Diabetes (Notes)

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What are 3 sources of glucose?: 1. Food intake - Carbs & Proteins
- carbs get broken down into glucose
2. Body Stores - Fat & Glycogen
3. Gluconeogenesis - Proteins and Fats get reprocessed
4. Glycogenolysis - glycogen gets broken down in the liver
What are 3 purposes of glucose?: 1. use it for ATP production
2. store as glycogen in the liver
3. store as fat in adipose tissue
What does the pancreas release that is important for the regulation of glucose? (name 2).: 1. Insulin
2. Glucagon
What does the liver release that is important for the regulation of glucose? (name 1).: Glycogen
What are 5 characteristics of insulin?: 1. Hormone
2. secreted by BETA cells, islets of Langerhans
3. secreted when there is an increase of insulin in the blood
4. short activity duration (Half-life of 5 MINS)
What are 3 uses for insulin?: 1. promotes entry of glucose into tissue cells (EXCEPT brain & RBC)
2. coverts glucose into energy storage (in the forms of glycogen & fat)
3. Facilitates amino acids, K+, Mg+, and phosphate into insulin-sensitive cells
What are 6 MOA (mechanisms of action) for insulin?: 1. circulates freely in blood but cannot diffuse through cell membrane
2. binds to receptor on cell membrane
3. phosphorylation of the receptor occurs
4. 2nd messenger system starts
5. GLUT4 transporter inserts into cell membrane
6. GLUT4 transports glucose into cell (***insulin is unable to transfer glucose into the cell by itself, it needs the help of GLUT4 transporter)
What is Glucagon?: 1. Hormone
2. secreted by ALPHA cells, islets of Langerhans
3. glucagon is secreted when blood glucose is LOW
4. readjusts as necessary based on low glucose levels
5. negative feedback to stop action
- short half-life of 5-6 mins
What are 4 uses for glucagon?: 1. Acts on the liver
2. stimulates GLYCOGENOLYSIS (breakdown of liver glycogen to glucose)
3. stimulates GLUCONEOGENESIS (formation of glucose from amino acids and fat)
4. stimulates lipolysis (breakdown of fats)
(*****NOT effective if there are no liver glycogen stores)
What happens if INTRACELLULAR glucose levels decrease?: more glucose will enter from the blood to restore to normal
What happens if INTRAVASCULAR glucose levels decrease?: glucagon will be released (from ALPHA cells in the pancreas) --> stimulate glycogenolysis and gluconeogenesis within the liver
What happens if INTRAVASCULAR glucose levels increase?: insulin will be released (from beta cells within the pancreas) to facilitate transport of glucose into the cells (with the aid of GLUT4 transporter)
What is the normal range for blood glucose levels?: 4 - 6 mmol/L
________ is an antagonist to insulin. They have opposite effects.: Glucagon
Blood glucose regulation is based primarily on 3 factors:: 1. insulin stimulated after eating
2. glucagon after eating protein or fat-rich meals and between meals when blood glucose drops
3. Constantly occurring - therefore makes it difficult to give insulin in diabetics to precisely match normal control
What is the basic response loop for blood regulation?: low or high blood sugar levels are detected --> interpreted by cells in the PANCREAS --> effector carries out response (high levels - INSULIN released from BETA cells, low levels - GLUCAGON released from ALPHA cells & HPA gets activated
(****low blood glucose levels --> decreased ATP production --> will stop the secretion of insulin)
What is hypoglycaemia?: low blood sugar
What are 2 ways to increased glucose?: 1. Glucagon - stimulates enzymes in the LIVER to break down GLYCOGEN into glucose
2. HPA
What is the difference between GLUCAGON & GLYCOGEN?: GlucAgon - produced from the ALPHA cells in the PANCREAS

GLYCOGEN - comprised of glucose and stored in the liver; glycogen stimulates enzymes to breakdown glycogen into glucose
How does hypoglycaemia activate the HPA axis?: low blood sugar is a stressor that activates HPA axis --> epinephrine is released from the adrenal medulla --> acts on liver to stimulate glycogenolysis

low blood sugar is a stressor that activates the HPA axis --> anterior pituitary releases ACTH --> adrenal cortex --> cortisol --> acts on liver to stimulate gluconeogenesis, lipolysis, and muscle protein catabolism
What are 5 S&S of hypoglycemia?: 1. headache
2. irritability/confusion (b/c of decreased glucose)
3. increased HR (epi increases firing rate of SA node)
4. pale/cold (catecholamines - vasoconstriction)
5. sweating (stimulation of sweat glands)
What are 5 effects of insulin?: 1. increases uptake of glucose by most cells
2. activates enzymes for glucose use & storage
3. inhibits enzymes for glucose production
4. activates enzymes for protein & fat synthesis
5. inhibits breakdown of proteins & fats
What is type 1 diabetes mellitus?: - NO insulin is produced
- defect in pancreatic BETA cells
- approximately 10% of people have this type of diabetes
What is type 2 diabetes mellitus?: - SOME insulin is made and released (INSUFFICIENT amount)
- defect in the # of insulin receptors OR sensitivity to insulin
- approximately 90% of people have this type of diabetes
How is diabetes diagnosed?: 1. S&S of hypoglycaemia
2. glucose in urine (glucosuria) - NOT an accurate way to diagnose (increased glucose urine levels depend on renal threshold for glucose - varies by individual)
3. Blood glucose levels - most accurate (4-6 mmol/L)
- diabetes if fasting level is greater than 7 mmol/L OR
- impaired glucose tolerance - glucose levels are greater than 11.1 mmol/L 2 hrs after taking 75g glucose OR
- random blood glucose levels greater than 11.1 mmol/L combined with thirst, excessive hunger, and excessive urine
In type 1 diabetes, why is no insulin produced?: Beta cells have been destroyed by auto-antibodies, viruses, drugs, or diseases
What happens in type 1 diabetes when there is no insulin being produced from the beta cells?: no insulin --> decreased glucose entry into cells --> glucose stays in blood (HYPERGLYCEMIA) & cells "starve" --> compensatory mechanisms occur
What happens when cells "starve" (in type 1 diabetes?: 1. decreased ATP production
2. decreased energy (tired)
3. Difficulty concentrating
4. HPA activated:
- epi/norepi increase glycogenolysis in the liver
- cortisol breaks down muscles/fat
- rapid weight loss but eating more
- ketones from lipolysis: acetone odour (fruity smell)
Explain the fluid shift of high serum glucose levels. (list 2 things): 1. fluid shifts from intracellular space to intravascular space (causing poor skin turgor & dry mucous membranes)
2. kidney increases excretion of fluid to get rid of glucose (causing polyuria & glucosuria)
What are 6 S&S of uncontrolled hyperglycemia in type 1 diabetes?: 1. hyperglycemia - increased blood sugar
2. Glucosuria - increased glucose in urine
3. Polyuria - increased kidney GFR to excrete more glucose --> frequent urination
4. Thirst
5. fatigue, difficulty concentrating (loss of consciousness when severe)
6. Weight loss (fat/muscle breakdown) - key tone production when severe
How do you treat type 1 diabetes?: - give exogenous insulin several times per day and/or by actual blood glucose levels
- subcutaneous injection
(***if taken by mouth, it is inactivated by digestive enzymes in the GI tract)
What are 3 diabetic complications?: 1. MECHANISM A:
Glycosylation of:
- RBC - reduced O2 carrying capacity (HbA1C)
- capillary basement membrane damage to blood vessels manifested as:
a) retinopathy
b) atherosclerosis (Htn, CVA, IHD)
c) nephropathy (kidney damage)
2. MECHANISM B:
non-insulin using cells metabolize glucose by polyol pathway --> sorbitol & fructose
- damages ion pumps
- attracts water (hyperosmolar)
- cataracts (lens thickening)
- peripheral neuropathy (nerve damage)
3. MECHANISM C:
- increased risk of infection
- rapid growth of germs because of sweet environment
- reduced defence against germs:
i) poor healing of skin --> decreased barrier
ii) affected WBCs:
a) function: decreased phagocytic activity
b) ability to get to site (altered blood supply)
What is called when Hb binds to glucose?: HbA1C
What is glycosylation?: It's when glucose binds to proteins, lipids, and other molecules
What is HbA1C?: the amount of glucose that the cell has been exposed to over 120 days (normal: less than 6%)
(****good measure for longer-term glucose control)
What are 2 long-term (chronic) problems of type 1 DM?: 1. insulin therapy inaffective --> high blood glucose persists
2. develop complications of diabetes
What are 2 acute (develop rapidly) problems of type 1 DM?: 1. no insulin at all
2. diabetic ketoacidosis (DKA)
What are 3 problems that atherosclerosis can lead to?: 1. Hypertension
2. Cardiovascular disease
3. Ischemic heart disease
What is diabetic ketoacidosis? (DKA): - profound hyperglycemia from no insulin that has exaggerated effects of compensation
What are 3 effects of diabetic ketoacidosis (DKA)?: 1. intracellular dehydration & hypovolemia
2. loss of consciousness
3. ketosis (ketones from lipolysis): acidic so get metabolic acidosis
What does the HPA axis release in the occurrence of diabetic ketoacidosis (DKA)?: 1. Epinephrine
2. Norepinephrine
3. Cortisol
4. Glucagon
How is diabetic ketoacidosis (DKA) diagnosed?: 1. S&S
2. blood glucose levels
3. arterial blood gases
What are 3 ways to treat DKA?: 1. Give fluids (***always give fluids 1st, then insulin)
2. Give insulin
3. Manage acidosis
What is type 2 diabetes? (List 3 characteristics): 1. Dysfunction of pancreatic BETA cells
2. Change in # or sensitivity of insulin RECEPTORS
3. More gradual onset

(***"adult-onset" is misleading because kids now get type 2
- 25% of Canadians over age 45 have diabetes
- for every known case, there is one unknown case)
What is the key risk factor for type 2 diabetes?: Obesity
What are the S&S of type 2 diabetes?: same as type 1 EXCEPT:
1. slower onset
2. no ketosis
3. higher glucose levels reached

(***differences are due to availability of SOME insulin - therefore S&S are not as drastic)
What are the long-term (chronic) problems associated with type 2 diabetes mellitus?: - SAME as type 1:
1. Glycosylation of capillary basement membrane (causing retinopathy, atherosclerosis, and nephronopathy)
2. Glycosylation of RBCs - causing reduced O2 carrying capacity of Hgb
3. Polyol pathway --> sorbitol & fructose
4. increased infection
What does HHNKS stand for?: Hyperosmolar Hyperglycemic Non-Ketotic Syndrome
What is hyperosmolar hyperglycemic non-ketotic syndrome (HHNKS)?: - occurs in people with type 2 diabetes
- has higher glucose levels (greater than 33 mmol/L)
- more severe dehydration

(***there are no ketones in type 2 diabetes, therefore no DKA; HHNKS occurs instead)
(***the higher your sugar, the more dehydrated you will be)
How do you treat HHNKS?: - same as for DKA:
1. Give fluids
2. Give insulin
3. Manage acidosis (***acidosis is not as severe for HHNKS because there are no ketones (which are acidic) as in DKA
What are 3 ways to treat type 2 diabetes?: 1. weight loss (may help restore some lost sensitivity of insulin receptors)
2. Diet control (reducing calorie intake means available insulin may be sufficient)
3. Drugs
What drugs are used with type 2 diabetes?: Oral hypoglycemic agents
(will learn more in pharmacology)
(****oral agents can't be given in type 1)
What are 3 effects of oral hypoglycemic agents?: 1. Increases the release of available insulin from beta cells (does not increase insulin production)
2. improves # or sensitivity of insulin receptors
3. delay carbohydrate digestion & absorption
When is exogenous insulin given in type 2 diabetes?: - if treatment of diet, wt. loss, and oral agents are insufficient

(***lower dose/frequency of insulin is required - most needs are met by own pancreas & drugs)
(*** avoid using: IDDM (type 1) & NIDDM (type 2) because type 2 diabetes is not insulin dependent but may be insulin requiring!)
Is type 1 or type 2 diabetes more serious?: neither is more serious.
- same complications
- HHNKS vs. DKA
- hypoglycemia if on oral drugs

(***type 1 treatment is more dramatic and intense - subcutaneous injections, constant monitoring, & worry re hypoglycemia)

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Created By daisy497