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54 Cards in this Set

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What are 5 sources of glucose?
1. Food intake (carbs & proteins)
2. Body stores (fat & glycogen)
3. CHO --> broken down into glucose units
4. Gluconeogenesis - proteins & fats get reprocessed
5. Glycogenolysis - glycogen stores in LIVER get broken down into glucose
What are 2 uses for glucose?
1. ATP production
2. Storage (liver - glycogen; adipose tissue - fat)
Where does insulin come from?
beta cells in the PANCREAS
Where does glucagon come from?
alpha cells in the PANCREAS
Where does glycogen come from?
storage site within the LIVER
What is insulin?
- hormone
- secreted when blood glucose levels are high
- short half-life = 5 mins
What is the effects of insulin?
- promotes entry of glucose into tissue cells (EXCEPT brain & RBCs)
- stimulates enzymes to convert glucose to glycogen and fat (which are energy stores)
- stimulates enzymes to synthesize protein (unable to store protein - gets broken down into amino acids and used elsewhere)
How does insulin work? (MOA)
- circulates freely in blood (not permeable to CM)
- binds to receptor on cell membrane
- receptor undergoes phosphorylation
- GLUT4 transporter is signalled to insert into cell membrane
- GLUT4 transports glucose into the cell (see textbook)
What is needed to complement insulin in transporting glucose into the cell?
GLUT4 transporter
What is glucagon?
- hormone
- secreted when blood glucose levels are low
- short half-life = 5-6 mins
What is the purpose of glucagon?
- acts on the LIVER
- stimulates enzymes to break down glycogen into glucose (glycogenolysis)
- stimulates gluconeogenesis
- stimulates lipolysis
(***Note: if there are no glycogen stores in liver, glucagon is not effective)
What is the range for normal blood glucose levels?
4 - 6 mmol/L
When is glucagon secreted?
- when glucose levels drop (between meals)
- after eating a protein or fat-rich meal
Besides glucagon, what is a backup mechanism for regulating hypoglycemia?
HPA axis
What does cortisol do to regulate hypoglycemia?
- stimulates lipolysis
- muscle and protein catabolism
- gluconeogenesis
What are the signs and symptoms of hypoglycemia?
1. Headache
2. Irritability / Confusion
3. Increased HR (epi on SA node)
4. Pale (catach - vasoconstriction)
5. Sweating (stimulating of sweat glands)

(***classic S&S of HPA stimulation)
What is type 1 diabetes?
- NO insulin is synthesized
- defect: in beta cells
What is type 2 diabetes?
- insufficient insulin (some insulin is made and released)
- defect: insulin receptors (due to numbers of receptors or sensitivity to insulin)
Where is the defect in type 1 diabetes?
pancreatic beta cells
Where is the defect in type 2 diabetes?
insulin receptors
(due to the number of receptors or the sensitivity of the receptors to insulin)
What are 2 clues to get a blood test for diabetes?
- signs and symptoms of hyperglycemia
- glucosuria

(*cannot diagnose diabetes by glucosuria)
Diabetes is diagnosed if fasting level is ________ OR
Impaired glucose tolerance - levels 2 hours after 75 g glucose _________ OR
Random BG level _________ combined with signs and symptoms of ________, ________ __________ & _______ __________.
greater than 7 mmol/L;
greater than 11.1 mmol/L;
greater than 11.1 mmol/L....thirst, excessive hunger, excessive urine
What are some ways in which beta cells can be destroyed? (Type 1 diabetes)
auto-antibody
virus
drugs
disease
What happens when there is decreased entry of glucose into the cells?
hyperglycemia --> increased osmotic pressure (hyperosmolarity) --> fluid shift from IC - IV [cells "starve"], triggering of osmoreceptors, and increased GFR in kidney
What happens when cells "starve"?
- decreased ATP production --> decreased energy --> tiredness/difficultly concentrating
- HPA activated (usual S&S):
> catechol - increased glycogenolysis in LIVER
> cortisol breaks down muscle / fat [keytones from lipolysis
> rapid weight loss (but eating more)
Explain hyperglycemia fluid shift.
- fluid shifts from IC to IV
- cells become dehydrated causing dry skin, poor skin turgor and dry mucous membranes
Explain how kidneys react to hyperglycemia.
try to get rid of glucose by excreting in urine
- glucosuria
- polyuria
Explain stimulation of thirst centre during hyperglycemia.
hyperglycemia --> increased osmotic pressure (hyperosmolarity) --> triggers osmoreceptors --> stimulates "thirst center" (hypothalamus) --> increased thirst --> polydipsia
What is the MOA for hyperglycemia?
hyperglycemia --> increase in osmotic pressure (hyperosmolarity) --> fluid shift from IC - IV causing poor skin turgor & dry mucous membranes; osmoreceptors are triggered --> stimulation of thirst centre (hypothalamus) --> increases thirst which leads to polydipsia; increased GFR in the kidney that causes polyuria & glucosuria
What are the signs and symptoms of Type 1 hyperglycemia?
- glucosuria
- polyuria
- thirst
- fatigue, decreased concentration
- loss of consciousness when severe
- weight loss (fat/muscle breakdown) - production of ketones when severe
How can you treat Type 1 diabetes?
- give (exogenous) insulin several times per day and/or by actual blood glucose levels
- subcutaneous injection (if given PO, it is inactivated by digestive enzymes)
- insulin pump
Is insulin still required if there is no activity/intake?
yes, insulin is still required for basic cell function
What are some long-term (chronic) complications of type 1 diabetes?
- high glucose levels persist
- could develop different types of complications (ex. glycosylation, polyol pathway activated, increased risk of infection)
What are some acute (rapidly develop) complications of type 1 diabetes?
- no insulin at all
- DKA (diabetic ketoacidosis)
How do diabetic complications arise from glycosylation in type 1 and type 2 diabetes?
- glycosylation of:
1. RBCs - reduces O2 carrying capacity (HbA1C)
2. Capillary basement membrane - causes damage to blood vessels. Manifested as:
- retinopathy (blindness)
- atherosclerosis (Htn, CVA, IHD)
- NEPHROpathy (kidney damage)
In type 1 and type 2 diabetes, where does glycosylation occur?
RBCs & capillary membranes (damaging blood vessels)
How do diabetic complications arise from activation of polyol pathway in type 1 and type 2 diabetes?
- cells that do not have insulin metabolize glucose by the polyol pathway creating sorbitol and fructose which can create problems such as:
- damaged ion pumps
- attracts water (hyperosmolar)
- cataracts (lens thickening)
- peripheral neuropathy (nerve damage)
How do diabetic complications cause increased risk of infection in type 1 & type 2 diabetes?
- rapid growth of germs because of sweet environment (food for bacteria)
- reduced defence against germs
- poor healing --> reduced barrier
- WBCs are affected (function & ability to get to the site)
What is HbA1C?
hemoglobin A1C is glycosylated hemoglobin
- Hb + glucose = HbA1C
- it is the amount of glucose that the RBC has been exposed to over 120 days
- used as a good measure of long-term glucose control
What is Diabetic Ketoacidosis (DKA)?
- significantly high glucose levels (hyperglycaemia) from no insulin
- occurs only in type 1
- HPA axis is stimulated
- S&S of intracellular dehydration & HYPOVOLEMIA
- loss of consciousness
- ketosis (lipolysis creates ketones)
How would you diagnose DKA?
- look for S&S
- check blood glucose levels
- analyze ABGs
How would you treat DKA?
- give fluids FIRST
- give O2
- then give insulin
- manage acidosis
What is type 2 diabetes?
insulin "resistance" caused by:
- INSUFFICIENT insulin available OR
- defect in insulin receptors (due to numbers or sensitivity)
What is the key risk factor for type 2 diabetes?
obesity (excess fat can decrease sensitvity of insulin receptors)
What is the major defect in type 2 diabetes?
insulin "resistance"
- dysfunction in beta cells
- insulin receptors - change in numbers or sensitivity
The result of cells "starving" and glucose remaining in blood is the same for both type 1 and type 2 diabetes. True or False.
TRUE
What are the signs and symptoms of type 2 diabetes?
same as type 1 (EXCEPT)
- slower onset
- no ketosis
- higher glucose levels reached
because it occurs for a longer period of time
*** S&S are less dramatic than type 1
What are some long-term (chronic) complications of type 2 diabetes?
- high glucose levels persist if PO or insulin therapy is ineffective
- develop complications of diabetes - same as type 1 (3 mechanisms: A,B,C)
What are the long-term complications of type 2 diabetes?
- same as type 1
- Mechanism A: glycosylation of RBCs (decreased O2 carrying capacity) and capillary basement membrane (retinopathy [blindness] atherosclerosis [HTN, CVA, IHD] & nephropathy [kidney damage])
- Mechanism B - polyol pathway --> sorbitol & fructose --> high levels cause damage (cataracts [lens thickening], peripheral neuropathy [nerve damage], damages ion pumps)
- Mechanism C: increased risk for infection because high glucose levels attract bacteria because it is food to them --> poor skin healing --> decreased barrier
What does HHNKS stand for?
hyperosmolar, hyperglycemic, non-ketotic syndrome
What is HHNKS?
- no ketones (as in DKA) --> acidosis is not as severe
- glucose levels >33 mmol/L which is higher compared to DKA --> leads to more severe dehydration
- treat same way as DKA (give insulin, fluids, O2, and manage acidosis)
What is the treatment for type 2 diabetes?
- weight loss - help restore some sensitivity of insulin receptors
- diet control - reducing calories means that available insulin may be sufficient
- Drugs - oral hypoglycemic agents (helps to RELEASE insulin, NOT produce it), improves # and sensitivity of insulin receptors, and delays CHO digestion and absorption)
- may also need to give insulin if other methods are insufficient (lower dose and frequency required than type 1)
****NOTE: oral agents cannot be given in type 1 because no insulin is produced, therefore, no insulin can be released - do not confuse this with taking insulin PO; insulin can never be taken PO because digestion enzymes deactivate it
Is it correct to use the terms IDDM & NIDDM?
No, because type 2 diabetes is not insulin dependant, but may still need insulin (insulin REQUIRING)
Why is type 2 diabetes just as serious as type 1 diabetes?
- HHNKS vs. DKA
- same complications
- risk of hypoglycemia for both - when taking insulin or oral agents