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54 Cards in this Set
- Front
- Back
What are 5 sources of glucose?
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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 |
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What are 2 uses for glucose?
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1. ATP production
2. Storage (liver - glycogen; adipose tissue - fat) |
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Where does insulin come from?
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beta cells in the PANCREAS
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Where does glucagon come from?
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alpha cells in the PANCREAS
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Where does glycogen come from?
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storage site within the LIVER
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What is insulin?
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- hormone
- secreted when blood glucose levels are high - short half-life = 5 mins |
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What is the effects of insulin?
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- 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) |
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How does insulin work? (MOA)
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- 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) |
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What is needed to complement insulin in transporting glucose into the cell?
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GLUT4 transporter
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What is glucagon?
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- hormone
- secreted when blood glucose levels are low - short half-life = 5-6 mins |
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What is the purpose of glucagon?
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- 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) |
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What is the range for normal blood glucose levels?
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4 - 6 mmol/L
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When is glucagon secreted?
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- when glucose levels drop (between meals)
- after eating a protein or fat-rich meal |
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Besides glucagon, what is a backup mechanism for regulating hypoglycemia?
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HPA axis
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What does cortisol do to regulate hypoglycemia?
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- stimulates lipolysis
- muscle and protein catabolism - gluconeogenesis |
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What are the signs and symptoms of hypoglycemia?
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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) |
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What is type 1 diabetes?
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- NO insulin is synthesized
- defect: in beta cells |
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What is type 2 diabetes?
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- insufficient insulin (some insulin is made and released)
- defect: insulin receptors (due to numbers of receptors or sensitivity to insulin) |
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Where is the defect in type 1 diabetes?
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pancreatic beta cells
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Where is the defect in type 2 diabetes?
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insulin receptors
(due to the number of receptors or the sensitivity of the receptors to insulin) |
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What are 2 clues to get a blood test for diabetes?
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- signs and symptoms of hyperglycemia
- glucosuria (*cannot diagnose diabetes by glucosuria) |
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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 |
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What are some ways in which beta cells can be destroyed? (Type 1 diabetes)
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auto-antibody
virus drugs disease |
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What happens when there is decreased entry of glucose into the cells?
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hyperglycemia --> increased osmotic pressure (hyperosmolarity) --> fluid shift from IC - IV [cells "starve"], triggering of osmoreceptors, and increased GFR in kidney
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What happens when cells "starve"?
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- 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) |
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Explain hyperglycemia fluid shift.
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- fluid shifts from IC to IV
- cells become dehydrated causing dry skin, poor skin turgor and dry mucous membranes |
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Explain how kidneys react to hyperglycemia.
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try to get rid of glucose by excreting in urine
- glucosuria - polyuria |
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Explain stimulation of thirst centre during hyperglycemia.
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hyperglycemia --> increased osmotic pressure (hyperosmolarity) --> triggers osmoreceptors --> stimulates "thirst center" (hypothalamus) --> increased thirst --> polydipsia
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What is the MOA for hyperglycemia?
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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
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What are the signs and symptoms of Type 1 hyperglycemia?
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- glucosuria
- polyuria - thirst - fatigue, decreased concentration - loss of consciousness when severe - weight loss (fat/muscle breakdown) - production of ketones when severe |
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How can you treat Type 1 diabetes?
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- 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 |
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Is insulin still required if there is no activity/intake?
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yes, insulin is still required for basic cell function
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What are some long-term (chronic) complications of type 1 diabetes?
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- high glucose levels persist
- could develop different types of complications (ex. glycosylation, polyol pathway activated, increased risk of infection) |
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What are some acute (rapidly develop) complications of type 1 diabetes?
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- no insulin at all
- DKA (diabetic ketoacidosis) |
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How do diabetic complications arise from glycosylation in type 1 and type 2 diabetes?
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- 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) |
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In type 1 and type 2 diabetes, where does glycosylation occur?
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RBCs & capillary membranes (damaging blood vessels)
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How do diabetic complications arise from activation of polyol pathway in type 1 and type 2 diabetes?
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- 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) |
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How do diabetic complications cause increased risk of infection in type 1 & type 2 diabetes?
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- 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) |
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What is HbA1C?
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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 |
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What is Diabetic Ketoacidosis (DKA)?
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- 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) |
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How would you diagnose DKA?
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- look for S&S
- check blood glucose levels - analyze ABGs |
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How would you treat DKA?
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- give fluids FIRST
- give O2 - then give insulin - manage acidosis |
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What is type 2 diabetes?
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insulin "resistance" caused by:
- INSUFFICIENT insulin available OR - defect in insulin receptors (due to numbers or sensitivity) |
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What is the key risk factor for type 2 diabetes?
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obesity (excess fat can decrease sensitvity of insulin receptors)
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What is the major defect in type 2 diabetes?
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insulin "resistance"
- dysfunction in beta cells - insulin receptors - change in numbers or sensitivity |
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The result of cells "starving" and glucose remaining in blood is the same for both type 1 and type 2 diabetes. True or False.
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TRUE
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What are the signs and symptoms of type 2 diabetes?
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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 |
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What are some long-term (chronic) complications of type 2 diabetes?
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- high glucose levels persist if PO or insulin therapy is ineffective
- develop complications of diabetes - same as type 1 (3 mechanisms: A,B,C) |
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What are the long-term complications of type 2 diabetes?
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- 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 |
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What does HHNKS stand for?
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hyperosmolar, hyperglycemic, non-ketotic syndrome
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What is HHNKS?
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- 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) |
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What is the treatment for type 2 diabetes?
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- 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 |
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Is it correct to use the terms IDDM & NIDDM?
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No, because type 2 diabetes is not insulin dependant, but may still need insulin (insulin REQUIRING)
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Why is type 2 diabetes just as serious as type 1 diabetes?
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- HHNKS vs. DKA
- same complications - risk of hypoglycemia for both - when taking insulin or oral agents |