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Flashcards in endocrine Deck (151):
1

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

2

LT damage of diabets

failure of different organs including the eyes, kidneys, nervous

system, heart and blood vessels

3

An anabolic hormone secreted by the Beta cells of the Islets of Langerhans
in the pancreas

insulin

4

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)

5

what does insulin impair?

-) glycogenolysis (break down of glycogen in liver)
(-) gluconeogenesis (inhibits glucose prod)
(-) hepatic glucose production
(-) lipolysis

6

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

7

threshold for DM with fBG

> 126

8

threshold for DM with random BG test

9

Hgb A1C level for dx of DM

>6.5%

10

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

11

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%

12

Reflects average level of hyperglycemia over prior 2-3 months.

Hgb A1c

13

hgb a1c normal level, pre diabetic level, diabetic level

6.5%

14

hgbA1c goal for diabetics; what plasma glucose level does it correlate with?

15

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
)

16

normal region for a woman to be tested for gestational diabetes (ACOG AND ADA)

24-28 weeks

17

FPG in pregnancy that is GDM (according to ADA)

FPG >92, if >125, diagnosis with full blown DM

18

gene that is associated with huge increased risk ofDM i

HLA dr3/dr4

19

factors causig DM I

complex genetics (but identical twins only have 30% risk), AI, environmental (viruses? chemicals? infant feeding?)

20

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

21

SX OF dm type ii

Polydipsia, polyuria, polyphagia, wt loss

22

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)

23

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

24

lab tests to distinguish type I and II

AI ab: GAD 65 most common (Glutamic acid decarboxylase (GAD) antibodies
)

25

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)

26

probably pathogenesis in gestational diabets

not totally understood, but Progesterone; estrogen; human placental lactogen; other placental hormones
may have a role

27

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

28

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)

29

acute complications of diabetes

Diabetic Ketoacidosis (DKA)
Hyperglycemic hyperosmolar state (HHS)
Hypoglycemia due to treatment

30

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

31

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

32

T or F: Diabetes Is a Cardiovascular Disease Risk Equivalent

t

33

study that demonstrated Lower risk of CVD events with intensive control (microvascular)

Diabetes Control and Complications Trial (DCCT)

34

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)

35

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

36

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)

37

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

38

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

39

non pharm of diabetes

exercise!! diet, behavioral therapy +/- non pharm

40

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

41

who should be considered by bariatric surgery?

BMI >35 + diabetes (type II)

42

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.

43

A1C goal of GDM

44

comorbidities of prediabetes

obesity, CVD, dyslipiedmeia, HTN, renal failure, cancer, sleep disorders

45

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

46

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

47

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

48

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

49

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

50

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

51

DKA labs:

BG >250
(+) betahydroxybutyrate
(+) urine and serum ketones
Arterial and venous pH 16

52

tx of DKA

insulin, hydration (nml saline), electrolyes

53

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!

54

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)

55

how does insulin affect K?

drives it into cells

56

A metabolic emergency in which uncontrolled hyperglycemia induces hyperosmolar state in the absence of significant ketoacidosis.

hhs: hyperosmolar hyperglycemic state

57

who is affected by HHS?

type 2 usu, rare type 1. often elderly.

58

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

59

tx of HHS

normal saline (slow!), insulin continuous IV, potassium (watch closely), monitor renal function

60

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

61

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

62

blood glucose

hypoglycemia

63

hypglycemia sx

64

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

65

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

66

Early morning hyperglycemia in the absence of nocturnal hypoglycemia. Probably due to increase in am GH, cortisol and relative insulin resistance

dawn phenomenon

67

Delayed “rebound” hyperglycemia following hypoglycemia. Due to effects of counter-regulatory hormones.
+/- am hyperglycemia, morning HA and nightmares

rebound hyperglycemia

68

T or F: only free hormone is active

T

69

which thyroid hormone is more active?

T3

70

where does thyroid effect in body?

Endocrine
Reproductive
GI
Skin
Eye
CV
Neuro
Pulm

71

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

72

most common cause of hyperthyroidism

Graves

73

causes of hyperthyroidism

Graves’ disease *
Toxic multinodular goiter
Toxic adenoma
Carcinoma / pituitary adenoma
Thyroiditis inflammation of thyroid gland that causes temporary hyperthyroidism
Thyrotoxicosis factitia

74

sequelae of hyperthyroidism

Atrial fib
CHF
Angina
MI
Sudden death
osteoporosis (minimal effect)

75

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

76

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)

77

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)

78

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

79

Sudden, SEVERE thyrotoxicosis
Some known precipitants
Trauma
Surgery
Infection
Ongoing disease
Fatal if untreated

thyroid storm

80

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)

81

test to observe/follow thyroid

US

82

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

83

tx of hyperthyroidism

antithyroid drug therapy, radioactive iodine ablation

84

most common clinical thyroid disorder

hypothyroidism

85

causes of hypothyroidism

Hashimoto’s thyroiditis *
Subacute thyroiditis
Painless thyroiditis
Postpartum thyroiditis
Post-therapeutic/Iatrogenic
T4  T3 conversion disorder

86

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

87

Initial hyperthyroidism, followed by hypothyroidism
Usually recovers to euthyroid over time
Symptoms last 2-4 months

subacute thyroiditis

88

Clinical syndrome found in acutely ill (hospital)
Decreased total/unbound T3
Normal T4 and TSH
Can also see elevated T3/T4 initially

euthyroid sick

89

most common type of thyroid cancer

papillary carcinoma

90

thryoid cancer assoc with increased calcitonin levels

medullary carcinoma

91

most aggressive thyroid cancer that is symptolmatic

anaplastic carcinoma, really rare but generally fatal (no cure)

92

Rapidly growing neck mass
Dysphagia, pain, dyspnea symptoms assoc with hashimotos

thyroid lymphoma

93

tx of thyroid cancer

surgery then radioactive Iodine thereafter then TSH suppression b/c TSH can stimulate thyroid to regrow

94

sx of pheochromocytoma (6 Hs)

• Hypertension
• Headache- throbbing
• Hyperhidrosis
• Heart consciousness or palpitations
• Hypermetabolism
• Hyperglycemia

95

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

96

• Paroxysmal Hypertension
• Small tumors that periodically release adrenaline

pheochromocytoma

97

best way to evaluate a pituitary mass

MRI

98

dx of acromegaly

• Random GH not useful
• IGF-1 best
• Oral glucose GH suppression testing is gold std

99

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)

100

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

101

most common iatrogenic cause of cushing's disease

steroid therapy

102

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 (

103

T or F: a patient with prolactinoma can't get pregnant

f

104

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

105

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

106

T or F: every patient with hyperprolactinemia has a prolactinoma

F

107

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

108

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%)

109

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?)

110

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

111

all pituitary hormones low makes you think of what? how to dx?

hypopituitaryism, dx: CT/MRI

112

sx of hyperparathyroidism

depression, fatigue, loss of appetite, constipation, osteoporosis, fractures, kidney stones

113

dx and tx of hyperparathyroid

DX: bone x-rays, Ca & PTH levels
TX: decrease high serum levels, surgical removal of parathyroid

114

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

115

painful spasms of face, hands, arms, and feet; seizures

hypoparathyrodism

116

what can cause low calcium

renal insuffiiency, drugs, vitamin D deficiency, rhabdo, hypomagnesemia (d/t PPIs), pancreatitis, sepsis, hypoalbuminemia

117

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

118

what should you always think of with hypercalcemia?

malignancy and hyperparathyroidism

119

Stones, Bones, Moans, Psychic Groans"

hypercalcemia

120

management of hypercalcemia

hydration first then diuretics

121

what molecule helps thyroid release thyroid hormone?

iodine

122

what does thyroid hormone do?

growth, development, metabolism, temperature and heart rate.

123

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

124

if TSH is high and thyroid hormones are high what does that signify?

hyperthryoidism (secondary from pituitary or tertiary from hypothalamus)

125

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

126

most common sx of hyperthyroid

weight loss, heat intolerance, fatigue, thinning of hair, eye tremor, eyelid lag, tachycardia, goiter, insulin resistance, ED, agitation, depression

127

MC etiology of hyperthryoid

graves

128

triad of grave's disease

hyperthyroidism, opthalmopathy, dermopathy

129

• A life-threatening hypermetabolic state due to hyperthyroidism

thyroid storm

130

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

131

dx of thyroid cancer

• Dx: fine needle aspiration of nodules >1 cm

132

mC cause of obesity

caloric intake more than expenditure

133

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

134

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

135

increased CVD risk of waist circumference is..? in males and females

≥ 40 inches in males and ≥ 35 inches in females

136

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

137

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

138

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

139

tx of obesity

Comprehensive lifestyle management
Diet, physical activity, behavior modification
Can encourage them to see a dietician
Medications
Surgery

140

qualifications for pharm management of obesity

>27 with comorbidities or >30 w/ out

141

indications for surgery in obesity

>35 with comorbidites, >40 without comorbidities

142

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

143

3 most common bariatric surgery


Gastric Sleeve, gastric bypass, gastric adjustable band

144

gold std of bariatric surgery

gastric bypass

145

how much of weight is lost with gastric bypass?

60%

146

bariatric surgery option that is reversible with no cutting involved

gastric adjustable band

147

common short term complications of

PE, dehydration/nausea, staple link leakage, constipation

148

LT complications of bariatric surgery

cholelithiasis, ulcers at site where stomach was cut, stomal stenosis, dumping syndrome, nutritional deficiencies

149

what's a good pneumonic for setting weight loss goals?

SMART: Specific, Measurable, Attainable, Realistic, and Timely

150

wt loss goals

Weight loss goals: 1-2 lbs./week
5-10% weight loss from baseline in 6 months

151

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