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Clinical Medicine > endocrine > Flashcards

endocrine Flashcards

1
Q

A complex metabolic disorder characterized by abnormally increased

blood glucose concentration caused by resistance to action of insulin,

insufficient secretion of insulin, or both.

A

diabetes mellitus

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2
Q

LT damage of diabets

A

failure of different organs including the eyes, kidneys, nervous

system, heart and blood vessels

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3
Q

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

A

insulin

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4
Q

function of insulins

A

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)

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5
Q

what does insulin impair?

A

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

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6
Q

A 29 amino acid polypeptide hormone secreted from the Alpha cells of the
Islets of Langerhans that is stimulated by hypoglycemia

A

glucagon (raises blood sugar) while insulin lowers blood sugar

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7
Q

threshold for DM with fBG

A

> 126

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8
Q

threshold for DM with random BG test

A
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9
Q

Hgb A1C level for dx of DM

A

> 6.5%

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10
Q

what’s an OGTT test? what’s the threshold for DM?

A

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

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11
Q

prediabets dx

A

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%

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12
Q

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

A

Hgb A1c

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13
Q

hgb a1c normal level, pre diabetic level, diabetic level

A

6.5%

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14
Q

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

A
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15
Q

what criteria make a woman high risk and she should be tested early for gestational DM? (ACOG)

A

~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
)

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16
Q

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

A

24-28 weeks

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17
Q

FPG in pregnancy that is GDM (according to ADA)

A

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

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18
Q

gene that is associated with huge increased risk ofDM i

A

HLA dr3/dr4

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19
Q

factors causig DM I

A

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

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20
Q

pathophys of DM i

A

Multiple autoimmune mechanisms
Insulitis (infiltration of islets with lymphocytes)
Islet cell antibodies (GAD, ICA, IAA)

~90% loss of b-cell function  clinical disease

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21
Q

SX OF dm type ii

A

Polydipsia, polyuria, polyphagia, wt loss

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22
Q

RFs for DMii

A 
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)
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23
Q

differences between type I and II

A

I has AI component, type II more common among 1st degree relatives, type II more likely obese, type II often asymptomatic and have comorbidities

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24
Q

lab tests to distinguish type I and II

A

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

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25
Q

why do we worry about gestational diabetes?

A

Increases risk of perinatal morbidity and mortality, including risk of preeclampsia, polyhydramnios, macrosomia, and malformations (though degree of risk debated)

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26
Q

probably pathogenesis in gestational diabets

A

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

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27
Q

etiology of maturity onset diabetes of the young

A

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

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28
Q

other etiologies of diabetes mellitius

A

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)

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29
Q

acute complications of diabetes

A

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

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30
Q

chronic complications of diabetes

A

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

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31
Q

what causes diabetic tissue damage?

A

hyperglycemia: repeated acute changes in cellular metabolism and LT changes in stable macromolecules (glycosylation of proteins) and accelerated by HTN and HLD

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32
Q

T or F: Diabetes Is a Cardiovascular Disease Risk Equivalent

A

t

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33
Q

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

A

Diabetes Control and Complications Trial (DCCT)

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34
Q

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.

A

EDIC (after DCCT)

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35
Q

major results of UKPDS (UK prospective diabetes study)

A

significant macrovascular risk reduction when on inventional group and Decline in beta-cell function correlated with loss of response to oral diabetes medications

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36
Q

what did these studies prove about DM? ADVANCE, ACCORD & VA-DT Results: Intensive vs Standard Glucose Control

A

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)

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37
Q

T or F: all diabetes need to get AIC down to

A 
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

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38
Q

potential benefits of bariatric surgery

A 
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
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39
Q

non pharm of diabetes

A

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

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40
Q

risks of bariatric surgery

A

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

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41
Q

who should be considered by bariatric surgery?

A

BMI >35 + diabetes (type II)

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42
Q

incretin effect

A

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.

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43
Q

A1C goal of GDM

A
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44
Q

comorbidities of prediabetes

A

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

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45
Q

prevention or delay of DMII in prediabetes

A

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

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46
Q

screen for pre diabetes if?

A 
>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
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47
Q

acute, severe and potentially life-threatening complication of diabetes characterized by marked hyperglycemia, dehydration, and ketoacidosis

A

diabetic ketoacidosis

Almost exclusively seen in Type 1 DM

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48
Q

DKA RFs

A

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

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49
Q

DKA preciptating factors

A 
Failure to take insulin
infxn
acute gastroenteritis, pneumonia
pyelonephritis
meningitis
Acute Vascular Event: Stroke, MI, mesenteric infarction
Severe emotional stress
Acute renal failure
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50
Q

DKA sx and signs

A 
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
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51
Q

DKA labs:

A

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

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52
Q

tx of DKA

A

insulin, hydration (nml saline), electrolyes

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53
Q

what do you always have to figure out in DKA

A

Precipitating factors may —the underlying cause may be what does the patient in—have to figure out why it happened!

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54
Q

T or F: in dKA, Total body K, Na, Mg, & P likely low despite variable serum values at presentation

A

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)

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55
Q

how does insulin affect K?

A

drives it into cells

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56
Q

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

A

hhs: hyperosmolar hyperglycemic state

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57
Q

who is affected by HHS?

A

type 2 usu, rare type 1. often elderly.

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58
Q

signs and sx of HHS

A

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

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59
Q

tx of HHS

A

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

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60
Q

major differences between HHS and DKA

A

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

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61
Q

causes of hypoglycemia other than tx of DM

A 
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
Q

blood glucose

A

hypoglycemia

63
Q

hypglycemia sx

A
64
Q

hypoglycemia preciptating factors

A 
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
Q

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/

A

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
Q

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

A

dawn phenomenon

67
Q

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

A

rebound hyperglycemia

68
Q

T or F: only free hormone is active

A

T

69
Q

which thyroid hormone is more active?

A

T3

70
Q

where does thyroid effect in body?

A 
Endocrine
Reproductive
GI
Skin
Eye
CV
Neuro
Pulm
71
Q

pertinnt H&P for thyroid

A 
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
Q

most common cause of hyperthyroidism

A

Graves

73
Q

causes of hyperthyroidism

A 
Graves’ disease *
Toxic multinodular goiter
Toxic adenoma
Carcinoma / pituitary adenoma
Thyroiditis inflammation of thyroid gland that causes temporary hyperthyroidism
Thyrotoxicosis factitia
74
Q

sequelae of hyperthyroidism

A 
Atrial fib
CHF
Angina
MI
Sudden death
osteoporosis (minimal effect)
75
Q

PE signs of hyperthyroidism

A

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
Q

dx test to tell you cause of hyperthryodiism

A

Radionuclide uptake scan (dx test it will tell you what the cause is)
123I(131I, Tc 99m)

77
Q

labs in thyroid diseases

A

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
Q 
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
A

grave’s disease

79
Q 
Sudden, SEVERE thyrotoxicosis
Some known precipitants
Trauma
Surgery
Infection
Ongoing disease
Fatal if untreated
A

thyroid storm

80
Q

tx of multi nodular goiter

A

observation, radioactive iodine (thyroid takes it up and it suppresses activity of it) or surgeyr (if compressive sx, or refuses iodine)

81
Q

test to observe/follow thyroid

A

US

82
Q

tender thyroid gland + recent infection makes you think of…? what do you expect in labs?

A

subacute thyroidits
labs: elevated TH, suppressed TSH (inflammation)
radionuclide study is best

83
Q

tx of hyperthyroidism

A

antithyroid drug therapy, radioactive iodine ablation

84
Q

most common clinical thyroid disorder

A

hypothyroidism

85
Q

causes of hypothyroidism

A 
Hashimoto’s thyroiditis *
Subacute thyroiditis
Painless thyroiditis
Postpartum thyroiditis
Post-therapeutic/Iatrogenic
T4  T3 conversion disorder
86
Q

hypothyroidism PE

A

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
Q

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

A

subacute thyroiditis

88
Q

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

A

euthyroid sick

89
Q

most common type of thyroid cancer

A

papillary carcinoma

90
Q

thryoid cancer assoc with increased calcitonin levels

A

medullary carcinoma

91
Q

most aggressive thyroid cancer that is symptolmatic

A

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

92
Q

Rapidly growing neck mass

Dysphagia, pain, dyspnea symptoms assoc with hashimotos

A

thyroid lymphoma

93
Q

tx of thyroid cancer

A

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

94
Q

sx of pheochromocytoma (6 Hs)

A
  • Hypertension
  • Headache- throbbing
  • Hyperhidrosis
  • Heart consciousness or palpitations
  • Hypermetabolism
  • Hyperglycemia
95
Q

labs, dx and tx of pheos

A

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
Q
  • Paroxysmal Hypertension

* Small tumors that periodically release adrenaline

A

pheochromocytoma

97
Q

best way to evaluate a pituitary mass

A

MRI

98
Q

dx of acromegaly

A
  • Random GH not useful
  • IGF-1 best
  • Oral glucose GH suppression testing is gold std
99
Q

difference between cushing’s syndrome and cushion’s diease

A
  • 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
Q

signs and symtpoms of cushion’s disease

A 
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
Q

most common iatrogenic cause of cushing’s disease

A

steroid therapy

102
Q

dx of cushings

A

• 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
Q

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

A

f

104
Q

what does prolactin do? when is it secreted? what inhibits it/

A
  • 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
Q

tx of hyperprolactinemia or prolactinomas

A
  • 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
Q

T or F: every patient with hyperprolactinemia has a prolactinoma

A

F

107
Q

most common causes of ACUTE adrenocrotical insufficiency

A

steroid withdrawal, adrenal crisis in chronic problem in kids with sepsis or surgical stress, adrenal hemorrhage or anticoagulation complications

108
Q

sx of adrenal insufficiency

A
  • Weakness (99%)
  • Skin pigmentation (98%)
  • Weight loss (97%)
  • Abdominal pain (34%)
  • Salt craving (22%)
  • Diarrhea (20%)
  • Constipation (19%)
  • Syncope (16%)
  • Vitiligo (9%)
109
Q

dx of adrenal insufficiency

A

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
Q

tx of adrenal insufficiency

A
  • 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
Q

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

A

hypopituitaryism, dx: CT/MRI

112
Q

sx of hyperparathyroidism

A

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

113
Q

dx and tx of hyperparathyroid

A

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

114
Q

PE of hyperparathyroidism

A
  • 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
Q

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

A

hypoparathyrodism

116
Q

what can cause low calcium

A

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

117
Q

signs and sx of hypocalcemia

A 
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
Q

what should you always think of with hypercalcemia?

A

malignancy and hyperparathyroidism

119
Q

Stones, Bones, Moans, Psychic Groans”

A

hypercalcemia

120
Q

management of hypercalcemia

A

hydration first then diuretics

121
Q

what molecule helps thyroid release thyroid hormone?

A

iodine

122
Q

what does thyroid hormone do?

A

growth, development, metabolism, temperature and heart rate.

123
Q

history and physical of thryoid

A 
•	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
Q

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

A

hyperthryoidism (secondary from pituitary or tertiary from hypothalamus)

125
Q

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

A

primary hyperthyroidism: thyroid making too much hormone which is turning off TSH

126
Q

most common sx of hyperthyroid

A

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

127
Q

MC etiology of hyperthryoid

A

graves

128
Q

triad of grave’s disease

A

hyperthyroidism, opthalmopathy, dermopathy

129
Q

• A life-threatening hypermetabolic state due to hyperthyroidism

A

thyroid storm

130
Q

sx of hypothryoidism

A
  • 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
Q

dx of thyroid cancer

A

• Dx: fine needle aspiration of nodules >1 cm

132
Q

mC cause of obesity

A

caloric intake more than expenditure

133
Q

health risks of obesity

A

pulmonary disease (OSA), non alcoholic fatty liver, gall bladder, gynecologic, OA, gout, stroke, cataracts, CHD, severe pancreatitis, cancer, phlebitis, skin infections

134
Q

rec’d for doing waist circumference, where do you measure it?

A

superior edge of iliac crest

Measured if BMI between 25-35
Unnecessary if BMI ≥ 35

135
Q

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

A

≥ 40 inches in males and ≥ 35 inches in females

136
Q

evaluation of obesity

A

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
Q

physical exam in obesity

A

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
Q

additional labs for obesity

A

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
Q

tx of obesity

A 
Comprehensive lifestyle management
Diet, physical activity, behavior modification
Can encourage them to see a dietician
Medications
Surgery
140
Q

qualifications for pharm management of obesity

A

> 27 with comorbidities or >30 w/ out

141
Q

indications for surgery in obesity

A

> 35 with comorbidites, >40 without comorbidities

142
Q

requirements for bariatric surgery

A

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
Q

3 most common bariatric surgery

A

Gastric Sleeve, gastric bypass, gastric adjustable band

144
Q

gold std of bariatric surgery

A

gastric bypass

145
Q

how much of weight is lost with gastric bypass?

A

60%

146
Q

bariatric surgery option that is reversible with no cutting involved

A

gastric adjustable band

147
Q

common short term complications of

A

PE, dehydration/nausea, staple link leakage, constipation

148
Q

LT complications of bariatric surgery

A

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

149
Q

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

A

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

150
Q

wt loss goals

A

Weight loss goals: 1-2 lbs./week

5-10% weight loss from baseline in 6 months

151
Q

steps of motivational interviewing

A

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

Clinical Medicine (19 decks)

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