1/303
Looks like no tags are added yet.
Name | Mastery | Learn | Test | Matching | Spaced | Call with Kai |
|---|
No analytics yet
Send a link to your students to track their progress
facts about obesity
-The united states is the most obsess nation
-42% obesity prevalence in adults- the rate in children in rapidly rising
-higher rates in African American and Hispanic ethnic groups
-women experience it more than men
-economic burden of $147 billion yearly- treating obesity and related complications
causes of obesity
-metabolic imbalance
-genetic link
-lifestyle
-medications
-societal changes
-inflammatory response
-hormonal/emotion
how does metabolic imbalance cause obesity?
-caloric intake is greater than energy expenditure-> positive energy balance-> fat storage
how does genetic links cause obesity?
-FTO is shown to be associated with obesity according to new research
-increases appetite and preferences for calorie dense foods
-other gene influence: leptin resistance, insulin sensitivity, and metabolic rate
how does lifestyle cause obesity?
-sedentary or active life style
-diet: nutritious foods vs empty calories/dense foods with no nutritional value: lower fiber and highly processed foods
how does societal changes cause obesity?
-increasingly bigger portion sizes
-urbanization results in less opportunity for activity
how does inflammatory response cause obesity?
adipocytes release pro-inflammatory cytokines-> systemic inflammation-> insulin resistance and atherosclerosis
what are the hormones of hunger?
ghrelin and NPY
what is ghrelin?
-excreted by the stomach
-raises appetite
-"hunger hormone"
What is NPY?
-excreted by the small intestine and hypothalamus
-raises appetite
-stimulated by fasting and stress
what are the hormones of satiety?
-signals the body to stop eating because it is full
-Insulin, somatostatin, cholecystokinin
what is insulin (in satiety)?
-excreted by pancreas
-decrease appetite
-promotes glucose uptake
-if it is chronically high it causes insulin resistance
What is somatostatin?
-excreted by pancreas and GI tract
-slows gastric emptying
-results in feeling full longer
what is cholecystokinin?
-excreted by the small intestine
-slows gastric motility
-"stop eating signal"
what is the hormone of adipose stores?
leptin (fat cells)
what is leptin
-released by adipose tissues
-decrease appetite and increases energy expenditure
-chronic obesity= leptin resistance
-· people who where obsess but lose weight will show drops in leptin levels but can regain it- direct response to weight loss and gain
what do GI microbes do in obesity?
-excreted by the colon
-modulate satiety hormones- high fiber diet improves balance
-a more processed diet results in decreased GI microbes than those who eats high fiber foods (fiber allows us to stay fuller longer, satisfied longer, less weight gain and helps with constipation
what is BMI
ratio of height and weight- it Is the gold standard but it is not the most accurate as it does not account for muscle and body frame
what are the categories of BMI?
· Normal: 18-24.9
· Overweight: 25-29.9
· Class 1 obesity: 30-34.9
· Class 2 obesity: 35-39.9
Class 3 (morbid) obesity: >40
how do you calculate BMI?
BMI= (weight in lbs/ height in inches^2) x 703
how do you calculate ideal body weight
-ideal body weight for men: 106+6lbs x (every inch over 5 feet)
-ideal body weight for women: 100+ 5lb x (every inch over 5 feet)
what are risk factors for obesity?
-occurs more in African Americans-> Hispanic-> Caucasian-> Asian
-lower socioeconomic status results in a higher obesity prevalence-> lack of funds for healthy groceries
-more common in women than men-> women have more adipose tissue because of periods, babies and breasts
-body shapes: android (more fat in the middle-increases risk for obesity) vs gynoid (more fat in the lower body- hips and thighs)
-waist circumference (visceral fat)
what are risks associated with android body type?
increased risk of cardiovascular issues and insulin resistance
what is the waist to hip ratio for women?
>0.80 (anything higher increases risk)
what is the waist to hip ratio for men?
· >0.90 (anything higher increases risk)
what is waist circumference for women?
>35 inches (anything higher increases risk)
what is waist circumference for men?
· >40 inches (anything higher increases risk)
what are medical complications with obesity?
-decreased life expectancy- depends on category but can be shortened by 6-20 years
-high mortality rate- comorbidities
-high morbidity rate
medical complications of obesity
-cardiovascular: hypertension, CAD, stroke
-endocrine: DM2, dyslipidemia and PCOS
-respiratory: sleep apnea, hypoventilation
-GI/hepatic: GERD, NAFLD, gallstones
-Musculoskeletal: OA, back pain
-cancer: breast, colon, endometrial
-reproductive: infertility, menstrual irregularities
-psychological: depression and body image disturbances
what medications affect obesity?
-antidepressants/mood stabilizers
-antipsychotics
-anticonvulsants
-insulins
-hormones- estrogen and progesterone)
-steroids- long term use of corticosteroids
how do antidepressants affect obesity?
cause appetite stimulation
how do antipsychotics affect obesity?
-causes insulin resistance
-increases appetite
how do anticonvulsants affect obesity?
slows down metabolism
how does insulin affect obesity?
glucose leads to fat storage
how do hormones (estrogen and progesterone) affect obesity?
water retention
how do long term use of corticosteroids affect obesity?
fluid retention and fat redistribution
what is the goal of obesity treatment?
create sustainable lifestyle changes and maintain long term weight loss
what are ways to treat obesity?
-diet/nutrition
-exercise
-portion control
-lifestyle modification
-medical treatment
-surgical treatment
-maintenance (hardest and often results in regaining the weight)
what are modifications to make in obesity management?
-behavioral therapy: group therapy and food diary-record caloric intake: makes people aware of what they are eating
-decrease caloric intake to at least 500 calories a day (1-2lb a week)
-smaller portions and limiting nonproductive foods: using a salad plate and slower eating
-limit processed foods: food without nutritional value-> focus on fruits, veggies, lean proteins and whole grains
-limit artificial sweeteners: limited nutritional value (tricks ghrelin and causes hunger)
-limit alcohol intake: empty calories
-sleep: stimulate ghrelin for energy
-150 minutes weekly of moderate aerobic activity and resistance training
-muscle strength conditioning: builds muscle-> increases fat burn-> decrease fat
One must burn 3500 calories more than they consume to lose one pound of fat
what is medical treatment for obesity?
-GI lipase inhibitor- orlistat (Xenical, Alli)
-selective serotonergic 5-HT2C receptor agonists- locaserin (beliq)
-GLP1 receptor agonist- liraglutide (saxenda)
-symoathomimetic amines- adipex-p, fastin (phentermine) and bontril (phendimetrazine)
-dual agents
orlistat (Xenical, Alli)
MOA: GI lipase inhibitor resulting in decreased fat absorption
SE: oily stools, GI upset- take with less fatty meals
Lorcaserin (beliq)
-MOA: 5-HT2C agonist-> appetite suppression
-SE: fatigue, dizziness and constipation
liraglutide (saxenda)
-MOA: GLP-1 agonist-> delayed gastric emptying and increase satiety
-SE: nausea, tachycardia; monitor for AFib
Phentermine/phendimetrazine
MOA: sympathomimetic amines-> appetite suppression
-SE: Increase heartrate, hypertension, insomnia and palpitations- only for short term use
dual agents
-MOA: suppress appetite+ slow emptying
-SE: varies by formulation
what should you monitor for for any of these medical interventions?
HR, BP, mood changes, adherence and side effects
what is the criteria for bariatric surgery?
for BMI 40 or greater OR BMI 35 or greater with severe comorbidities after failed conservation therapy
what are types of bariatric surgery?
-orbera balloon (non-invasive)
-roux-en-Y gastric bypass
-gastric banding
-sleeve gastrectomy
-biliopancreatic duodenal switch
orbera balloon
-MOA: space-occupying balloon-> early satiety
-notes/risks: temporarily, endoscopic removal
Roux-en-Y gastric bypass
-MOA: small stomach pouch + bypass small intestine
-notes/risks: malabsorption; lifelong vitamin B12 supplements
Gastric banding
-MOA: adjustable band that restricts intake
-notes/risks: risk of slippage, less effective long-term
sleeve gastrectomy
-MOA: removes about 75% of the stomach
-notes/risks: restrictive; fewer malabsorption issues
biliopancreatic diversion
-MOA: major bypass
-notes/risks: high complication rate; rarely used
pre and post-op nursing considerations?
Diet progression: clear → pureed → soft → solid (if advanced too soon → vomiting → rupture risk).
Monitor for infection: fever, drainage, wound changes.
Fluid/electrolyte balance: cannot eat & drink simultaneously.
Nutrition: lifelong vitamin B12, iron, calcium, protein.
Avoid NSAIDs: ↑ risk of ulcers & GI bleeding.
Mobility: prevent DVT/VTE.
Skin integrity: folds, wound care.
Psychosocial: body image, depression, adjustment to new lifestyle.
complications from bariatric surgery?
-hemorrhage
-anastomotic leak
-bile reflux
-DVT/VTE
-dysphagia
-bowel outlet obstruction
-dumping syndrome
nursing focus for hemorrhage or anastomotic leak
watch for tachycardia, hypotension, shoulder pain and fever
nursing focus for dumping syndrome
nausea, vomiting, sweating after meals; avoid high sugar foods and eat slowly
nursing focus for bile reflux
burning epigastric pain- treat with bile-acid binders
nursing focus for bowel obstructions
monitor bowel sounds and distention
nursing focus for dysphagia?
eat slowly and chew thoroughly
what is important to know about the pituitary gland?
-master gland
-controls others (thyroid, adrenal and gonads)
-in the base of the brain connected to the hypothalamus
which part of the pituitary gland produces its own hormones?
anterior pituitary gland
what is the main anterior pituitary hormone we are focusing on?
growth hormone
what does growth hormone do in children?
regulates bone and tissue growth
what does growth hormone do in adults?
regulates metabolism- maintain muscle mass, tissue repair and energy balance
what is the role growth hormone?
-increase protein synthesis in many tissues
-increase the breakdown of fatty acids in adipose tissues
-increase blood glucose levels
what stimulates the production of GH?
deep sleep, exercise, stress, fasting and hypoglycemia
what inhibits the production of GH?
obesity, depression, hypothyroidism, high blood glucose
what is the overproduction of GH called?
acromegaly
What causes acromegaly?
pituitary adenoma secreting GH - after epiphyseal plate closure
what is the effects of acromegaly?
enlarged hands, feet, facial bones, thick skin, organ enlargement, joint pain, hypertension and cardiomegaly
what is the nursing/medical care for acromegaly?
-surgical removal of tumor (transsphenoidal hypophysectomy)
-meds (octreotide- GH inhibitor)
what is the pathophysiology of acromegaly?
growth hormone overproduction-> liver releases IGF-1-> stimulates tissue growth
what are manifestations of acromegaly?
-enlarged hands, feet, facial bones (frontal bossing, wide nose and jaw protrusion)
-deepened voice (thickened vocal cords)
-headache, visual disturbances (tumor compresses optic chiasm)
-sleep apnea, hypertension, heart failure and hyperglycemia
what are treatment goals for acromegaly?
-normalize GH levels
-prevent complications (cardiomegaly and diabetes)
-surgical tumor removal if possible
nursing care for acromegaly?
-neurological status and visual changes
-post op:
--avoid coughing, sneezing and straining (increased intracranial pressure)
--monitor nasal drainage for CSF leak (glucose test)
--keep head of bed elevated
--monitor for DI or SIADH post-surgery
what is the function on the posterior pituitary gland?
to store hormones (ADH and oxytocin)
what is the function of ADH?
controls the excretion of water by the kidneys- it is stimulated by an increase in the osmolarity of the blood or by the decrease in blood pressure
-Increase ADH-> water retention and decreased urine output
-decrease ADH-> water loss and increased urine output
what is the underproduction or resistance to ADH?
diabetes insipidus
what is the pathophysiology of DI?
ADH deficiency or renal resistance-> kidneys cant retain water-> massive dilute urine output
what is the cause and key feature of central (neurogenic) DI?
-cause: decreased ADH from hypothalamus/pituitary damage (head trauma, surgery, tumor)
-responds to desmopressin
what is the cause and key feature of nephrogenic DI?
-causes: kidneys resistant to ADH (lithium, renal damage, hypercalcemia, hypokalemia)
-no response to desmopressin
what is the cause and key feature of dipsogenic DI?
-cause: excess fluid intake due to thirst center defects
-decreased plasma osmolarity and normal ADH
what is the cause and key features of gestational DI?
-placental enzyme breaks down ADH
-temporary; occurring during pregnancy
what are clinical manifestations of DI?
-Polyuria: >250 mL/hr (can reach 3-20 L/day)
-Urine: dilute, specific gravity 1.001-1.005
-Polydipsia: intense thirst (prefers cold water)
-Dehydration: dry mucous membranes, hypotension, tachycardia
-Hypernatremia: confusion, irritability, seizures if severe
what are diagnostic tests for DI?
-fluid deprivation test
-plasma urine osmolarity
-desmopressin challenge
-MRI
DI findings of fluid deprivation test?
-urine stays dilute despite dehydration
DI findings of plasma and urine osmolarity?
increase plasma osmolarity, decrease urine osmolarity
DI findings of desmopressin challenge?
central DI will improve, nephrogenic does not
DI findings of MRI?
check for pituitary lesions or tumors
what are treatment goals for DI?
-replace ADH
-control urine output
-enhance ADH action
-restore fluids
what is an intervention for replacing ADH?
Desmopressin (DDAVP) intranasal/oral- drug of choice
what is the intervention for controlling urine output?
vasopressin (caution with CAD-> causes vasoconstriction)
what is an intervention for enhancing ADH action
chlorpropamide, thiazide diuretics for mild cases
what is an intervention for restoring fluids?
IV or oral hydration, monitor Is&Os
nursing care for DI
-Monitor vitals, I&O, daily weights.
-Watch for dehydration and electrolyte imbalance.
-Educate:
--Lifelong desmopressin use (central DI).
--Signs of hyponatremia (water intoxication).
--Maintain adequate fluid intake.
-Prevent complications → dehydration → ↓ cardiac output → ↓ renal perfusion.
what is the overproduction or excess release of ADH
Syndrome of inappropriate antidiuretic hormone (SIADH)
what is the pathophysiology of SIADH?
-excess ADH-> kidneys retain water-> dilutional hyponatremia and concentrated urine
what are causes of SIADH?
-malignancy: small cell lung cancer is the most common
-CNS disorders: head injury, brain surgery, infection and tumor
-medications: SSRIs, tricyclics, vincristine, thiazides, nicotine
-pulmonary disease: pneumonia or pneumothorax
clinical manifestations of SIADH?
-Low urine output (oliguria)
-Water retention / weight gain
-Hyponatremia → confusion, lethargy, seizures
-No peripheral edema (fluid is intracellular)
-Serum: ↓ Na⁺, ↓ osmolarity
-Urine: ↑ Na⁺, ↑ osmolarity