endocrine Flashcards
A complex metabolic disorder characterized by abnormally increased
blood glucose concentration caused by resistance to action of insulin,
insufficient secretion of insulin, or both.
diabetes mellitus
LT damage of diabets
failure of different organs including the eyes, kidneys, nervous
system, heart and blood vessels
An anabolic hormone secreted by the Beta cells of the Islets of Langerhans
in the pancreas
insulin
function of insulins
regulating glucose homeostasis by stimulating glucose
uptake by cells and by suppressing hepatic gluconeogenesis (body makes glucose
Out of other substances)
(+) glycogen synthesis
(+) glucose transport to muscle and adipose
(+) protein synthesis
(+) uptake of amino acids by peripheral tissues
(+) transport of Triglycerides(TG) to adipose tissue
(+) fat synthesis (lipogenesis)
what does insulin impair?
-) glycogenolysis (break down of glycogen in liver)
(-) gluconeogenesis (inhibits glucose prod)
(-) hepatic glucose production
(-) lipolysis
A 29 amino acid polypeptide hormone secreted from the Alpha cells of the
Islets of Langerhans that is stimulated by hypoglycemia
glucagon (raises blood sugar) while insulin lowers blood sugar
threshold for DM with fBG
> 126
threshold for DM with random BG test
Hgb A1C level for dx of DM
> 6.5%
what’s an OGTT test? what’s the threshold for DM?
Oral Glucose Tolerance Test (OGTT)
2-hr plasma glucose following 75 g OGTT (measure BG at 0,1, and 2 hrs)
Diagnostic 200 mg/dL
prediabets dx
FPG 100-125 mg/dL (=impaired fasting glucose IFG0
random glucose 140-199
OGTT 140-199m((impaired glucose tolerance (IGT) ))
AIC 5.7-6.4%
Reflects average level of hyperglycemia over prior 2-3 months.
Hgb A1c
hgb a1c normal level, pre diabetic level, diabetic level
6.5%
hgbA1c goal for diabetics; what plasma glucose level does it correlate with?
what criteria make a woman high risk and she should be tested early for gestational DM? (ACOG)
~Obesity
~Personal history of GDM or previous macrosomic infant
~Family history of diabetes in a first degree relative
~Polycystic ovarian disease (PCOS)
Ethnicity: AA, pacific islander, hispanic
Age: >35
)
normal region for a woman to be tested for gestational diabetes (ACOG AND ADA)
24-28 weeks
FPG in pregnancy that is GDM (according to ADA)
FPG >92, if >125, diagnosis with full blown DM
gene that is associated with huge increased risk ofDM i
HLA dr3/dr4
factors causig DM I
complex genetics (but identical twins only have 30% risk), AI, environmental (viruses? chemicals? infant feeding?)
pathophys of DM i
Multiple autoimmune mechanisms
Insulitis (infiltration of islets with lymphocytes)
Islet cell antibodies (GAD, ICA, IAA)
~90% loss of b-cell function clinical disease
SX OF dm type ii
Polydipsia, polyuria, polyphagia, wt loss
RFs for DMii
Obesity (BMI > 30) Genetic predisposition FH type 2 Metabolic Syndrome (abd obesity, low HDL, etc) Race/Ethnicity (esp native american, pacific islander, AA, hispanic GDM / child > 9 lbs Mother GDM, DM SGA infants (small gestational age)
differences between type I and II
I has AI component, type II more common among 1st degree relatives, type II more likely obese, type II often asymptomatic and have comorbidities
lab tests to distinguish type I and II
AI ab: GAD 65 most common (Glutamic acid decarboxylase (GAD) antibodies
)
why do we worry about gestational diabetes?
Increases risk of perinatal morbidity and mortality, including risk of preeclampsia, polyhydramnios, macrosomia, and malformations (though degree of risk debated)
probably pathogenesis in gestational diabets
not totally understood, but Progesterone; estrogen; human placental lactogen; other placental hormones
may have a role
etiology of maturity onset diabetes of the young
autosomal dominant genetic defect in beta cell function (often confused with type I b/c of early onset) and type II b/c can be tx’d with drugs
other etiologies of diabetes mellitius
exocrine (pancreatitis, cytstic fibrosis–kills off beta cells, pancreatectomy), severe protein/calorie malnutrition, other endocrine disorders: bushings, acromegaly, hyperandrogegism, PCOS, medications (corticosteroids, HCTZ, HIV meds, antipsychotics)
acute complications of diabetes
Diabetic Ketoacidosis (DKA)
Hyperglycemic hyperosmolar state (HHS)
Hypoglycemia due to treatment
chronic complications of diabetes
Microvascular
Retinopathy: background/proliferative
Neuropathy: peripheral/autonomic/mononeuropathy multiplex
Nephropathy
Macrovascular
Coronary artery disease
Cerebrovascular disease
Peripheral artery disease(PAD)
Combined:
Lower Extremity Complications: combination of peripheral neuropathy and PAD can’t feel foot and can’t get blood there to heal it, leads to amputations
Impotence and ED
what causes diabetic tissue damage?
hyperglycemia: repeated acute changes in cellular metabolism and LT changes in stable macromolecules (glycosylation of proteins) and accelerated by HTN and HLD
T or F: Diabetes Is a Cardiovascular Disease Risk Equivalent
t
study that demonstrated Lower risk of CVD events with intensive control (microvascular)
Diabetes Control and Complications Trial (DCCT)
study that showed these results:
Intensive diabetes therapy during the DCCT later reduced the occurrence of first CV event by 42% (p=0.018) and risk of CV death, MI and CVA by 58% (p=0.016) compared to conventional therapy
Risk reductions exceeded those of other interventions such as cholesterol and BP lowering medications.
These results confirm the benefit of “metabolic memory” of the earlier excellent control.
EDIC (after DCCT)
major results of UKPDS (UK prospective diabetes study)
significant macrovascular risk reduction when on inventional group and Decline in beta-cell function correlated with loss of response to oral diabetes medications
what did these studies prove about DM? ADVANCE, ACCORD & VA-DT Results: Intensive vs Standard Glucose Control
All 3 studies confirmed reduction in microvascular complications with better glucose control but NO no significant reduction in CVD outcomes with intensive glycemic control (once you have type II it doesn’t show reduced risk)
T or F: all diabetes need to get AIC down to
False: needs to be individualized: Certain populations (children, pregnant women, and elderly) require special considerations in pregnant women want really good control, in elderly risk of hypoglycemic events is worse than goal of preventing hyperglycemic complications
More stringent glycemic goals (i.e., a normal A1C,
Less intensive glycemic goals are indicated in patients with severe or frequent hypoglycemia, elderly, multiple comorbid illnesses
potential benefits of bariatric surgery
Weight loss, Reduced need for medications , Improved diabetes control Remission of diabetes Improvements in blood pressure, blood lipids, sleep apnea, osteoarthritis, quality of life Reduced long-term mortality
non pharm of diabetes
exercise!! diet, behavioral therapy +/- non pharm
risks of bariatric surgery
periop, anastomotic leaks, wound infxns, thromboembolism, pneumonia, Late complications including nausea, vomiting, anastamotic ulcers, internal hernias, gallstones, oxalate nephropathy, dumping syndrome, nutritional deficiencies (iron, calcium, vitamins B1, B12, D) and, postprandial hypoglycemia
who should be considered by bariatric surgery?
BMI >35 + diabetes (type II)
incretin effect
The Incretin Effect Is Diminished in Subjects With Type 2 Diabetes. Incretin effect=something is different when you give glucose IV AND you eat something (we don’t know why). When you eat something it stimulates more incretin release. Incretins also slow down gastric motility and decrease appetite. Why they give incretin to DMII.
A1C goal of GDM
comorbidities of prediabetes
obesity, CVD, dyslipiedmeia, HTN, renal failure, cancer, sleep disorders
prevention or delay of DMII in prediabetes
loss of 7% of body weight, and should increase their moderate physical activity to at least 150 min/week + behavioral counseling program. F/U counseling and maintenance
screen for pre diabetes if?
>45, or BM >25 + one of the following: Inactivity Extreme obesity 1º relative with DM Previous IGT / IFGT Associated conditions Delivery > 9# baby HTN Hyperlipidemia PCOS Acanthosis Nigricans H/O premature cardiovascular disease Prior h/o GDM
acute, severe and potentially life-threatening complication of diabetes characterized by marked hyperglycemia, dehydration, and ketoacidosis
diabetic ketoacidosis
Almost exclusively seen in Type 1 DM
DKA RFs
DMI
undx’d type 1 diabetes
Interruption of insulin therapy,
– Insulin pump failure or infusion site failure
Stress of an acute or chronic illness
Psychological problems with compliance and SBGM
Alcohol and drug addiction
DKA preciptating factors
Failure to take insulin infxn acute gastroenteritis, pneumonia pyelonephritis meningitis Acute Vascular Event: Stroke, MI, mesenteric infarction Severe emotional stress Acute renal failure
DKA sx and signs
sx: Vomiting Nausea, anorexia Abdominal pain Thirst Polyuria Weight loss Weakness Mental status changes
signs: Kussmaul respirations with fruity (acetone) breath Dehydration Warm, dry, flushed skin Hypotension Postural dizziness Tachycardia Shock CNS depression, coma
DKA labs:
BG >250
(+) betahydroxybutyrate
(+) urine and serum ketones
Arterial and venous pH 16
tx of DKA
insulin, hydration (nml saline), electrolyes
what do you always have to figure out in DKA
Precipitating factors may —the underlying cause may be what does the patient in—have to figure out why it happened!
T or F: in dKA, Total body K, Na, Mg, & P likely low despite variable serum values at presentation
T:
Initially 30% may have elevated serum potassium
due to insulin deficiency, metabolic acidosis, and hyperosmolar state
Could be dangerously high
A net total body potassium deficit exists
due to GI losses, increased renal excretion, and hyperaldosteronism secondary to dehydration (3-5 mEq/kg deficit)
how does insulin affect K?
drives it into cells
A metabolic emergency in which uncontrolled hyperglycemia induces hyperosmolar state in the absence of significant ketoacidosis.
hhs: hyperosmolar hyperglycemic state
who is affected by HHS?
type 2 usu, rare type 1. often elderly.
signs and sx of HHS
Dehydration
Sodium variable (normal 135-160)
Hypotension ( 800 mg/dL)
High serum osmolality (>330 400 mOsm/L)
Weight loss, polyuria, and polydipsia
Renal insufficiency elevated BUN (prerenal)
Lactic acidosis may also be present
tx of HHS
normal saline (slow!), insulin continuous IV, potassium (watch closely), monitor renal function
major differences between HHS and DKA
coma common in HHS, kussmaul respirations in DKA, much higher glucose in HHS, ketones, acidosis, and low bicarb in DKA, elevated BUN in HHS, type1 more common in DKA, type 2 more common in HHS
causes of hypoglycemia other than tx of DM
high insulin states (insulinoma, admin of insulin, drugs that induce insulin secretion--sulfonylureas) low insulin states: liver failure Malnutrition Excessive alcohol ingestion GH or cortisol deficiency Tumors that produce IGF Low carbohydrate intake
blood glucose
hypoglycemia
hypglycemia sx
hypoglycemia preciptating factors
Intentional or accidental overdose insulin Most common in Type 1 DM Inadequate food intake Increased exercise Decreased insulin requirement Potentiating medications
Rapidly fluctuating blood glucose
Type 2 diabetics taking insulin or sulfonylureas
if you find a diabetic patient and sx are vague and you aren’t sure if its HHS, DKA or hypoglycemia, what do you do/
50 grams of glucose/dextrose will do no harm to the patient with DKA or HHS until further evaluation can be implemented.
failure to do so: convulsions, coma,d eath
Early morning hyperglycemia in the absence of nocturnal hypoglycemia. Probably due to increase in am GH, cortisol and relative insulin resistance
dawn phenomenon
Delayed “rebound” hyperglycemia following hypoglycemia. Due to effects of counter-regulatory hormones.
+/- am hyperglycemia, morning HA and nightmares
rebound hyperglycemia
T or F: only free hormone is active
T
which thyroid hormone is more active?
T3
where does thyroid effect in body?
Endocrine Reproductive GI Skin Eye CV Neuro Pulm
pertinnt H&P for thyroid
Head/neck surgery or radiation FH malignant disease Sxs of hyper/hypoT Pain Growth/change Compression findings (can’t swallow as well or need lots of water to get food down or can’t lie flat in bed or it move neck and it feels tight) Presence of bruit Size Margins Consistency Adenopathy If nodule found: Location Mobility Size
most common cause of hyperthyroidism
Graves
causes of hyperthyroidism
Graves’ disease * Toxic multinodular goiter Toxic adenoma Carcinoma / pituitary adenoma Thyroiditis inflammation of thyroid gland that causes temporary hyperthyroidism Thyrotoxicosis factitia
sequelae of hyperthyroidism
Atrial fib CHF Angina MI Sudden death osteoporosis (minimal effect)
PE signs of hyperthyroidism
endo: Goiter, bruit, Ca, PTH, insulin resistance
neuro: Restlessness (scatter brained), tremor, fatigue, DTR, confusion, decreased cognition, insomnia
GI: Wt,appetite, diarrhea, lipid ∆, vit stores
skin Sweating, flushing, hair/nail ∆
eyesEyelid, tremor, infiltrate
CVTachy, SVT, LVH, CO, peripheral resistance
pulmDyspnea, vital capacity
reproOligo/amenorrhea, erectile dysfunction
dx test to tell you cause of hyperthryodiism
Radionuclide uptake scan (dx test it will tell you what the cause is)
123I(131I, Tc 99m)
labs in thyroid diseases
TSH
Free T4
Total T3 or Free T3
TSI (thyroid stimulating immunoglobulin)+ in graves only
Radionuclide uptake scan (dx test it will tell you what the cause is)
123I(131I, Tc 99m)
what do these symptoms make you think of? what lab will confirm it? sx: Diplopia, blurred vision Lacrimation or dryness Photophobia Heat intolerance Tachycardia Tremor Weight loss signs: Pretibial myxedema Exophthalmos, lid lag*, EOM paralysis Brisk DTRs Periorbital edema, papilledema Goiter 3x normal size (normal 20g), symmetric, +/- bruit, NT *Von Graefe's sign is the lagging of the upper eyelid on downward rotation of the eye
grave’s disease
Sudden, SEVERE thyrotoxicosis Some known precipitants Trauma Surgery Infection Ongoing disease Fatal if untreated
thyroid storm
tx of multi nodular goiter
observation, radioactive iodine (thyroid takes it up and it suppresses activity of it) or surgeyr (if compressive sx, or refuses iodine)
test to observe/follow thyroid
US
tender thyroid gland + recent infection makes you think of…? what do you expect in labs?
subacute thyroidits
labs: elevated TH, suppressed TSH (inflammation)
radionuclide study is best
tx of hyperthyroidism
antithyroid drug therapy, radioactive iodine ablation
most common clinical thyroid disorder
hypothyroidism
causes of hypothyroidism
Hashimoto’s thyroiditis * Subacute thyroiditis Painless thyroiditis Postpartum thyroiditis Post-therapeutic/Iatrogenic T4 T3 conversion disorder
hypothyroidism PE
Gen: fatigue, wt gain, cold intolerance
Skin: coarse, dry, scaly, cool extremeties
Hair: coarse, dry, sparse
HEENT: facial puffiness, periorbital swelling, hoarseness, eyelid droop
CV: bradycardia, pericardial effusion
Pulm: pleural effusion
GI: constipation
: depression
Neuro: forgetful, paresthesias, *delayed relaxation of DTRs with brisk contraction
Heme: menorrhagia/irregular, anemia
Initial hyperthyroidism, followed by hypothyroidism
Usually recovers to euthyroid over time
Symptoms last 2-4 months
subacute thyroiditis
Clinical syndrome found in acutely ill (hospital)
Decreased total/unbound T3
Normal T4 and TSH
Can also see elevated T3/T4 initially
euthyroid sick
most common type of thyroid cancer
papillary carcinoma
thryoid cancer assoc with increased calcitonin levels
medullary carcinoma
most aggressive thyroid cancer that is symptolmatic
anaplastic carcinoma, really rare but generally fatal (no cure)
Rapidly growing neck mass
Dysphagia, pain, dyspnea symptoms assoc with hashimotos
thyroid lymphoma
tx of thyroid cancer
surgery then radioactive Iodine thereafter then TSH suppression b/c TSH can stimulate thyroid to regrow
sx of pheochromocytoma (6 Hs)
- Hypertension
- Headache- throbbing
- Hyperhidrosis
- Heart consciousness or palpitations
- Hypermetabolism
- Hyperglycemia
labs, dx and tx of pheos
labs: • Plasma Free Metanephrines
• Urine Metanephrines (24h co
dx: CT/MRI or MIGB scan if available
tx: surgery (laparascopic for small or open for >7 cm) or drugs: beta blockers, alpha adrenergic receptor antagonists
- Paroxysmal Hypertension
* Small tumors that periodically release adrenaline
pheochromocytoma
best way to evaluate a pituitary mass
MRI
dx of acromegaly
- Random GH not useful
- IGF-1 best
- Oral glucose GH suppression testing is gold std
difference between cushing’s syndrome and cushion’s diease
- Cushing’s syndrome is a syndrome due to excess cortisol from pituitary, adrenal or other sources (exogenous glucocorticoids, ectopic ACTH, etc.)
- Cushing’s disease is hypercortisolism due to excess pituitary secretion of ACTH (about 70% of cases of endogenous Cushing’s syndrome)
signs and symtpoms of cushion’s disease
Symptoms • Mood changes (depression and euphoria) • Easy bruising • Weakness • Weight gain • Menstrual changes- key clue of endocrine problems • Back pain Signs • Truncal Obesity (90%) • Hypertension (85%) • Glucose Intolerance (80%) • Hirsutism (70%) • Wide, purple abdominal and thigh striae (65%) • Osteoporosis (55%) • Moon facies • Plethoric face • Buffalo hump (Thoracic kyphosis) • Myopathy • Supraclavicular fat pad development • Hypertrichosis • Peripheral Edema
most common iatrogenic cause of cushing’s disease
steroid therapy
dx of cushings
• ACTH, AM cortisol
• 24 hour urine cortisol
• midnight salivary cortisol
• Low dose Dexamethasone Suppression Test - screening
− Dexamethasone 1 mg at 11pm
− Plasma Cortisol in following morning (8 am)- positive if > 10 ug/dL (
T or F: a patient with prolactinoma can’t get pregnant
f
what does prolactin do? when is it secreted? what inhibits it/
- Primary function is to enhance breast development during pregnancy and to induce lactation
- Secretion is pulsatile; it increases with sleep, stress, pregnancy, and chest wall stimulation or trauma
- Inhibited by dopamine
tx of hyperprolactinemia or prolactinomas
- Pharmacotherapy dopamine agonists DOC like bromocriptine, pergolide and cabergoline
- Surgical resection TOC if intolerable AE of drug tx or large tumors with other hyperfunctional tumors (GH, ACTH secreting)
- Radiotherapy
- Follow up and monitoring will depend on size and other features of tumor
T or F: every patient with hyperprolactinemia has a prolactinoma
F
most common causes of ACUTE adrenocrotical insufficiency
steroid withdrawal, adrenal crisis in chronic problem in kids with sepsis or surgical stress, adrenal hemorrhage or anticoagulation complications
sx of adrenal insufficiency
- Weakness (99%)
- Skin pigmentation (98%)
- Weight loss (97%)
- Abdominal pain (34%)
- Salt craving (22%)
- Diarrhea (20%)
- Constipation (19%)
- Syncope (16%)
- Vitiligo (9%)
dx of adrenal insufficiency
adrenocorticotropic hormone stimulation test with dexamethasone–cortisol level should double in response to ACTH stimulation test. − In adrenal insufficiency, serum cortisol levels fail to rise after ACTH administration.
may see peaked T waves on EKG (from hyperkalemia and dehydration?)
tx of adrenal insufficiency
- Emergent – IV Hydrocortisone (100 mg q6h or constant infusion of 10mg/hr)
- Non emergent – oral hydrocortisone usually twice daily in AM and afternoon- to avoid fatigue, and they don’t feel the effect of low cortisone while sleeping
all pituitary hormones low makes you think of what? how to dx?
hypopituitaryism, dx: CT/MRI
sx of hyperparathyroidism
depression, fatigue, loss of appetite, constipation, osteoporosis, fractures, kidney stones
dx and tx of hyperparathyroid
DX: bone x-rays, Ca & PTH levels
TX: decrease high serum levels, surgical removal of parathyroid
PE of hyperparathyroidism
- Trousseau’s sign: temporarily occlude arterial blood flow with inflated BP cuff, above the normal systolic pressure- positive when the hand and fingers contract from ischemia- hypocalcemia
- Chvostek’s sign: tap on the facial nerve just below the temple- positive when nose, eye, lip & facial muscles twitch- hypocalcemia
painful spasms of face, hands, arms, and feet; seizures
hypoparathyrodism
what can cause low calcium
renal insuffiiency, drugs, vitamin D deficiency, rhabdo, hypomagnesemia (d/t PPIs), pancreatitis, sepsis, hypoalbuminemia
signs and sx of hypocalcemia
Symptoms • Nonspecific • V/D • Nervousness • Weakness • Paresthesias • Muscle stiffness and muscle cramps • Headache • Abdominal pain signs • Tetany • Carpopedal Spasm -Trousseau's Sign (hand and fingers contract from ischemia) • Chvostek's Sign (tap on facial nerve and muscles twitch) • Hair Loss • Cataracts • Papilledema
what should you always think of with hypercalcemia?
malignancy and hyperparathyroidism
Stones, Bones, Moans, Psychic Groans”
hypercalcemia
management of hypercalcemia
hydration first then diuretics
what molecule helps thyroid release thyroid hormone?
iodine
what does thyroid hormone do?
growth, development, metabolism, temperature and heart rate.
history and physical of thryoid
• Head/neck surgery or radiation • FH malignant disease • Sxs of hyper/hypoT • Pain • Growth/change • Compression findings (can’t swallow as well or need lots of water to get food down or can’t lie flat in bed or it move neck and it feels tight) • Presence of bruit • Size • Margins • Consistency • Adenopathy • If nodule found: o Location o Mobility o Size
if TSH is high and thyroid hormones are high what does that signify?
hyperthryoidism (secondary from pituitary or tertiary from hypothalamus)
if TSH is low and thyroid hormones are high what does that signify?
primary hyperthyroidism: thyroid making too much hormone which is turning off TSH
most common sx of hyperthyroid
weight loss, heat intolerance, fatigue, thinning of hair, eye tremor, eyelid lag, tachycardia, goiter, insulin resistance, ED, agitation, depression
MC etiology of hyperthryoid
graves
triad of grave’s disease
hyperthyroidism, opthalmopathy, dermopathy
• A life-threatening hypermetabolic state due to hyperthyroidism
thyroid storm
sx of hypothryoidism
- Gen: fatigue, wt gain, cold intolerance
- Skin: coarse, dry, scaly, cool extremeties
- Hair: coarse, dry, sparse
- HEENT: facial puffiness, periorbital swelling, hoarseness, eyelid droop
- CV: bradycardia, pericardial effusion
dx of thyroid cancer
• Dx: fine needle aspiration of nodules >1 cm
mC cause of obesity
caloric intake more than expenditure
health risks of obesity
pulmonary disease (OSA), non alcoholic fatty liver, gall bladder, gynecologic, OA, gout, stroke, cataracts, CHD, severe pancreatitis, cancer, phlebitis, skin infections
rec’d for doing waist circumference, where do you measure it?
superior edge of iliac crest
Measured if BMI between 25-35
Unnecessary if BMI ≥ 35
increased CVD risk of waist circumference is..? in males and females
≥ 40 inches in males and ≥ 35 inches in females
evaluation of obesity
If BMI ≥ 25 OR a waist circumference greater than ≥ 35 in (women) or ≥40 in (men):
Determine etiology: Secondary causes? Medical history Physical exam findings Laboratory findings Determine type and severity of obesity (BMI, waist circumference) Determine health risks/co-morbidities Guide treatment and management
physical exam in obesity
BMI/wt/ht +/- waist circumference
Thyroid goiter Hypothyroidism, look for nodules
Proximal muscle weakness, purple striae, HTN, osteoporosis Cushing’s Syndrome
Acne/hirsutism PCOS
additional labs for obesity
Fasting labs—FLP, fasting glucose, a1c
LFTs
TSH
If PCOS prolactin, FSH, LH, testosterone
If Cushing’s a 24-hour urine collection with analysis for urinary free cortisol
tx of obesity
Comprehensive lifestyle management Diet, physical activity, behavior modification Can encourage them to see a dietician Medications Surgery
qualifications for pharm management of obesity
> 27 with comorbidities or >30 w/ out
indications for surgery in obesity
> 35 with comorbidites, >40 without comorbidities
requirements for bariatric surgery
BMI ≥ 40 kg/m2 or BMI ≥ 35 kg/m2 with significant obesity-related co-morbidities
ages 16-70 y.o
Acceptable operative risk
Failure of non-surgical weight loss programs
Psychologically stable with realistic expectations and education on dietary restrictions
No eating disorders
Well-informed and motivated patient
Supportive family/social environment
Absence of active alcohol or substance abuse
Absence of uncontrolled psychotic or depressive disorder
3 most common bariatric surgery
Gastric Sleeve, gastric bypass, gastric adjustable band
gold std of bariatric surgery
gastric bypass
how much of weight is lost with gastric bypass?
60%
bariatric surgery option that is reversible with no cutting involved
gastric adjustable band
common short term complications of
PE, dehydration/nausea, staple link leakage, constipation
LT complications of bariatric surgery
cholelithiasis, ulcers at site where stomach was cut, stomal stenosis, dumping syndrome, nutritional deficiencies
what’s a good pneumonic for setting weight loss goals?
SMART: Specific, Measurable, Attainable, Realistic, and Timely
wt loss goals
Weight loss goals: 1-2 lbs./week
5-10% weight loss from baseline in 6 months
steps of motivational interviewing
Establish rapport
Assess readiness for change if not ready, move on or investigate why
Assess motivation and confidence
Patient identifies problems and solutions
Identify next action and follow up
