Med Con 1-Diabetes Pathophysiology

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what is a PT's role in diabetes management? (use phases)
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what is a PT's role in diabetes management? (use phases)
phase 1:
-recognize s/s of diabetes in undiagnosed individuals
-identify emergencies of high/low blood glucose
-risk assessment

phase 2:
-recognize the relationship between DM and orthopedic conditions
-differential diagnoses of complications of DM from MSK conditions

intervention: connect DM and MSK condition
-lifestyle changes: self management education and support
-appropriate prescription of exercise
-monitor appropriately
-identify emergencies
what is a PT's role in diabetes prevention?
primary prevention: recognize risk factors and initiate early education (physical activity)

secondary prevention: [they have diabetes]
-advocate for health behaviors
-recognize signs of poor glucose control
-foot exam/care
-incorporate education: diet, smoking, PA, resistance training

tertiary prevention:
-wound care, amputation, CV events, peripheral vascular disease, kidney failure DUE TO THEIR DIABETES
-maximize function and address items above
what is diabetes mellitus?
metabolic disease resulting in hyperglycemia due to deficits in insulin secretion, insulin action, or both
what organs play a role in glucose metabolism?
1. pancreas
2. liver
3. kidney
4. skeletal muscle
5. GI
6. adipose tissue

7. brain (but no medication for it)
do all cells require glucose?
yes
which organs do not depend on insulin for glucose transport? why?
-Exercise muscle doesn't need glucose but resting muscle does
-Brain and liver doesn't depend on insulin for glucose transport bc the liver doesn't need insulin to get it in there
why does the brain need glucose? how does this happen?
Bc the brain can only use proteins and glucose for energy to make ATP

AKA
-neurons can't store glucose so they depend on the bloodstream to deliver a constant supply of fuel
-fatty acids can't cross blood-brain barrier bc they are bound to albumin in plasma
-insulin mediates glucose uptake into adipose tissue and skeletal muscle through GLUT4 glucose transporters
-brain and liver don't require insulin for efficient uptake of glucose bc they don't use GLUT4
what is the primary cause of type 1 diabetes?
a. beta cells are destroyed by poor diet
b. beta cells are destroyed by an autoimmune process
c. excessive insulin production by pancreas
d. low insulin production by pancreas
b. beta cells are destroyed by an autoimmune process
what are some diabetes complications?
macrovascular complications:
-CV disease: coronary heart disease, stroke, peripheral arterial disease(PAD)/amputation

microvascular complications:
-eye disease (retinopathy)
-kidney disease (nephropathy)
-nerve disease (neuropathy)
what happens in type 1 diabetes?
cell-mediated autoimmune destruction of beta-cells of the pancreas
-rate of destruction is variable
-absolute insulin deficiency
what are the s/s of type 1 diabetes?1. hunger 2. weakness 3. weight loss 4. fatigue 5. dizzinesswhat are some clinical manifestations of diabetes (type 1 and 2)?1. polyuria 2. polydipsia 3. weakness, fatigue, and dizziness 4. blurred visionwhat are the clinical manifestations for type 1 diabetes specifically?1. polyphagia 2. ketonuria 3. weight losswhat is the pathophysiologic basis for polyuria? what is it?excessive urination; water is not reabsorbed from renal tubules bc of osmotic activity of glucose in the tubuleswhat is the pathophysiologic basis for polydipsia? what is it?excessive thirst; polyuria causes dehydration, which causes thirstwhat is the pathophysiologic basis for weakness, fatigue, and dizziness?dehydration leads to postural hypotension; energy deficiency and protein catabolism contribute to fatigue and weaknesswhat is the pathophysiologic basis for blurred vision?chronic exposure of the lenses and retina to hyperosmolar fluids causes blurring of visionwhat is the pathophysiologic basis for polyphagia?starvation secondary to tissue breakdown causes hungerwhat is the pathophysiologic basis for ketonuria?fatty acids are broken down so ketones are present in urinewhat is the pathophysiologic basis for weight loss?glucose is not available to the cells; body breaks down fat and protein stores for energy; dehydrationtrue or false: type 1 diabetes is a lifestyle diseasefalsewhat is the primary cause of type 2 diabetes? a. destruction of beta cells in pancreas b. blood glucose is low c. liver and muscle tissue is resistant to insulin d. defective insulin secretionc. liver and muscle tissue is resistant to insulinwhat happens in type 2 diabetes?cells in the muscles, liver, and fat tissue become resistant to insulin. insulin secretion becomes defective and insufficient to compensate for insulin resistance. CAN be prevented with weight loss, increase activity level, and better eating habits OR insulin resistance develops. beta-cells must make more insulin to accommodate for lack of insulin action (Secondary hyperinsulinemia). relative insulin deficiency results in rise in blood glucose (type 2 DM). insulin resistance creates liver imbalance and gluconeogenesis increaseswhat are some modifiable risk factors for diabetes?1. overweight/obesity: -body mass index > 25 mg/m2 -visceral fat -waist circumference: f>35 in; m>40 in 2. inactivity: <30 min of mod-vig/day, 5 days/wk 3. hypertension: -elevated: 120-129/<80 -HTN stage 1: 130-139/80-89 -HTN stage 2: >140/>90 -HTN stage 3: >180/>120 (req emergency care) 4. smoking 5. diet: refined grains, red/processed meat, sugar-sweetened bev, lack of mod alcohol intake 6. psychosocial: depression, increased stress, low social support, poor mental health 7. abnormal fasting cholesterol: -triglycerides > 150 mg/dL -high-density lipoprotein: f<50 mg/dL; m<40 mg/dLwhat are some nonmodifiable risk factors for diabetes?1. age: > 45 yrs 2. sex: male 3. socioeconomic: lower level edu, occupation, housing conditions, income 4. race/ethnicity: american indian, alaska native, african american, hispanic, asian americans, pacific islander 5. family history/genetic predisposition 6. history of gestational diabetes 7. low birth weightwhat symptoms is associated with diabetes and is a major problem in the US today?obesity and diabetes are linked by a common dependence on insulin action in peripheral tissues and brain. CNS ensures a steady supply of energy substrate. so reduced CNS insulin signaling from either defective secretion/action contributes diabetes and obesitywhat is the incretin effect?it's released from special endocrine cells in the gut after eating. -increases the release of insulin from beta-cells -lowers blood glucose levels -DPP-4 is an enzyme that degrades GLP-1what is DPP-4?an enzyme that degrades GLP-1what is gestational diabetes? what happens?diabetes that begins in pregnancy, typ around 24-28 weeks (6 months) 1. placental hormones cause insulin resistance; increasing insulin release from mom 2. glucose crosses placenta, but insulin doesn't so the baby increases insulin secretion to take care of the extra glucose coming in from momm 3. baby stores extra fat and grows large bc they are making more insulin (insulin is anabolic) 4. at birth, the baby is producing too much insulin; risk of hypoglycemia when mom is no longer contributing glucose about 60% of mom with gestational diabetes develop type 2 DMwhat is the normal range for the hemoglobin A1c level?4-5.6%how often do you test for A1c?every 3 monthswhat is the normal fasting blood glucose?70-100 mg/dLwhat hemoglobin A1c levels are considered pre-diabetes?5.6-6.5%what hemoglobin A1c levels are considered diabetes?>6.5%define fastingnot having anything to eat or drink except water for at least 8 hours before testwhat is the cut off score for fasting plasma glucose for diabetes?>126 mg/dLwhat is the oral glucose tolerance test?2 hr test that checks blood glucose levels before and 2 hours after you drink a special sweet drink. it tells the doctor how your body processes glucosehow is diabetes diagnosed with A1c?normal=less than 5.6% pre-diabetes: 5.6-6.5% diabetes: greater than 6.5%how is diabetes diagnosed with fasting plasma glucose?normal: 70-100 mg/dl pre-diabetes: 100-126 mg/dl diabetes: greater than 126 mg/dlhow is diabetes diagnosed with oral glucose tolerance test?normal: less than 140 mg/dl pre-diabetes: 140-199 mg/dl diabetes: 200+ mg/dlwhat organs play a role in glucose metabolism? how could the organ function by influenced to improve blood glucose metabolism?1. kidneys: inhibit (-) glucose reabsorption 2. pancreas: (+) insulin; (-) glucagon 3. adipose tissue: (+) FFA storage; (-) lipolysis 4. gut (stomach+Small intestine): (-) glucose reabsorption; (+) incretin release 5. skeletal muscles: (+) glucose uptake; (+) insulin sensitivity 6. liver: (-) gluconeogenesis; (-) lipolysis; (+) glucose uptakewhat are the types of medications for diabetes?1. sulfonylurea 2. biguanides 3. thiazolidinedione 4. incretin mimetic (GLP-1 agonist)-"glutide" 5. SLGT-2 inhibitors "-gliflozen" 6. DPP-4 inhibitors "-gliptin" 7. a-glucosidase inhibitorswhat medication is given first to someone who has pre-diabetes? (what medication does everyone pre-diabetes and diabetes have?) then what?metformin, then sulfonylureaswhat are medications for people who are at low risk of diabetes?metformin and acarbosewhat medications are given to patients with type 1 diabetes?none! they are on insulin (type 2 on meds; type 1 given insulin)what type of diabetes are insulin-dependent?type 1what is given for rapid acting type 1 diabetes?lispro (humalog)what is given for long acting type 1 diabetes?glargine (lantus)what are the recommendations for glycemic goals in adults with diabetes?lowering A1c to below or ~7%: reduces microvascular and neuropathic complications associated with long-term reduction in macrovascular disease -for complex older adults, <8 may be more appropriate target. hyper and hypoglycemia can lead to fall and mental status changes in older adultswhat are the types of acute complications in diabetes?1. acute hypoglycemia 2. acute hyperglycemia: diabetic ketoacidosis (DKA) in type 1 3. acute hyperglycemia: hyperglycemic hyperosmolarity state (HHS) in type 2what happens in acute hypoglycemia?-common in type 1 > 2 -low blood sugar levels -caused by excessive insulin intake or activity *uncommon unless taking insulin or sulfonylurea -symptoms vary: headaches, confusion, sleepy, shaky, hungry, sweating MED. EMERGENCY: BG < 70 mg/dl w/ symptomswhat happens in acute hyperglycemia in type 1 diabetics?-DKA-buildup of acid in the blood -absolute insulin deficiency so cells can't use glucose so uses fats instead, which makes ketones and metabolic acidosis occurs -arterial pH < 7.3 -develops over hours to 1-2 days MED. EMERGENCY: BG > 250 mg/dl, ketones w/ symptomswhat happens in acute hyperglycemia in type 2 diabetes?-hyperglycemic hyperosmotic state-buildup of glucose in blood without ketones -too much sugar in blood for long period of time; osmolarity changes -resulting dehydration is responsible for symptoms -severe relative insulin deficiency -arterial pH > 7.3 -develops over days to weeks MED EMERGENCY: BG > 600 mg/dl w/ symptomsdifferentiate ketosis vs. ketoacidosis-ketosis-presence of ketones; triggered by low carb diet; body burns fats instead of relying on glucose -ketoacidosis-high blood sugar levels and high urine and blood ketone levels causing metabolic acidosis