Obesity and Diabeetus Flashcards

1
Q

Obesity

A

chronic, relapsing disease r/t abnormal or excessive accumulation of fat and weight gain

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2
Q

Obesity patho

A

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

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3
Q

obesity management

A

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
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4
Q

BMI classification

A

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

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5
Q

bariatric surgery

A

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)

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6
Q

types of bariatric surgery

A
  1. Sleeve gastrectomy: most common- large portion of stomach lumen removed (looks like an extension of esophagus, connecting to duodenum
  2. 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
  3. 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
  4. gastric banding: least invasive but highest rate of inefficacy or failure- reduces circumference of stomach
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7
Q

post-op bariatric mgmt

A

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

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8
Q

post-op bariatric surgery complications

A

change in bowel habits, infection, hemorrhage, venous thromboembolism, bile reflux, dumping syndrome, dysphagia, bowel or gastric outlet obstruction

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9
Q

Dumping syndrome

A

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

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10
Q

Insulin

A

hormone secreted by the beta cells of islets of lagerhands of pancreas
- anabolic, “storage” hormone
- needed for metabolism of carbs, proteins, and fats

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11
Q

Type 1 diabetes

A

insulin isn’t secreted from pancreas (No Key to open the cells for glucose)
RF: genetic predisposition

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12
Q

Type 2 diabetes

A

deficiency in insulin action/production (broken key for the cell door)
RF: liefstyle factors
- largely preventable

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13
Q

classic symptoms of diabetes

A

Polyuria, polydipsia, polyphagia (very hungry)

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14
Q

common diabetic manifestations

A

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

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15
Q

diabetic labs

A
  • serum glucose (BG)- diabetic symptoms and casual BG >200 or fasting plasma > 126, 2 hr post load glucose > 200
  • A1C >6.5%
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16
Q

Oral antidiabetic agents

A

used for Type 2 diabetics who require more than diet and exercise

-may be used in combo with long-acting insulin

17
Q

hypoglycemia

A

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

18
Q

hypoglycemia mgmt

A
  • 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)
19
Q

DKA

A

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

20
Q

DKA risk factors

A
21
Q

manifestations of DKA (Patho)

A

hyperglycemia s/s (poluria, polydipsia, fatigue, blurred vision, weakness, HA, hypotension

ketosis and acidoses related s/s (GI symptoms, acetone breath, kussmaul breathing)

22
Q

DKA labs

A

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)

23
Q

DKA management

A

correct acidoses, dehydration and e- loss FIRST!!

  • then correct hyperglycemia with insulin
    -monitor BG, renal function and UO
    -EKG, e- levels, VS, lung sounds
24
Q

Hyperglycemic hyperosmolar syndrome (HHS)

A

insulin deficiency initiated by an illness/increased insulin demand
- ketosis is minimal or absent
- most common in type 2

25
Q

HHS labs

A

BG >600, serum osmolality (>320), chem (Na) and other e-, BUN and creatinine are elevated

26
Q

HHS manifestations

A

hypotension, profound dehydration, tachycardia, variable neuro signs (caused by cerebral dehydration)
- high mortality rate

27
Q

HHS treatment

A

rehydration, correct e-, insulin

-prevention: BG monitoring, dx and mgmt of diabetes, self-care