Diabetes Flashcards
Type 1 DM
“juvenile-onset”
or “insulin-dependent”
Most often occurs under 30
Absent or minimal
insulin production
due to an autoimmune
process
Result of pancreatic beta cell destruction
Prone to ketoacidosis
Causes from autoimmune otherwise unknown
Type 1B DM Vs Type 1A DM
1B caused by nonimmune factors
of unknown (idiopathic) etiologies
1A caused by an immune mechanism
When do manifestations of DM type1 appear?
when
the person’s pancreas can no longer produce insulin
Type 2 DM
by far, the most
prevalent type of DM, accounting for over 90% of patients with
DM
Usually occuring after 35
Pancreas produced insuffiencent insulin OR tissue does not respond to it
polydipsia
Excessive thirst
Lipodystrophy
(hypertrophy or atrophy of
subcutaneous tissue) may occur if the same injection sites are used frequently
Somogyi effect
Usually occurring during the hours
of sleep, the Somogyi effect is associated with a decline in
blood glucose level in response to too much insulin.
Glycemic Index
is the term used to describe the rise in
blood glucose levels after a person has consumed carbohydrate-containing
food.
Diabetic ketoacidosis (DKA)
Diabetic ketoacidosis (DKA) is an acute metabolic complication
of DM occurring when fats are metabolized in the absence
of insulin. It is caused by a profound deficiency of insulin and
is characterized by hyperglycemia, ketosis, metabolic acidosis,
and dehydration (volume depletion). It is most likely to occur
in people with type 1 DM but may be seen in type 2 DM in
conditions of severe illness or stress
Is diabetes increasing?
Yes, particularly type 2
Who are the most likely to develop DM?
Indigenous population
Type 2 diabetes is increasing?
Obesity rates rising
More sedentary lifestyles
People living longer
Increased immigration from high DM prevelant areas
How was DM diagnosed in ancient times
Whether there was sugar in a persons urine (attracting ants)
Pioneer in DM treatment
Candian scientist “Banting”
Depancreatizing dogs
DM used to be konwn as what type of disease
Wasting away
What is Diabetes Mellitis
Metabolic disorder characterized by presence of hyperglycmeia due to defective insulin secretion, defective insulin action OR both
Multisystem disease
Classicifications of DM
Prediabetes
- Impaired glucose tolerance (IGT) or impair fasting glucose (IFG)
FPG= 6.1-6.9 mmol/L
Type 1 DM
Type 2 DM
Notmal Blood Glucose
4.0-6.0 mmol/L
Blood glucose in a prediabetic state
Stays relatively high (above 6)
IGT
Impaired Glucose Tolerance
2 hour glucose levels bw 7.8 and 11.0
Gestational Diabetes
Develops during pregnancy
Usually no longer present after giving birth
Can present as type 1 or 2
Secondary diabetes
Diebetic symptoms related to underlying condition i.e. pancreatic disease, endocrine pathologies, drugs/medical therapy
Cause abnormal blood sugar levels, usually is resolved when issue is solved
Diebetes Insipidus
Not diabetes at all
Nothing to do with pancreas or blood sugar
To do with kidneys, related to pit gland and management of Vasopressin
Pts have polyuria and polydipsia
Metabolic Syndrome
Collection of risk factors increasing persons chance of developing CV disease and DM
Abdominal obesity
Hypertension
Dyslipidemia
Insulin resistance
Dysglycemia (Abnormalities in blood glucose levels)
Often in individuals with sedentary lifestyle
Primary prevention for Type 2: Modifiable risk factors
Obesity
Physical inactivity
HTN
Abnormal cholesterol/lipid levels (Dyslipidemia)
Non- modifiable risk factors for type 2 DM
Age (usually over 45)
Hx of gestational DM
Family Hx
Race/ethnicity
What is the bodys natural response to high blood sugar?
Hormonal regulation
Releases insulin homrone to move blood sugar into cells to be utilized
Body’s response to low blood sugar
Releases counter-regulatory hormones to bring BS up to compensate for normal eating patterns
Which cells in pancreas regulate insulin?
Beta Cells
What does insulin do?
Increases cellular uptake of glucose
Which cells regulate glucogon
Alpha cells
Role of Glucogon
Glucagon increases release of glucose by liver to increase blood sugar
Other hormones that work to increase blood glucose
Epinephrine
Growth Hormone
Cortisol
Stimulate glucose output by the liver
Decrease movement of glucose into cells
Counter-regulatory hormones
When do we need stored glucose
Fasting, intense aerobic exercise
Basal rate of insulin
Constant supply of insulin that is necessary to regulate insulin, sets the baseline
Bolus release of insulin
After meals, body releases large dose of insulin to maintain blood sugar (meet needs of dietary intake)
Specifics of DM type 1
Acute symptoms
Lack of insulin secretion
Destruction of beta-cells resulting in decreased or absent insulin secretion
Manifestation seen when 80%-90% of normnal beta-cell funciton is destroyed
Possible causes of DM type 1
Immune system disorder (genetic predispositon)
Viral component working in combination with genetic
Autoimmune disorder
Specificcs of type 2 DM
Insuline Resistance
- Body tissues do not respond to
Decreased responsiveness of beta cells to hyperglycemia
Decreased abilty to produce insulin
Inappropriate glucose production by liver (Not a primary factor)
Alteration in production of hormones and cytokines by adipose tissue
Livers role in blood glucose regulation
Glucose and glucagon storage/release
Type 1 DM Presents
Pre-adolecents mainly
Usually abrupt diagnosis
- Present usually with Ketoacidosis (Very high blood sugar)
Cachexic appearance (Gaunt, thin, wasting away)
Often Diagnosis precipitated by stess or illness
Often difficult to control BS
Type 2 DM Presents
Typically older age (Adult onset DM)
Slow gradual onset
Combination of genetic and environmental factors
Oral hypoglycemics agents or insulin may be necessary
Relatively stable BS
Diagnosis of DM (Labs)
done with blood test
- Random Plasma Glucose Value
Symptoms of DM RPGV: >/= 11.1mmol/L
Fasting plasma glucose (FPG) >/= 7.0 mmol/L
A plasma glucose value in the 2-h sample (2hPG) of a 75g oral glucose tolerance tst (OGTT) >/= 11.1 mmol/L (simulated test for insulin bolus)
A1C>/=6.5% (In adults)
A fasting plasma glucose
A1C test is of
The amount of glucose attatched to hemoglobin in the blood stream, should be below 6% in normal adults
Positive A1C DM test
> /= 6.5%
Type 1 DM Symptoms
Polyuria
Polydipsia
Polyphagia
Weight loss
Ketonuria & Ketoacidosis
- Fruity breath, N/V, ABD pain
- Very ill person
- Weakness/fatigue
- Visual changes
Type 2 DM symptoms
“Classic “ manifestations w/ gradual onset
Symptoms associated with prolonged hyperglycemia
- Chronic blurred vision
- Recurrent infections (Skin, vaginal yeast)
- Neurophatic pain
- No typical weight loss, often weight gain (especialy middle fat, possible thin limbs)
Often fatigue is the only symptom
Goals for management of Diabetes
Reduce symtoms
Prevent and manage acute complications
Delay onset and progression of long term complications
Attaining desierable wieght
GLycogen
Stored glucose in liver and muscle
Glucose
Source of energy in the body
Glucagon
Strongly opposes the action of insulin, stimulates conversion of flycogen to glucose
Gluconeogenesis
Making glucose from non-carb sources
Glycogenolysis
GLycogen breakdown to make glucose
Endogenous insulin
Insulin in the body made by the bodyEx
Exogenous insulin
Externally made insulin
4-7 BG
Is generally acceptable
What is a hemoglobin A1C
65-85% of people with DM will die of
Heart disease or stroke
What ethnic group is the most likely to develop DM
Indigenous
Hypoglycemia
Not enough glucose in the blood stream
Do DM 1 and DM 2 look different
Yes
DM 2 - Usually caused by insulin resistance. Usually a slow and steady progression - Often fatigue is the only symptom
Type 2 DM
Gradual onset
May have classic manifestations
Symptoms associated with prolonged hyperglycemia (Chronic blurred vision, recurrent infections
ABCDESSS of Diabetes Care
A1C Targets
BP targets
Cholesterol Targets
Drugs for CV and/or Cardio-renal protection
Exercise Goals and healthy eating
Screening for complications
Smoking Cessation (Exacerbates CV issues)
Self Management
Types of Insulin
Rapid - Lispro
Short (Fast) Acting (Humulin R)
Intermediate acting (Cloudy) - NPH
Extended long acting (Cloudy) - Glargine
Premixed (Cloudy) -
Why don’t we massage an insulin injection site?
Affects absorption
When someone is sick does BS go up or down
Generally up, infections INCREASE hyperglycemia
May need INCREASED insulin, unless risk of dehydration
How is diabetes diagnosed (Test)
Plasma BG test NOT a finger prick
How to treat DMs at risk of dehydration to to vomiting OR diarrhea?
Rehydrate appropriately (Water, broth, diet soft drinks, sugar free Kool Aid, diet Jello-O, avoid caffeinated beverages)
Hold SADMANS meds. Restart once able to eat/drink normally
SADMANS meds *** KNOW THIS
[S sulfonylureas, other secretagogues A ACE-inhibitors D diuretics, direct renin inhibitors M metformin A angiotensin receptor blockers N non-steroidal anti-inflammatory drugs S SGLT2 inhibitors]
When DM type 1 are sick, if CBG> 14mmol/L what should they do?
Check urine for ketones
Exercise effect on BG
Increase glucose uptake
Decreased insulin resistance
Effect of stress on BG
Increases insulin resistance and BG
Exercise Precautions
SMBG before and after
Keeo log of activity and BG
Avoid exercise when hypoglycemia is present
Exercise 1-2 hr after meals
Carry carbs and medic alert tag
