ENDO #2 Flashcards

(49 cards)

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
Management guidelines
1st = DM Ed. Class TLC - diet etc. Pharm mgmt
26
MOA of Metformin / SGLT2’s / DPP4 / GLP1s
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
When to start insulin
T1 DM identified | Or DKA / HHS episode
28
Dawn vs Somogyi
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
Acute complications of hypoglycemia
``` Lower than 60 Behavioral changes Impaired glucagon response Sympathetic adrenal blunting CKD/ GASTROPARESIS ```
30
Diff between DKA and HSS
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
Good treatment for DKA and HSS
``` 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
Mgmt of chornic complications for micro and vascualr complications
Best TXM = glycemic control / tobacco cessation / HTN mgmt Vision screen —> ophthalmology 5 years after T1 Dx Initial @ Dx then Annual —> T2
33
Other meds to prescribe in a patient with diabetes
Consider HTN (ACEI/ARBs) ``` Diabetic neuropathy (Gabapentin/ Nortriptyline/ Capsaicin cream) Peripheral neuropathy = amitriptyline Nephropathy= dialysis GASTROPARESIS = metoclopramide Skin = steroids ```
34
Mechanism of ca metabolism PTH Vit D Calcitonin
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
What organs and how do organs regulate calcium
Kidneys = releases Vit D ; renal tubular reapportion of phosphates by PTH Bones Skin
36
Hyper calcemia presentation (GMOBS)
``` Groans - Met Acidosis ; kidney stones Moans - Myalgia / muscle weak Overton’s - depression / anxiety Bones - bone pain / fx / Stones - kidney stones ```
37
Hypo calcemia presentation
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
Causes of hyper v hypo Ca
Hyperparathyroid = PTH elevated or suppressed Squamous cell cancer of the lungs = PTHrP Immobilized Diet Hypo CKD Alcoholism Diuretics
39
Can HCTZ be used with hyper or hypo CA
Hypocalcemia can be used as txm
40
High vs low PTH
41
3 etiologies involved in hyper ca+
Suppressed PTH Normal minimal PTH Elevated PTH
42
DEXA scan points
Greater than -1 = NML -1 - -2.5 = OSTEOPENIA Less than -2.5 = OSTEOPOROSIS
43
3 etiologies of Hypocalcemia
Increased loss Elevated PTH Suppressed PTH
44
What is the most common cause of Hypocalcemia
CKD
45
What is the most common cause of hypocalcemia with an elevated PTH
Vit D Deficiency
46
3 main types of primary hypergonadism
Congenital - Klinefelters 47XXY Cryptorchidism/Bilateral anorchia Seminiferous tubules dysgenesis
47
4 reasons for acquired hypogonadism
Infection - mumps Aging - trauma Chemotherapy Radiation therapy
48
Reasons for secondary hypogonadism (3)
Kallmann = congenital Panhypopituiriasm = AI, Trauma, Infection Hyperprolactin
49
At what glucose level are you Tired/Thirsty/Dry vs. | Shaky/Sweaty/Wet
T/T/D = over 200 SS//W = less than 60