Obesity and Diabeetus Flashcards
Obesity
chronic, relapsing disease r/t abnormal or excessive accumulation of fat and weight gain
Obesity patho
metabolic imbalance. increase in body fat cause adiposopathy (adipose tissue promotes development of metabolic, biochemical and psychosocial diseases and disorders)
- impairs normal body functions
- chronic inflammation
- causes morbidity
obesity management
BMI is the definitive measure
- screenings for CV diseases, cholesterol, triglyceride, T2DM, non-fatty liver disease, and OSA
- lifestyle modification
- pharm: anti obesity meds- inhibit GI absorption of fats (ozempic), others alter brain receptors for satiety or reduce cravings
- check your bias and language
BMI classification
Overweight/pre-obese: 25-29.9
Class 1 obesity:30-34.9
Class 2 obesity: 35-39.9
Class 3 obesity (extreme/severe obesity: >40
bariatric surgery
treats obesity after nonsurgical attempts at weight control fail
- patient must meet certain criteria (ADL, support system, failure with nonsurgical, ability to adhere to post mgmt, BMI>30 with T2DM and poor glycemic contorol, >35 with comorbidities, >40 without excessive surgical risk)
types of bariatric surgery
- Sleeve gastrectomy: most common- large portion of stomach lumen removed (looks like an extension of esophagus, connecting to duodenum
- Roux-en-Y gastric bypass (RYGB): 2nd common, has pouch for food - stomach is still in place to produce digestive juices- duodenum and stomach bypassed, jejunum connect to gastric food pouch from esophagus
- Biliopancreatic diversion w/ duodenal switch: results in most post-op weight loss (ideal for high BMI pt)- “reroutes” everything- duodenum attached to gall bladder, jejunum connected to stomach pouch and routes to colon
- gastric banding: least invasive but highest rate of inefficacy or failure- reduces circumference of stomach
post-op bariatric mgmt
IV fluids, drains, early ambulation, pain mgmt, antiemetics
diet: clear diet x48H, progress to full, sugar free liquid puree, pureed, soft, solid food around 8 weeks
post-op bariatric surgery complications
change in bowel habits, infection, hemorrhage, venous thromboembolism, bile reflux, dumping syndrome, dysphagia, bowel or gastric outlet obstruction
Dumping syndrome
rapid transit of food from stomach into intestines causes release of metabolic peptides
- vasomotor and GI symptoms
- occurs within minutes to 2 hours after eating
- s/s: tachy, dizzy, sweating, n/v/d, bloating, cramping
- symptoms resolve after defecation
- reactive hypoglycemia
Insulin
hormone secreted by the beta cells of islets of lagerhands of pancreas
- anabolic, “storage” hormone
- needed for metabolism of carbs, proteins, and fats
Type 1 diabetes
insulin isn’t secreted from pancreas (No Key to open the cells for glucose)
RF: genetic predisposition
Type 2 diabetes
deficiency in insulin action/production (broken key for the cell door)
RF: liefstyle factors
- largely preventable
classic symptoms of diabetes
Polyuria, polydipsia, polyphagia (very hungry)
common diabetic manifestations
fatigue, weakness, visions change, tingling/numbness in extremities, dry skin, skin lesions/wounds that are slow to heal, recurrent infections
type 1- may have sudden weight loss, n/v
diabetic labs
- serum glucose (BG)- diabetic symptoms and casual BG >200 or fasting plasma > 126, 2 hr post load glucose > 200
- A1C >6.5%
Oral antidiabetic agents
used for Type 2 diabetics who require more than diet and exercise
-may be used in combo with long-acting insulin
hypoglycemia
caused by too much insulin/antidiabetic agents, excessive physical activity or not enough food
s/s: headache, tinnitus, trembling, irritability, sweatiness, blurry vision, tachy, hunger, anxiety, weakness/fatigue
hypoglycemia mgmt
- give 15-20g of concentrated carb
- retest BG in 15 min, retreat if ,70
- give snack and notify provider
- if <54 and unable to swallow or unconscious: subQ or IM glucagon or 25-50 mL of dextrose (D50W)
DKA
Diabetes along with 1of 3 causes: infection, insulin deficiency, or undiagnosed/untreated diabetes
- most common in type 1
- s/s: hyperglycemia, dehydration and acidosis
-PREVENTION IS KEY
DKA risk factors
manifestations of DKA (Patho)
hyperglycemia s/s (poluria, polydipsia, fatigue, blurred vision, weakness, HA, hypotension
ketosis and acidoses related s/s (GI symptoms, acetone breath, kussmaul breathing)
DKA labs
BG: 250-800mg/dL
Ketoacidosis labs: low pH, low bicarb, low pCO2, ketone bodies in blood and urine
- electrolyte imbalance: hyperkalemia, increase in creatinine, hematomacrit, BUN (dilutional)
DKA management
correct acidoses, dehydration and e- loss FIRST!!
- then correct hyperglycemia with insulin
-monitor BG, renal function and UO
-EKG, e- levels, VS, lung sounds
Hyperglycemic hyperosmolar syndrome (HHS)
insulin deficiency initiated by an illness/increased insulin demand
- ketosis is minimal or absent
- most common in type 2
HHS labs
BG >600, serum osmolality (>320), chem (Na) and other e-, BUN and creatinine are elevated
HHS manifestations
hypotension, profound dehydration, tachycardia, variable neuro signs (caused by cerebral dehydration)
- high mortality rate
HHS treatment
rehydration, correct e-, insulin
-prevention: BG monitoring, dx and mgmt of diabetes, self-care