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ENDO > ENDO #2 > Flashcards

ENDO #2 Flashcards

1
Q

What are appropriate interventions for weight loss by BMI

A

BMI over 40 or over 35 with Comorbids (HTN or T2DM) = bariatric surgery

BMI over 30 or over 27 with Comorbids (HTN or T2DM) = obesity med specialist

Everyone get nutrition and exercise

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2
Q

When is medication indicated for Obesity

A

After diet and exercise

BMI over 30 or over 27 with Comorbids ( HTN.T2DM.CVD)

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3
Q

BMI obesity classes

A

Under = less than 18.4

NML = 18.5-24.9

Over Wt. = 25-29.9

Class 1 = 30 -34.9

Class 2 = 35-39.9

Class 3 = Over 40

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4
Q

Rule outs of secondary Causes of obesity

And what are the secondary effects

A

Cushings (fast wt gain-truncal) - Dex Mex Test

Acromegaly - IGF1

Thyroid- TSH/Free T4

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5
Q

What are the secondary effects of metabolic syndrome and DM

2

A

High cholesterol

CAD

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6
Q

Different causes of hirsutism (5)

A

Idiopathic

PCOS

Steriogofnic enzyme defects

Cancer

Rare Pharm.

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7
Q

Concerning signs of hirsutism that may indicate a neoplasm is the cause

A

Pure adrenal tumors
Outside of perimenapausal period
Rapid severe hair growth

VIRILIZATION

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8
Q

What meds cause hirsutism

A

Minoxidil; hair loss TXM drug

Cyclophosphene - organ transplant drug

Older progestins - northindrone

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9
Q

Difference hirsutism vs virilization

A

Hirsituism = hair only

Virilization = deepening of the voice with increased muscle growth and male hair distribution

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10
Q

What are we worried about with virilization

A

Cancer

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11
Q

Effective treatment for hirsituism (7)

A

Change OCP ; anti androgen progestin

Spironolactone = anti androgen [ good for hair acne and androgenic]
+METFORMIN

Flutamide + Bicalutamide = bind test. And suppress
[severe txm]

Finasteride = inhibit 5 alpha reductase [BAD PREG.]

Simvastatin = red. hirsutism [ good with OCP’s ]

Clomiphene = fertility restored aid PCOS + infertility

Cosmetic and end stage Laser Therapy.

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12
Q

Causes of gynecomastia

Primary vs Secondary

A

Physio vs Endo

Neonate
Puberty
Aging
Obesity

Endo
Hyper/Hypoo thyroid
Liver Dz

Cancer
Meds

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13
Q

Features suspicious for malignancy in gyneocmastia

A

Asx
Location NOT below the Areola
Unusually firm
Nipple bleeding or with discharge

W/ abnormal tests and thyroid exam

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14
Q

What meds are used for gyenocmastia

A

Pubertal = self limited

Stop offending drug and switch

If painful,
SERM = tamoxifen/raloxifene

If hypogonadism = test r2

Radiation then last, Surgery

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15
Q

Pubertal gynecomastia vs breast cancer

Presentation

A 
Puberty 
Uni / Bi lateral 
Tender discoid enlargement 
2-3 cm in diameter 
TENDER 
Subsides at 1-2 years self limited wt loss helps!
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16
Q

What are lab tests for gynecomastia

A

PRL HcG LH
Testosterone
Estradiol
TSH/FT4

Karotype —> Klinefelters

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17
Q

When do we work up gynecomastia

A

Not physio or if caused by a condition known (Ex: thyroid disorder).

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18
Q

Primary hypogondsiam vs.

Secondary hypogonadism

A

Primary = testes dont produce testosterone (Hypergonad)

Secondary = pituitary or hypothalamus can’t secrete LH/FSH (Hypogonad)

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19
Q

What are the lab for male hypogonadism (Test/LH/FSH)

Primary vs secondary

A

Testosterone - taken in the MORNING!

Total test = 54-75% bount to SHBG
Free test = 23% (MOST AFFECTED - HYPOGONAD)

LH/FSH high Test low = Primary

LH/FSH low/ nml Test low = Secondary

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20
Q

Indications and contra to replacement therapy for male hypogonadism\ with side effects

A 
Patches = non scrotal area 
Topical = risk of female transfer 
Pellets/Injections = pulm oil microembolism 
Intraday = URI rxn 
Side effects :
Acne 
Decreased HDL 
Sleep apnea 
Osteoporosis
21
Q

Defects in androgen action

A

Causes resistance

Think - normal testosterone with elevated LH/FSH

22
Q

Patho for DM 1 and 2

A

1 = Auto immune B cell destruction
“Deficient Insulin” Wt. Loss / DKA

2= overwhelmed Insulin
“Resistance” Obesity Fam Hx HHS

23
Q

S/sxs of T1/T2 DM

A

T1:
Polyuria / Polydipsia / Polyphasia Blurred vision / Wt. Loss

T2:
Skin Infections candidiasis vaginitis “acanthosis Nigerians”: dark back of the neck fold

24
Q

Labs for DM dx

A

All abnormal= Repeated

Fasting glucose (over 126)
HbA1c (over 6.5%)
Random Glucose ( over 200 w/ sxs)
OGT (over 200)

25
Q

Management guidelines

A

1st = DM Ed. Class
TLC - diet etc.
Pharm mgmt

26
Q

MOA of Metformin / SGLT2’s / DPP4 / GLP1s

A

Metformin = Biguanide
Dec Lipids/Slight Wt. Loss
(Not in renal insuff. Or lactic acidosis)

SGLT2’s= Flozins ; dec. Absoroption / renal threshold / inc. glucose secretion through urine
Wt. Loss
(Not in renal dysfunction)

DPP4’s =-GLIPTONs ; prevent incretin degradation stabilize insulin secretion dec glucose release
Wt. neutral/ low Hypoglycemia risk
(Not for renal impaired/PANCREATITIS/URI sxs)

GLP1-agonists—tides ; stimulate glucose, dec. Insulin release
Wt. Loss, help post praindal glucose
(Not forMEN2 / Medullary thy cancer gastropaerresis bad)

TZD=- ZONE’s senstizers to peripheral tissues insulin
Dec. Lipids slow progression
(Not for HF /Active Liver Dz)

SU= -tamide/zide/glinide
Stim insulin form panc. B cells good longevity
(Not for severe liver dz or renal dz)

AGI’s =-Bose/Miglitol glucose absorber by delaying carb absorption
good Wt. Loss/post praindal glucose
(Not for CKD / GI sxs)

27
Q

When to start insulin

A

T1 DM identified

Or DKA / HHS episode

28
Q

Dawn vs Somogyi

A

Dawn = ELEVATED
Slightly @ 0200 - 0300 ; dec. Sensitive to insulin b/w 0500-0800
TXM = Increase the dose! (Bed time)

Somogyi = LOW to NML
@ 0200 - 0300 ;
TXM = Decrease the dose! (Bed time)

29
Q

Acute complications of hypoglycemia

A 
Lower than 60 
Behavioral changes 
Impaired glucagon response 
Sympathetic adrenal blunting 
CKD/ GASTROPARESIS
30
Q

Diff between DKA and HSS

A

DKA
T1 common ; deficient insulin. Rapid mobilization of energy stores in muscle and fat Increase Flux of AA to ketones.
Greater than 250 mg/ dL hyperglycemia

HHS 
[NO KETOSIS] 
CHF or CKD underlying makes it worse 
Partial insulin def. / dec. Glucose to muscle fat and liver 
Insidious Onset. 
B/w 800- 2400 mg/dL
31
Q

Good treatment for DKA and HSS

A 
DKA
IV Fluids = 1st 
Insulin R2 if K+ over 3.5 = reg insulin 
IF K+ Low = R2 KCl- First! 
IF ACIDOSIS Sodium Bicarbonate 
ABX~

HHS
Fluids = 1st
NML Saline
Glucose less than 25 = dextrose and saline

0.05 Insulin infusion if still greater than 250 glucose = 2nd Line

32
Q

Mgmt of chornic complications for micro and vascualr complications

A

Best TXM = glycemic control / tobacco cessation / HTN mgmt

Vision screen —> ophthalmology
5 years after T1 Dx
Initial @ Dx then Annual —> T2

33
Q

Other meds to prescribe in a patient with diabetes

A

Consider HTN (ACEI/ARBs)

Diabetic neuropathy (Gabapentin/ Nortriptyline/ Capsaicin cream) 
Peripheral neuropathy = amitriptyline 
Nephropathy= dialysis 
GASTROPARESIS = metoclopramide 
Skin = steroids
34
Q

Mechanism of ca metabolism
PTH
Vit D
Calcitonin

A

Increase in PTH = Decrease in Ca2+

Mg regulates PTH

PTH = inhibits phosphate ca reabsorption

Vit D = increased Ca2+ absorption from intestine

Calcitonin = Increase PTH secretion ; dec. CA2+

35
Q

What organs and how do organs regulate calcium

A

Kidneys = releases Vit D ; renal tubular reapportion of phosphates by PTH

Bones

Skin

36
Q

Hyper calcemia presentation (GMOBS)

A 
Groans - Met Acidosis ; kidney stones 
Moans - Myalgia / muscle weak 
Overton’s - depression / anxiety 
Bones - bone pain / fx / 
Stones - kidney stones
37
Q

Hypo calcemia presentation

A

CAT’s GO NUMB
Convulsions arrhythmias tetany seizures numb hands feet mouth

Paresthesias 
Muscle cramps 
Tingles 
Irritability and Confusion 
Anxiety and Depression 
LARYNGEAL AND BRONCHOSPASMS 
PROLONGED QT INTERVAL
38
Q

Causes of hyper v hypo Ca

A

Hyperparathyroid = PTH elevated or suppressed
Squamous cell cancer of the lungs = PTHrP
Immobilized
Diet

Hypo
CKD
Alcoholism
Diuretics

39
Q

Can HCTZ be used with hyper or hypo CA

A

Hypocalcemia can be used as txm

40
Q

High vs low PTH

A
41
Q

3 etiologies involved in hyper ca+

A

Suppressed PTH
Normal minimal PTH
Elevated PTH

42
Q

DEXA scan points

A

Greater than -1 = NML

-1 - -2.5 = OSTEOPENIA

Less than -2.5 = OSTEOPOROSIS

43
Q

3 etiologies of Hypocalcemia

A

Increased loss
Elevated PTH
Suppressed PTH

44
Q

What is the most common cause of Hypocalcemia

A

CKD

45
Q

What is the most common cause of hypocalcemia with an elevated PTH

A

Vit D Deficiency

46
Q

3 main types of primary hypergonadism

A

Congenital -

Klinefelters 47XXY

Cryptorchidism/Bilateral anorchia

Seminiferous tubules dysgenesis

47
Q

4 reasons for acquired hypogonadism

A

Infection - mumps
Aging - trauma
Chemotherapy
Radiation therapy

48
Q

Reasons for secondary hypogonadism (3)

A

Kallmann = congenital
Panhypopituiriasm = AI, Trauma, Infection
Hyperprolactin

49
Q

At what glucose level are you Tired/Thirsty/Dry vs.

Shaky/Sweaty/Wet

A

T/T/D = over 200

SS//W = less than 60

ENDO (3 decks)

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