss, and smoking cessation, statins, fibrates)
Anti-platelet Agents
Just know you need to take an aspirin

-Platelets in diabetes have decreased function activation (thromboxane A)
-Give antiplatelet aggregators
-Aspirin- 81- 325 mg/ daily,
-Clopidogrel - Plavix daily, 1st year after acute coronary syndrome
Regular Insulin
-Short acting
-Onset: 30-60 min
-Peak: 2.5-5 hours
-Duration: 6-8 hours
Lispro (Humalog)
-Rapid acting
-Onset: 5-15 min
-Peak: 1-1.5 hours
-Duration: 3-5 hours

-Give SC only 5-15 minutes before a meal
-Very quick acting but action lasts for only 5 hours
-Good for those who eat irregularly
-Lispro does not provide basal insulin needs; use NPH, Lantus, or other long-acting insulin
-Can be mixed with NPH
-Do not mix with Lantus
-Monitor BG levels, hypoglycemia, allergic reaction,
Aspart (novolog)
-Rapid acting
-Onset: 5-15 min
-Peak: 1-1.5 hours
-Duration: 3-5 hours
-Intermediate acting
-Onset: 60-90 min
-Peak: 4-10 hours
-Duration: 16-24 hours
70% NPH, 30% Regular
-Pre mixed combo
-Onset: 30-60 min
-Peak: 3-4 hours and 8-12 hours
-Duration: 12-18 hours
Levimir (Determir)
-Long acting
-Onset: 2 hours
-Duration: 20-24 hours
Lantus (Glargine)
-Long acting
-Onset: 2-4 hours
-Duration: 20-24 hours

-Introduced June 2001
-Produced by recombinant DNA using E coli (HUMAN)
-Give SC only, NEVER IV.
-The exact time it lasts is individual as with all insulins
-Monitor for hypoglycemia, allergic reactions, injection site reactions, lipodystrophy
-Given at bedtime once per day
-Clear unlike most long acting insulins
Oral Diabetic Agents
-1st Generation Sulfonylureas (1950) e.g.- orinase, dymelor, tolinase, diabinese
-2nd Generation Sulfonyureas (1980)- Glucotrol, glyburide, diabeta,

Both categories of drugs stimulate the pancreas to produce more insulin; side effects of 1st generation tend to involve hypoglycemia, the heart and liver. The 2nd generation have lower rates of side effects.
2nd Generation Sulfonylureas
-glimepiride (Amaryl); glipizide (Glucotrol & Glucotrol XL); glyburide (Diabeta, Glynase, Micronase)
-Lowers blood glucose by stimulating release of insulin from the pancreas; increases sensitivity to insulin at receptor sites; may decrease hepatic glucose production;
-Side Effects: hypoglycemia, disulfiram like reaction with alcohol; weight gain
Biguanides (1990's)
-Biguanides: Metformin (glucophage),
-Increases sensitivity to insulin; decreases hepatic production of glucose; decreases intestinal absorption of glucose
-Decreases amount of insulin needed by Type 2's
Monitor for lactic acidosis; does not cause hypoglycemia
Thiazolidinediones (Glitazones): 1990's
-Rosiglitazone (Avandia); pioglitazone (Actos)- decreases insulin resistance by increasing insulin action at receptors and post receptor level in hepatic and peripheral tissue;
-Monitor for hypoglycemia, fluid retention; may decrease effect of oral contraceptives; usually given with insulin or sulfonylurea but can be used as monotherapy; check liver enzymes q 2 months for first year
Exenatide (Byetta)
-Byetta stimulates insulin secretion, slows emptying of the stomach and inhibits production of glucose by the liver. It also appears to suppress appetite and helps weight loss. This would be a particular advantage with type 2 diabetes; given SC
-Major concern is the increased incidence of pancreatitis linked to use of this drug
DDP-4 Enzyme Inhibitors
-Introduced in 2006
-Drug: Sitagliptin (Januvia)
-Mechanism of Action (MOA) - blocks DDP-4 enzyme inhibitors and thereby increases the release of insulin after blood glucose rises (glucose dependent).
-Less potential for hypoglycemia
-repaglinide (Prandin)
-Stimulates insulin secretion via closing or inhibition of ATP-sensitive K channels in beta cells; monitor for hypoglycemia; monitor for URI
-Usually given with metformin
Mr. Carlos Ramirez is 48 years old and arrives at the ED two days ago with a blood glucose of 395 mg/dl. His wife and two children, ages 8 and10, accompany him.
1. What are his signs and symptoms and why?
2. What kind of diabetes does he probably have?
Carlos tells the RN that he has been urinating large amts for several months and has lost 25 lbs over the last two months, is always hungry, eats all the time, and has blurry vision.
What is the diagnosis? What is the immediate treatment
Carlos states that he knows that diabetics can't have foods containing sugar because his grandmother had diabetes before she died. How should the nurse respond?
We now know that a person with diabetes can have a diet with some sugar in it. We call it the consistent carbohydrate diet. I will get a dietician to help you and your wife learn about it.
Glucose Goal Premeal
130 mg/dl
Carb goal for meals
3 carbs
The nurse decides to discuss the children's weight with their mother since they look like they are overweight. The rationale for this decision is based on the father's diagnosis of diabetes AND (select all that apply):
Carlos is referred to a certified diabetes diabetes nurse educator (CDE) who teaches him self management lifestyle changes. One of these changes involves his need to give insulin. Which of the following should the CDE emphasize?
Carlos has an A1C done the day before he goes home. He tells his CDE that he is discouraged because he knows that the A1C should be <7% and his is 12.2%. How should the CDE respond? (check all that apply).
The RN teaches Carlos how to check his blood glucose per fingerstick. How often and when should he check his glucose levels when he goes home?
Carlos is placed on insulin 10 Units Lantus in the PM and on correction factor insulin before breakfast.
Explain the concept of correction factor, basal and bolus insulin.
What is the rationale for using insulin in this patient rather than an oral medication?
John, age 17, is participating in a walk- a - thon and suddenly starts staggering and quickly becomes unconscious. His girlfriend states he has Type 1 diabetes and takes Lantus insulin. Paramedics are called but there is no equipment to check his blood glucose before they arrive. How should he be immediately treated ? If her were awake, how would the treatment differ?
Desired outcomes
-Quality of life - many people with diabetes are found to have high stress levels and depression
-"Good glycemic control" and BP 130/80 or < 7.0
-Prevent or treat early the potential acute complications of DM - hypoglycemia and DKA
-Prevent or delay chronic complications, such as kidney disease, CAD, foot ulcers, neuropathy
-Routine checks for microalbuminuria - an early indication of kidney disease or dysfunction
-An educated patient!