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IPAP > Endo Block 2 > Flashcards

Endo Block 2 Flashcards

1
Q

What is the most convenient population level measure of overweight and obesity currently available?

BMIs of what percentage are categorized as overweight, Class 1-3?

A

BMI- kg/m^2

Normal: 18.5-24.9
Over: 25-29.9
Class 1: 30-34.9
Class 2: 35-39.9
Class 3: Greater than 40
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2
Q

What are four cons of using BMI as a measurement tool?

Upper body obesity that is located ? and ? is more significant than lower body obesity of fat located ? or ?

A

Mis-classifies 25% of PTs
No account for fat location
Not accurate for sedentary/body builders
Not distinguished between fat/lean mass

Abdomen/flank
Thigh/buttocks

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3
Q

Fat that is located ? is more hazardous to health and is composed of ? fat

Females must have a minimum body fat of -% to have a regular menstruation?

A

Abdominal fat
Visceral

13-17%

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4
Q

Upper body obesity and abdominal fat is associated w/ abnormal adipose lipolysis leading to ? and higher incidences of ? complications

What is the number one cause of high output heart failure?

What is the number one public health concern linked to increasing levels of obesity?

A

Insulin resistance
Metabolic

Obesity

DM

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5
Q

Men must have _% body fat

What is the name of an environment that can increase the chance of a PT becoming obese?

A

3%

Obesigenic

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6
Q

What are the 5 parts of the motivational interview?

What is the most common genetic cause of obesity?

What is an independent predictor of metabolic abnormalities associated w/ obesity over and above the effects of exercise?

A 
Nutrition intervention
Physical activity
Behavior therapy
Pharmacotherapy
Bariatric surgery

Prader-Willi Syndrome- demonstrates hyperphagia (compulsive overeating over long periods of time)

Sedentary activities

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7
Q

If an adopted PT is concerned about weight gain, how can this be predicted?

What are the typical features of Prader-Willi Syndrome?

A

Biological parents weight

Hypotonia
Almond shaped eyes
Narrow bifrontal diameter
Thin upper lip

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8
Q

What is done during PE for an obesity work up?

What diabetic drugs can cause weight gain?

A

BMI, degree/distribution of body fat, nutritional status, signs of secondary cause

Insulin
Sulfonyureas
Thizolidinediones

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9
Q

How much weight loss can be expected with conventional diet techniques?

What is the more important part of obesity management?

A

20% lose 20lbs and maintain for 2yrs
5% maintain a 40lbs loss
Avg= 7% loss from baseline

PT-Provider contact

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10
Q

Trimble’s obesity management plan and associated goals?

Define Very Low Calorie Diet

A

Diet/Exercise= greatest loss
Only diet= moderate loss
Only exercise= small loss
No Tx= no loss

800-1000cal/day x 4-6mon w/ average loss of 15%
Significant weight gain after 18mon

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11
Q

What are six classes of drugs that are known to cause weight gain?

What class of medication can be considered for these PTs that have underlying psych issues?

A 
Psych/Neurological
Steroid hormones
Anti-diabetes (Insulin, Sulfonylureas, Thiazolidinediones)
Anti-histamines
Anti-HTN
Anti-retroviral therapy

SSRIs

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12
Q

How much exercise is recommended per week by the College of Sports Med?

How much moderate exercise is recommended per day?

A

150min moderate
75min vigorous
Equivalent mod/vigorous combo
Weights 2x/wk

1hr

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13
Q

When are meds added to obesity management?

What GI agent is used for management and how does it exert it’s effect in PTs?

A

BMI >30
BMI >27 w/ obesity related RFs: HTN, DM2, CVD

Orlistat- Inhibits intestinal lipase/fat absorption
S/e- oily stool/diarrhea, incontinence

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14
Q

What CNS stimulant/anorexants are used for obesity management and how does it do it?

A

Lorcaserin- SSRA, promotes satiety for moderate weight loss >5%
S/e= HA, breast tumors

Phentermine- inc NorEpi/dopamine uptake suppressing appetite x 3mon

Phen/Topiramte- migraine prophylaxis, weight loss effect. C/i- hypothyroid, glaucoma
D/c if no loss in 4wks

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15
Q

What antidepressant/opioid agonist is used for obesity management?

A

Bupropion/Naltrexone- regulates dopamine reward system, cravings and overeating behaviors
S/e- GI upset
Caution in Psych Hx
C/i- HTN, opioid use, seizure, eating d/o

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16
Q

What GLP-1 agonist can be used for obesity management

A

Liraglutide- DM management med, increases insulin secretion, decreases inappropriate glucagon and slows gastric emptying
S/e- tachy, HA, hypoglycemia, nausea
C/i- medullary thyroid CA, MEN2a

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17
Q

What are the general contraindications for using weight loss meds?

A 
Uncontrolled CAD
Pregnancy/feeding
Hx of psych dz
<18y/o
Certain med use- MAOIs
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18
Q

When is bariatric surgery a consideration for obesity management?

What is the name of the gastric bypass procedure?

A

> 40% BMI or >35 w/ co-morbidities

Roux-en-Y gastric bypass
Restrictive/malabsorptive surgery, distal stomach resected. Remaining pouch is anastomosed to retro-colic segment of jejunum leaving gastric capacity at 30-50mL
Dec food intake/absorption of ingested food

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19
Q

What is the name of the Lap Band procedure?

Define Sleeve Gastronomy

A

Vertical banded gastroplasty
Prosthetic band dec size of gastric outlet
Multiple f/u visits for adjustment

Creation of sleeve over bougie, removing portion of greater curvature
Dec ghrelin levels x 1yr
Restricts food intake

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20
Q

Define Dumping Syndrome

What does Hirsutism mean?

A

Bariatric surgery complication when PT has to defecate nearly immediately after eating

Latin- shaggy, hairy
Excessive terminal hair growth that appears in women in a male pattern

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21
Q

Androgens act on sex-hormone responsive hair follicles causing a transition from ? to ?

Half of women with Hirsutism will have ?

A

Vellus into terminal

Hyperandrogenism

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22
Q

What will be seen in women with hirsutism that have increased follicle sensitivity to normal levels of androgens?

What is the Hirsutism is pathological?

How is Hirsutism scored?

A

Normal labs- genetics

Elevated circulating androgens, will have elevated labs

Ferriman-Gallwey score
Norm: <8
Max: 36

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23
Q

Where does DHEA S come from?

Where does Androstenedione released from?

Where is testosterone ( the most potent) secreted from?

A

Adrenal gland

Ovary and adrenal gland

Ovary/adrenal gland

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24
Q

What is the most potent androgen in females?

65% is bound to ? protein
33% is bound to ? protein

A

Testosterone

Sex hormone binding globulin
Albumin

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25
Q

How and where is free testosterone converted into dihydrotestosterone?

Why is this conversion important?

A

In the skin by 5a-reductase

5-DHT stimulates androgen dependent hair follicles

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26
Q

What are the 5 etiologies of hirsutism?

Which etiology is most common in middle eastern and Mediterranean groups?

A 
Idiopathic/familial
PCOS
Steroidogenic enzyme defect
Neoplastic d/o
Rare/pharmacologic

Idiopathic/Familial

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27
Q

What lab results would be seen in Med/Middle eastern females w/ Hirsutism?

What is believed to be that cause of this?

A

Normal androgen levels
Onset at puberty
Regular menses, PE

Higher 5a-reductase activity

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28
Q

What is beleived to be the most common cause of Hirsutism in females?

How is this acquired?

A

PCOS- function d/o of ovaries

Functional d/o of ovaries
Familial passsage of autosomal dominant trait

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29
Q

50% of Hirsutism PTs have elevated levels of ?

What criteria is used to Dx Hirsutism?

A

Testosterone

Rotterdam Criteria
1- extra androgen (hirsutism, acne, androgenic alopecia)
2- ovarian dysfunction/polycystic morphology (oligo/amenorrhea, infertility)
3- Absence of other causes of excess testosterone (pregnancy, thyroid, neoplasm)

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30
Q

What are the S/Sxs associated with the 3 parts of Rotterdam criteria?

A

Androgen excess/Elevated testosterone- Hirsutism, Acne, Androgenic alopecia

Ovarian dysfunction- Oligo/Amenorrhea w/ anovulation, infertility

Absence of other causes of testosterone- pregnancy, thyroid dysfunction, neoplasm, Cushings, Hyperprolactinemia

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31
Q

What are two unique facts about a PCOS Dx?

How is PCOS Tx?

A

30% of PCOS women doen’t have cystic ovaries
30% of normal menstruating women do have cystic ovaries

Restore cycles/fertility
Reduce Sxs- hair, oil, weight

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32
Q

Congenital adrenal hyperplasia is a defected level of ? enzyme?

What are the two types?

A

21-hydroxylase

Classic- complete deficiency; ambiguous genitals, virilized when treated w/ CCS

Non-classic: partial deficiency; PCOS and adrenal adenomas are more likely to develop
Irregular menses, gradual onset of hirsutism

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33
Q

What neoplastic d/os can cause Hirsutism?

A

Ovarian tumors
Adrenal carcinoma
Pure androgen secreting adrenal tumor

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34
Q

What are the 4 features of neoplastic d/o hirsutism?

What is the next step for this PT?

A

Onset out of peri-menarchal period
Rapid/severe hair progression
Recent menstrual irregularity
Signs of virilization (deep voice, inc muscles)

Measure androgen levels

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35
Q

What are the rare causes of hirsutism?

What medications can cause hirsutism?

A

Acromegaly
Cushings

Minoxidil- Tx of androgenic alopecia (frontal balding)
Cyclosporine- imm suppressant
Phenytoin- anti-seizure
Anabolic steroids
Progestins in OCPs (Norethindrone)
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36
Q

Key S/Sxs of Hirsutism

A 
Inc hair
Inc sebaceious activity
Menstrual irregularities
Anovulation
Amenorrhea
Defeminization
Virilization
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37
Q

What lab is the most useful test for evaluating Hirsutism?

A

Serum androgen to find adreanl/ovarian neoplasm

Free testosterone- most important
Androstenedione
DHEA-S

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38
Q

If female PT has testosterone levels >200ng/dl what is the next step?

What if these tests are negative?

A

Pelvic exam and US

Bilateral CT of adrenal glands

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39
Q

What are the second and third labs evaluated during hirsutism?

A

Serum androstenedione- >1000 suggests ovarian/adrenal neoplasm. Do pelvic US and bilateral CT adrenal scan

Serum DHEA-S- >700mcg= adrenal source
Order bilateral adrenal CT scan

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40
Q

What labs are ordered for a hirsutism work up?

What images are ordered for hirsutism after PE and labs?

A 
LH/FSH
17-hydroxyprogesterone
Fasting insulin/glucose
TSH/FT4/PRL
UA- cortisol
Lipids

Adrenal CT- elevated DHEAS, elevated testosterone after negative pelvic and US
Pelvic US- elevated testosterone/androstenedione
Pelvic MRI- visualized tumors of ovary

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41
Q

When are neoplastic origins of hirsutism treated?

A

Surgery

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42
Q

What are the non-surgical Tx options of hirsutism and are c/i in pregnancy?

A

Spirinolactone- K sparing w/ anti-androgenic action

Flutamide- non-steroid, non-selective anti-androgen

Finasteride- 5a-reductase inhibitor, only used in post-menopause females

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43
Q

What med can be added to spirinolactone to increase it’s efficacy?

What drug combo is more effective than spirinolactone?

A

OCPs
Metformin

OCPs and Flutamide

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44
Q

What are the new combined OCPs used to reduce hirsutism and acne?

What are the s/e of using these combos

A

Desogestrel
Drospirenone
Norgestimate

Inc DVT risk, use lower estrogen formulas

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45
Q

When/why is metformin used for hirsutism?

What is it’s use combined with?

A

PCOS to improve menses and promote weight loss

W/ Sironolactone

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46
Q

When/why is Simvastatin used for hirsutism?

When is Clomiphene used?

A

Reduces hirsutism and testosterone levels in PCOS, improved when sued w/ OCPs

Fertility aid in PCOS and infertility

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47
Q

What cosmetic therapies can be used for hirsutism?

What are the etiologies of gynecomastia?

A

Vaniqa cream- dec hair growth in 4-8wks

Physiologic
Endocrine Dz
Systemic Dz
Neoplasms
Meds- 59 total
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48
Q

What are the 4 physiological causes of gynecomastia?

A

Neonatal- transient and self resolving, due to high estrogen from pregnancy

Puberty- very tall/overweight boys, 60% of normal boys affected and self resolves in 1yr

Aging- seen w/ dec testosterone and weight gain, increased SHBG reduces free testosterone

Obesity- inc fat increases aromatse activity converting testosterone into estradiol (usually pseudo-gynecomastia)

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49
Q

What’s the difference between glandular and fatty gynecomastia?

What are the 5 etiologies of gynecomastia?

A

Glandular- tender
Fatty- non-tender

Physiologic
Endocrine dz
Neoplasm
Systemic Dz
Meds- 59 of them
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50
Q

What are the endocrine abnormalities that can cause gynecomastia?

What are the 3 systemic diseases that can cause gynecomastia?

A

Androgen insensitivity
Hypogonadism- Klinefelters
Hyperprolactinemia
Hyperthyroidism

Liver, renal dz
Spinal cord injury

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51
Q

What types of neoplasms can cause gynecomastia?

A

Steroid producing (estrogen)
hCG producing in lung, teste, hepatocellular, gastric carcinoma
Breast Ca- unilateral, irregular, painless, firm/fixed to underlying tissue

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52
Q

At a BioChem level, what causes gynecomastia?

Male breast cancer has a higher incidence rate in ? PT population?

A

Testosterone converted by aromatase into estradiol in adipose/extra-gonadal tissues

Klinefelters

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53
Q

What are 5 meds that can cause gynecomastia?

A

Spironolactone*- only common

Cimetidine

Ketoconazole

5a-reducatse inhibitors for BPH (Proscar, Avodart)

Exogenous steroid/androgen

HIV Tx w/ highly active antiretroviral therapy- especially Efacirenz or Didanosine

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54
Q

FSH stimulates ? process

LH stimulates ? process?

Gynecomastia presents as ? development while CA presents as ?

A

F- binds to Sertoli cells in seminiferous tubules to stimulate spermatogenesis

L- Leydig cells in testes to produce testosterone

G: concentric
C: ecentric, off to side

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55
Q

Gynecomastia is usually located ? when compared to where female breast cancer usually shows

How is gynecomastia Dx?

A

CA- supper lateral quad, gynecomastia- under nipple

Clinically

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56
Q

DDx of gynecomastia

A

Unilateral, Painless, Eccentric= Breast Ca, Lipoma, Neurofibroma

Bilateral, Painless= obesity, pseudogynecomasti

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57
Q

What labs are ordered for gynecomastia?

How is Klinefeltors Dx’d?

A

PRL, hCG, LH, testosterone, estradiol, TSH

Persistent gynecomastia w/out identifiable etiology

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58
Q

If a male has one of what 5 conditions, no work up is needed for gyneocmastia

A 
Hypogonadism
Liver Dz
Testicular tumor
Hyperthyroid
Medication Hx
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59
Q

Lab results for gynecomastia

A

PRL and b-hCG
High PRL= hyperprolactinemia, pituitary lesion
High b-hCG= malignancy in liver, lung, testis

Testosterone/LH
Low T, High LH= primary hypogonadism
Low T, low LH= secondary hypogonadism

Estradiol
Inc in testicular tumors, liver dz, obesity, inc levels of b=hCG

TSH/FT4
Hyperthyroid inc SHBG, dec free testosterone

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60
Q

What imaging is needed for gynecomastia PTs?

A

Mammography, CXR
US for suspicious mammogram findings

Needle biopsy w/ cytology for suspicious unilateral/asymmetric enlargement to distinguish tumor from mastitis

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61
Q

How is pubertal gynecomastia Tx?

A

Observe, f/u Q6mon
Self resolving in 1-2yrs

Painful/Persistant: SERM (Ramoxifen, Faloxifene) better for glandular type
Aromatase inhib (Anast/Letrozole)
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62
Q

How is hypogonadism related gynecomastia Tx?

This Tx can only occur after ?

A

Testosterone replacement, can worsen condition

Lab confirmed Dx

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63
Q

When is radiation therapy used for gynecomastia?

When is surgery used as a last resort?

A

Prostate CA + gynecomastia

Persistent and severe cases

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64
Q

Testosterone + aromatase= ?

Testosterone + 5a-reductase= ?

A

Estradiol- wolffian duct, brain, muscles, body hair, spermatogenesis, libido

5a-DHT- (masculine effects) External genitals,
Male body hair pattern
Temporal baldness

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65
Q

What are the three effects testosterone exerts?

Most important androgen in men is testosterone due to its impact on what non-endocrine organs?

A

1: Direct impact on androgen receptors
2: converted to estradiol/5a-DHT
3: non-endocrine organ impact

Muscle, adipose, bone, metabolism, brain function

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66
Q

Define Hypogonadism

What are the two types?

A

Deficient testosterone secretion from testes (low testosterone)

P: failure of testes to produce (hypergonadotropic hypo- high LH/FSH)
S: hypothalamus/pituitary failure to secrete gonadotropins
(hypogonad- low LH/FSH)

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67
Q

S/Sxs of hypogonadism

Hypogonadism can occur in what four time frames?

A

Low libido
ED, Fatigue, depression
Reduced endurance

Early prenatal
Late prenatal
Pre-puberty/puberty deficient
Post-puberty deficient

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68
Q

Define Early Prenatal Hypogonadism

Define Later Prenatal Hypogonadism

A

1st trimester T deficiency
Ambiguous genitalia
Pseudohermaphroditism- ovary or testi
True hermaphrodite: both

Deficiency of testosterone during 3rd trimester= micropenis, cryptochordism

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69
Q

Define Puberty Hypogonadism

Define Post-puberty hypogonadism

A

T deficiency at puberty
Dec strength/endurance
High voice/Dec hair
No sexual maturity or differentiation

Mid life lack of testosterone
Dec libido/energy/hair
Impotence/Wrinkles

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70
Q

Define Eunochoidal Proportions

What d/o is this normally seen in?

A

GH stims bones to grow out of proportion
Testosterone=closed plates
Arm span>height by +5cm
Crown-pubis

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71
Q

What 4 labs need to be drawn in the morning due to diurnal release?

What class drug is given to PTs w/ BPH?

A

GnRH, LH, FSH, Testosterone

5a-reductase inhibitor

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72
Q

How much of testosterone is bound and where is it bound to?

What part of life has a lower portion of free testosterone?

A

54-75% to SHBG
44% to albumin

Elderly, higher SHBG levels

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73
Q

What are the three main types of hypogonadism?

A

Primary- defect of testes (hypergonad hypogonad)
Low T, Inc LH/FSH

Secondary- defect of hypothalamus/pituitary
(hypo, hypo)
Low T, L or N LH/FSH (inappropriately normal)

Androgen defect/resistance
Inc T, Inc LH/FSH but effects of low T

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74
Q

What can cause Primary Hypogonadism?

A

Congenital: Klinefelter, Cryptochordism, Bilatearal anorchia

Acquired: age trauma infection(mumps/gonorrhea, leprosy) chemo/radiation

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75
Q

What is the most common congenital/chromosomal abnormality among males causing primary hypogonadism?

What are the comorbidities that come w/ this Dx?

A

Klinefelter 47XXY

Breast Ca
DM
CPDz
Osteoporosis
Varicose veins
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76
Q

What type of testicular development does Klinefelters cause and how is it Dx?

A

Firm, Fibrotic, Nontender, Small <2cm (N=>3.5)
High LH/FSH, low T
Keryotyping

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77
Q

How is Cryptorchidism Tx non-surgically?

If surgical Tx must be done for cryptorchidism, what age is it done at?

What are the associated risks w/ infertility?

A

hCG 1500mg x 3 days

Orchipexy @12-24mon

75% if bilateral
50% if unilateral

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78
Q

Define Vanishing Testicle Syndrome

A

Primary Hypogonadism. Bilateral Anorchia

Testes @ 14-16wks of gestation, empty scrotum
Normal growth/development until secondary sexual development fails to show at puberty

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79
Q

How is Bilateral Anorchia Dx?

How are all forms of Primary Hypognoadism Tx?

A

hCG stimulation test
+ test= no inc of testosterone
Crypto= inc of testosterone

Testosterone IM Q2-3wks
Testosterone patches
Topical application= most stable levels, transfer risk 
Buccal- Q12hrs
PO from not avail in US
Pellets- SQ administration
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80
Q

When does monitoring needs to be done for PTs taking testosterone?

What also needs to be checked every 6-12mon in these PTs?

A

Starting 14 days after initiation

Lipids, LFTs, CBC, PSA, DRE
Repeat Q6mon

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81
Q

What are the 5 s/e of testosterone replacement?

What are the c/i of using this therapy?

A 
Dec HDL
Acne
Gynecomastia
Liver abnormalities
Polycythemia

Prostate hyperplasia/CA
Boys <13y/o

82
Q

What are the four causes of Secondary Hypogonadism?

A

Congenital: Kallmann (most common cause of 2* Hypo)

Acquired: Panhypopituitary, Hyperprolactinemia

Other-meds age obesity illness ETOH drugs

83
Q

Define Kallmann Syndrome

What odd Sx do they present with?

A

X-linked inheritance causing isolated gonadotropin deficiency

GnRH cells near olfactory bulbs= anosmia

84
Q

How do PTs w/ Kallmann Syndrome present?

How are they Dx?

A

Prepubertal testes (small/rubber)
Eunuchoidal build
+/- gynecomastia
50% unilateral renal agenesis

Low T, Low/N LH/FSH

85
Q

What is the most common cause of hyperprolactinemia

What are the two major causes of “other” etiologies of Secondary Hypogonadism

A

Pituitary adenoma
Inhibits GnRh and T
Dec LH efficacy

Obesity
Poor health

86
Q

How is Secondary Hypogonadism Tx?

Defective androgen action/resistance only happens in ? PTs?

A

Weight loss
Underlying issue
Testosterone + other hormone for fertility

High T, FSH, LH in 46XY
Phenotype female
Genotype male

87
Q

How/why are PTs w/ 46XY Dx?

What PE finding is indicative of this Dx?

A

Amenorrhea

No uterus is palpable
blind pouch w/out uterus, cervix, Fallopian tubes

88
Q

How are PTs w/ CAIS Tx?

Where is 5-AR Deficiency frequency increased?

A

Remove testes
Estrogen Tx

Dominican republic
New Guinea
Turkey

89
Q

DHT is needed for neonatal target organ development during what point of development?

How doe these PTs present to clinic and on lab results?

A

8-12wks

Poorly developed prostate/external genitals
Appears female
Crytorchid tested
Normal T/FSH/LH

90
Q

Define Guevedoce

What other findings are seen with 5a-reductase deficiency?

A

Penis development at 12 from inc T due to alternate DHT production pathways

Masculinity
Adams apple
Deep voice

91
Q

A cells make ?
B cells make ?
D cells make ?
F cells make ?

A

Glucagon
Insulin
Somatostatin
Ghrelin

92
Q

Glucagon acts on ? to convert ?

Glucagon promotes ?

A

Hepatocytes- glycogen to glucose

Gluconeogenesis- formation of glucose from lactic acid and amino acids

93
Q

What is the most important regulator of glucagon and insulin levels?

DM is a syndrome of disordered ? and inappropriate ?

A

Blood glucose

Metabolism, Hyperglycemia

94
Q

Define DM Type 1

What is the greatest risk factor for DMT2 insulin resistance?

A 
Usual PT= kids
Autoimmune destruction of B-cells/Catabolic d/o
REQUIRES insulin
UnTx= Ketosis 
Not linked w/ FamHx

Visceral Obesity- adipocytes secrete adipokines, impair insulin signaling

95
Q

Define MODY

How does this get passed through generations?

A

Maturity Onset Diabetes of Young
Non insulin dependent DM
<25, non-obese PTs due to impaired glucose-induced secretion of insulin

Autosomal dominant

96
Q

What are secondary causes of hyperglycemia?

What does Diabetes, Insipidus, and Mellitus mean?

A

Insulin insensitivity: Tumors, Steroids, Liver dz
Red insulin secretion
Pheo, Pancreatitis, Drugs

D: excessive urine/siphon
I: tasteless
M: honeyed, sweet

97
Q

Metabolic Syndrome puts PTs at risk to develop ?

What waist size is dangerous for this development?

What organ system is first to start the decline towards metabolic syndrome?

A

DM2, CVD

> 40 / >35

Renal function: hyperuricemia

98
Q

3 of what 5 criteria are needed to Dx metabolic syndrome?

What Dx is given to these PTs?

A 
Ab obesity: >102/88cm
TG: >150
HDL: < 40/50
BP: +130/85
Fasting glucose: +110

Pre-Diabetic

99
Q

What are the characteristic S/Sxs of DM1

A 
Polyuria- osmotic diuresis
Polydipsia
Polyphagia
Blurry vision-  hyperosmolar fluids
Weight loss
PHOTN
Pareasthesia
DKA
100
Q

Since DM2 is ASx, what is a common initial complaint in women?

What derm issue is seen in DM2 PTs?

A

Vaginitis

Acanthosis Nigricans- hyperpigmented thickened skin on neck/groin/axilla

101
Q

What is the equivalent to DKA of DM2?

What is not a screening test for DM?

A

Hyperglycemic Hyperosmolar Coma

UA

102
Q

What are the two tests primarily used for DM?

What diabetic like issue is seen on UA of pregnant PTs?

A

Plasma glucose
HbA1c

Nondiabetic glycosuria

103
Q

What ketonuria levels require hospitalization?

How long does glycated HgB circulate in blood?

A

> 3.0mmol

120d
Reflects glycemia for up to 12wks previously

104
Q

How often is A1C measured in diabetics?

What can this measurement be used for?

A

Q3-4mon

Screening/Dx

105
Q

What are the normal plasma glucose levels?

What are normal, impaired and diabetic OGTT results?

What are normal, impaired and diabetic A1C levels?

A

Fasting: +126= DM
Fasting: 100-125= impaired
Random: +200 w/ Sxs= DM

N: <140
I: 140-199
D: >200

N: <5.7
I: 5.7-6.4
D: 6.5 or higher

106
Q

What steps can be done to prevent/delay development of DM2?

What is the next step for suspected DM but normal plasma glucose?

A

Dec weight 5-10%
Diet, Exercise, Drugs

OGTT

107
Q

What can cause a false high OGTT result?

A

Low RBC turnover:
Fe, B12, Folate deficient
Kidney/liver failure

Rapid RBC turn over:
Bleeding
Anemia
Transfusion
Hemolysis
Kidney/Liver Failure
108
Q

What is the first and descending complications to occur with an average A1C of 6.5% or higher?

What blood measurement is used for A1C scores if PT hs abnormal HgB or hemolytic states?

A

Retinopathy
Nephropathy
Neuroapthy/Microalbuminuria
Skin/membrane

Serum Fructosamine- nonenzymatic glycosylation of serum protein (albumin) from past 1-2wks

109
Q

What two measurements can be taken to differentiate between Dm1 and DM2

An abnormal lab should be confirmed on a different day using ? test?

A

Insulin
C-peptide: fragment of proinsulin, mirrors levels

Fasting glucose

110
Q

What are the levels of FPG, HbA1C, random and 2hr OGTT needed for Dx and won’t be on test

A

FPG: +126mg
HbA1c: +6.5%
Random: >200mg w/ Sxs
OGTT: >200mg

111
Q

What is the first step in diabetic management?

What Sxs are seen in DM w/ glucose levels >200 or <60

A

Self management, education and support

+200: Thirst, dry, tired
-60: Shaky, sweaty, weak
Don’t use UA for monitoring

112
Q

Medical Nutritional Therapy can decrease HgA1C by how much?

What is the most important part of DM Diet?

A
  1. 0-1.9% for DMT1
  2. 3-2% for DMT2

Healthy eating patterns, especially Mediterranean style pattern (high in/soluble fiber)

113
Q

Low glycemic index foods are _ or less

High glycemic index foods are _ or more

A

55 or less

70 or more

114
Q

What is the “magical pill” for health and diet?

This “magic pill” mimics what class of drug?

These two things can reduce the effects of ? DM Sx?

A

Protection from polyphenols- inhibits glucose absorption, oxidative stress and inflammation

A-glucosidase inhibitors

Neuropathy

115
Q

What is the first, last and anytime line of Tx of diabetes?

What are the next two steps?

A

Therapeutic lifestyle change

Weight loss
Exercise

116
Q

Since all DM PTs are ImmComp, what vaccines do they need?

What meds are considered in all PTs w/ DM?

A

Influenza
Penumococcal- at Dx and repeat at 65 if first dose was prior to 65y/o

Glycemic agents
ASA
Lipid lowering
ACE/ARB

117
Q

What is the JNC 8 B goal for PTs w/ DM?

GLP-1 RA meds are only used for ? type of DM?

This is the 1st line medication for all new cases of DM2

A

<140/90

Only DMT2

Metformin

118
Q

Glycemic control agents are used for DM, what are the classes and meds of each class?

A 
Biguinide: metformin
DPP4i: -gliptin
GLP-1RA:  tide
SGLT2i: -gliflozing
TZD: glitazone
AGI: -acarbose

SU/GLN: -glipizide/-glyburide

119
Q

What is the MOA of Metformin?

What are the advantages, disadvantages and c/i of using metformin?

A

Dec gluconeogenesis, inc hepatic insulin sensitivity

A: Lipids, no hypoglycemia, weight loss

D: lactic acidosis

C: CKD, alcoholics, CHF

120
Q

What two classes are included under “Incretin Therapy”?

Meds in this class end w/ ?

What is the DPP4/Metformin combo pill?

A

DPP4 inhibitors
GLP-1 agonists

-gliptin

Janumet

121
Q

What is the MOA of DPP4s?

What are the advantages, disadvantages and c/i of using DPP4 inhibitors?

A

Prevent degradation of incretins which stimulate insulin release, dec glucagon

Low hypoglycemia risk

Reactions, pancreatitis, URI

Renal impairment,

122
Q

What are GLP-1 agonists effect on hypoglycemia and weight?

When are GLP-1 agonists used in DM therapy?

A

Hypo: neutral
Weight: decrease

No solo use, added to Metformin or Sulfonylureas

123
Q

What is the MOA of GLP-1 agonists?

What are the advantages, disadvantages and c/i of using this drug?

A

Stimulate insulin release, reduce glucagon and slow GI emptying

Weight loss, addresses post-prandial glucose, weekly administration

GI, pancreatitis, medullary thyroid CA, injection

MEN2, medullary CA, gastroparesis

124
Q

What DM Tx med is also a formulation for obesity Tx?

What are SGLT-2 inhibitors effect on hypoglycemia and weight?

A

GLP1 agonist: Liraglutide

Hypo: neutral
W: loss

125
Q

What is the MOA of SGLT-2 inhibitors?

What is an FDA benefit of this med?

What are the advantages disadvantages and c/i of using SGLT-2 inhibitors?

A

ONLY med to work at level of kidney
Dec re-absorption, inc urinary excretion

Approved for reducing CV risk
Weight loss

Inc urination, reduced BP, UTIs

126
Q

What are TZDs effect on hypoglycemia and weight gain?

What are their MOA?

A

Hypo: neutral
Weight: GAIN

Sensitizes peripheral tissue to insulin

127
Q

What are the advantages, disadvantages and c/i of TZDs?

A

Improved lipids, slows DM progression

Inc risk of MI, edema, Osteoporoses, weight inc

NYHA 3,4
Liver Dz

128
Q

What is the effect of sulfonylurea on hypoglycemia and weight?

What is their MOA?

A

Severe hypo
Weight gain

Stims insulin release

129
Q

What are the 1st and 2nd generation sulfonyureas?

What are the advantages, disadvantages and c/i of using them?

A

1st: Tolbutamide
2nd: Glipizide- long acting

Longevity, cheap

Only PO med to cause Hypoglycemia (SFN>GLN)

Liver/renal dz

130
Q

What is the MOA of AGIs?

What are the advantages, disadvantages, c/i of using these?

A

Delay carb absorption

Weight neutral, address post-prandial glucose

GI

Intestine d/o, Cirrhosis

131
Q

What PT populations have an A1C goal of <6.5, <7, <7.5, <8 ad <8.5

A
  1. 5: pregnant adults if able w/out hypoglycemia/polypharm
    7: non-pregnant healthy adult
  2. 5: Older/healthy adult, children, adolescents
    8: Hx of severe hypoglycemia
  3. 5: Older adult, frail, limited life span
132
Q

What is the DM2 oral agent algorithm?

What DM med is started/used first for PTs w/ A1C >9 w/ Sxs?

A 
If HbA1C <9
Nutrition/exercise
Metformin x 3mon (D-Day)
3mon: D+3, Dual therapy
3mon D+6, Triple therapy
3mon: D+9, Insulin w/ PO agents (never more than 3 PO agents), except

Insulin + metformin

133
Q

Major s/e of Metformin, Pioglitazone, GLP-1, DPP4, SGLT2 classes?

A

Met: lactic acidosis

Pio: fluid retention, Fxs, bladder CA

GLP: N/V/pancreatitis

DPP4: pancreatitis (only moderate efficacy class)

SGLT2: UTI, GU fungal infxn, dehydration

134
Q

What are the two groups of insulin and what belongs in each?

A

Bolus-
Rapid: Lispro, Aspart, Glulisine
Short: Regular

Basal-
Intermediate: NPH
Long: Glargline, Detemir

135
Q

What type of insulin is used in the ER to Tx DKA?

DMT2 Pts need to stop taking ? med if insulin is added to their Tx routine?

A

Short acting- Regular, can be given IV

Sulfonylureas- only PO agent that causes hypoglycemia

136
Q

When adding insulin to DMT2 PTs, what type is usually added first?

Define Dawn Phenomenon and Somogyi Effect and how each one is Tx?

A

NPH/Long acting (Glargine, Detemir) at bed time

Dawn: inc 02-0300 glucose levels, inc bed time dose
Somogyi: low 02-0300 glucose levels, reduce bedtime insulin dose

Both result in morning hyperglycemia, 02-0300 check to differentiate

137
Q

Why do Dawn and Somogyi Phenomenons happen?

A

D: reduced tissue sensitivity to insulin that develops between 05-0600 due to GH

S: surge of Epi produces high glucose by 0700

138
Q

What DMT2 medication is used for DM and weight loss?

Hypoglycemia is the most common complication inf DM PTs being Tx w/ and feel Sxs when levels are below ?

A

GLP1 receptor agonists - add on therapy on to Metformin or Sulfonylurea

Insulin
<54mg

139
Q

What are the first 3 Sxs of hypoglycemia?

What class med can blunt these Sxs?

Neurological Sxs don’t show until blood glucose is below ?

A

Tachy, Palpitation, Termulousness

BBs

<50mg

140
Q

How can mild/mod hypoglycemia be Tx?

How is severe cases Tx?

A

15g of carbs

Glucagon kit- 1mg
Given to every PTs receiving insulin

141
Q

What is given in the ER for hypoglycemia?

Who is most likely to have DKA?

A

IV glucose 50ml
IM glucagon 1mg if glucose is unavailable

DMT1 w/ pump
DMT2 during trauma/sepsis

142
Q

How can early DKA be detected quickly in PTs w/ pumps?

What is the cut off indicator that PTs need to seek medical help while self-monitoring w/ DKA during sick day?

A

UA ketones

Test urine ketone Q2-4hrs
>250mg x >6hrs
4-6ox fluid Q30m

143
Q

How does DKA present?

A 
Polyuria/dipsia x 1-2 days
N/V/Fatigue
Hypothermia
Tachy w/ HOTN
pH <7.4 (6.9-7.2)
Hyper-K on lab, actually depleted in body
144
Q

How is DKA Tx?

What is one of the most serious shortcoming of DKA Tx?

What is the fluid of choice for Tx DKA?

What fluid is used if PT presents w/ hypernatremia (Na>150)

A

IV fluid, Insulin, K, BiCarb

Fluid deficit: 4-5L

  1. 9% NS: 1L over 1-2hrs
  2. 45% NS
145
Q

What can be induced if Tx w/ DKA fluid resuscitation is too aggressive?

During DKA Tx, when is fluid Tx switched?

A

> 5L in 8hrs= ARDS, Cerebral edema

<250mg= switch to 5% glucose solution

146
Q

Insulin replacement falls where in the DKA Tx algorith?

What is the f/u step to this sequence

A

After fluids IF K is >3/5meq

If K is <3.5, delay insulin until K is normal

147
Q

How much K is given to PTs during DKA Tx?

How does hyper/hypo-K show on EKG?

A

KCl 10-30meq during 2 or 3rd hr of Tx

Hyper= peaked T
Hypo: flat T, U wave

148
Q

When is NaBicarb used for DKA Tx?

What is the last step of consideration when Tx DKA?

A

pH <7.0
1-2 ampules added to 1L of 0.45% of saline

ABX- cholecystitis, polynephritis may be severe in these PTs

149
Q

What is the second most common form of hyperglycemic coma?

What PT population is it normally seen in?

A

HHS- hyperglycemia w/ no ketosis

Middle age/elder w/ DM2

150
Q

PTs suffering from HHS usually have what underlying systemic Dz or are taking ? meds?

Why is HHS more deadly than DKA?

A

CHF, CKD
Thiazides, Glucocorticoids

Slow onset w/ 10x higher glucose levels

151
Q

What will be seen on PE of PT w/ HHS?

What will be seen on labs?

A

Profound dehydration w/ no Kussmaul respirations

Hyperglycemia
Hyponatremia
Prerenal azotemia
NO ketosis or acidosis

152
Q

How is HHS Tx?

A

IV fluid, insulin, K
4-6L over 8-10hrs
Hypovolemia+oliguria= NS 0.9%
No hypovolemia= 0.45% NS

Once glucose is <250, start 5% dextrose, 0.45% or 0.9% NS

Insulin- only if glucose >250

KCl- added earlier than DKA Tx, not if CKD/oliguria is present

153
Q

What are the DMT1 complications?

What are the DMT2 complications

A

Renal Dz
Blindness
Neuropathy
Death from end stage renal dz

Renal dz
Blindness
Neuropathy
Macrovascular Dz= MI*/stroke

154
Q

What is the difference of the anion gap between HHS and DKA?

Chronic DM complications include what 5 systems?

A

HHS: Norm
DKA: High (>10)

Ocular
Nephropathy
Neuropathy
CV
Skin/membrane
155
Q

What are the two categories of diabetic retinopathy?

A

Nonrpoliferative “background”:
Microaneurysms
Exudates
Dot hemorrhage

Proliferative “malignant”
Cotton wool spots
Leading cause of blindness in US

156
Q

How is proliferative retinopathy Tx?

A

Photocoagulation
Bevacizumab- injection to stop growth of new vessels
HTN management
Tobacco cessation

157
Q

When do DMT1 or DMT2 get eye exams ? that coincide for testing for?

What are seen as kidney function begins to decline?

A

1: 5yrs after Dx then annually
2: at Dx, then annually
Microalbuminuria

Albuminuria to urea/creatinine accumulation in blood

158
Q

What is the TOC for diabetic nephropathy

What levels/how many positive tests are needed for Dx?

A

Morning spot urine for albumin/creatinine ratio, can’t be detected by urine dipstick

30-300mcg
2-3pos tests within 3-6mon before Dx

159
Q

How id DM microalbuminuria Tx?

How is progressive diabetic nephropathy Tx?

A

ACEI (even in T1 PT w/ normal BP)
ARBs
Low protein diet

Dialysis due to macro proteins in urine

160
Q

What is the most common form of diabetic peripheral neuropathy

What is “rocker bottom” foot deformity

A

Distal symmetric polyneuropathy (glove/stocking or Charcot) starting w/ the longest axons

Charcot arthropathy- joint subluxation, periarticular Fxs

161
Q

What type of diabetic neuropathy is reversible?

What nerves are most likely to be involved by this?

A

Isolated peripheral

Femoral and CNs (CN3 palsy)

162
Q

How is painful diabetic neuropathy Tx?

Autonomic neuroapthy in DM can effect what 4 things?

A

Amitriptyline- TCA
Duloxetine- SNRI
Gabapentin
Capsaicin cream

BP/P, GI tract, Bladder, ED

163
Q

What med can be used for DM w/ GI tract autonomic neuropathy induced gastroparesis

What can be used for diarrhea

A

Metoclopromide 30min before meals/bed, only for 3mon

Broad spectrum ABX Loperimide

164
Q

What can be used for ED from DM?

Half of PTs w/ DM will develop ? after 20yrs of the Dz

A

Sildenafil
Papaverine- intracavernous injection

Peripheral vascular dz:
Ischemia of LE
ED
Intestinal angina
Gangrene of feet
165
Q

What meds are given to DM w/ PVDz?

What are the lipid goals for these PTs?

A

ACE/ARB
ASA
Statin

LDL <100/<70 w/ CAD
HDL >40
TG <150

166
Q

DM get annual foot exams to check for ulcers IAW ? program

What three factors lead to diabetic foot problems?

A

LEAP: lower extremity amputation prevention w/ monofilament test, 10g pressure, 10 spots

Ischemia
Peripheral neuropathy
Secondary infection

167
Q

DMT2 can have increased risk of developing ? fungal infection?

What skin finding can be seen on shins/dorsal surface of foot?

When are DM PTs referred to Endocrinology?

A

Thrush

Necrobiosis Lipoidica Diabetricorum

Type 1: at Dx
Type 2: if difficulty w/ reaching goals

168
Q

What hand issue can be seen in DM w/ long standing diabetes?

What labs are drawn at each DM visit?

A

Dupuytrens contracture

Fasting CMP: 110-120
HbA1C: <7%
Microalbumin for DMT2 (at Dx and annually)
Lipid- annual
Ophthalmology- dx and annual
169
Q

What vaccines do DM PTs need?

Leading cause of death for type 1/2 DM?

A

Pneumovax
Influenza

1: Renal Dz
2: MI

170
Q

What is normal Ca level?

What organs are directly and indirectly responsible for Ca regulation?

A

Serum: 8.5-10.5mg
Ionized/Free: 4.6-5.3mg

Direct: parathyroid, kidney w/ Ca sensing receptors
Indirect: intestine

171
Q

What hormones regulate serum Ca?

What stimulates for the major one to inc/dec?

A

PTH, Vit D, Calcitonin

Stim: falling Ca/Mg level
Inhib: rising free Ca/Mg level

172
Q

What does PTH stimulate/inhibit

Where is calcitonin made and what does it do?

A

Resorption of bone to inc systemic Ca/Phosph

Opposite of PTH
Parafollicular cells in thyroid gland in response to elevated serum Ca level to Inhibits osteoclasts
Produced in

173
Q

When are calcitonin levels monitored?

What are the first and second most common causes of Hypercalcemia?

A

Thyroid Ca

High Ca, High PTH
Primary hyperparathyroidism (adenoma, hyperplasia, CA)

Norm Ca, High PTH: (familial hypocalciuric hypercalcemia)

High Ca, Low PTH:
Secondary malignancy, non parathyroid CA (milk alkali syndrome)
Can be from any type of CA

174
Q

What is the first step in investigating hypercalcemia?

What are the S/Sxs of hypercalcemia

A

What is the PTH doing?

Mild: ASx
Severe: >14mg, CA concern
Groans Moans Overtones Bones Stones

175
Q

What is the first part of Tx for parathyroid adenomas?

What monitoring steps are done for ASx PTs?

A

Hydration

F/u Q6mon: BP, SrCr
Yearly: Urine Ca, Kidney function
Bone density Q2yrs

176
Q

What Ortho Dx is indicative of Hypercalcemia?

What is a rare but serious cause of High Ca/High PTh?

How is MEN induced parathyroid hyperplasia Tx?

A

Osteitis Fibrosa Cystica

MEN 1, 2, 4

Subtotal parathyroidectomy, 3.5 glands removed

177
Q

What are the three types of hyperparathyroidism?

What lab results are seen in Parathyroid CA?

A

Benign parathyroid adenoma
Parathyroid hyperplasia
Parathyroid CA

Sever hyperCa, Very high PTH corrected w/ surgery

178
Q

What lab results are seen in Familial Hypocalciuric Hypercalcemia?

How is it Tx?

A

Defective Ca receptors in parathyroid leading to:
Normal PTH
Permanent HyperCa, HypoCalciruia

None avail, autosomal dominant d/o

179
Q

How do you tell between parathyroid cancer and small lung cell cancer?

What protein will increase in PTs w/ parathyroid malignancy?

What will be seen on labs?

A

High PTH= parathyroid
Low PTH= SCLCa

PTHrP

Severe HyperCa
Low PTH
High PTHrP

180
Q

What types of CA can cause PTHrP increases?

Define Milk Alkali Syndrome

A

Squamous CA of lung, esophagus, head/neck
Renal, Bladder, Ovarian, Breast CA

Triad of HyperCa, Metabolic alkalosis, Acute kidney injury

181
Q

What vitamin increase can suppress PTH?

Where can this increase be causes by if it wasn’t ingested?

A

Vit D

Lymphoma
Granulomatous Dz: Sarcoidosis, TB, Histoplasmosis, Coccidiomycosis
Thyrotoxicosis
Immobilization- ICU PT, Dx of exclusion

182
Q

How is hypercalcemia managed?

A 
Hydration/Activity
Furosemide- + calciuresis
No thiazides, Vit A/D, Antacids
Avoid Vit A/D
Dialysis if renal failure
183
Q

When are Bisphosphonates used for hypercalcemia?

What is the MOA in Tx?

A

Hyperparathyroidism, Malignancy,
Immobilization
Surgery Pre-Op-

Inhibits osteoclast reabsoprtion of Ca

184
Q

What is the TOC in malignancy associated hypercalcemia

What Tx is added for post-menopause PTs?

A

IV Bisphosphonates

Estrogen

185
Q

What is the most common cause of hypocalcemia?

Elderly hospitalized PTs w/ hypocalcemia, variant PTH levels are likely to be deficient in ?

A

CKD

Vit D

186
Q

Hypoalbuminemia is a common cause of low ?

If this is due to hypoalbuminemia, it’s not clinically significant if ?

A

Total serum Ca

Ionized Ca is normal

187
Q

If albumin is low, check ? or calculate the correct one

What can cause HypoCa w/ High PTH

What causes HypoCa w/ low PTH

A

Ca

Pseudohypoparathyroid (PTH resistance)
Vit D deficient/resistance

Hypoparathyroidism (PTH deficiency)

188
Q

What are the S/Sxs of HypoCa

A 
CATS go numb
Convulsion
Arrhythmia
Tetany
Seizure
Numb/parasthesia in hands, feet, mouth

Chvetskys
Trousseaus

189
Q

What are the lab results in true HypoCa

What all is checked?

A

Serum Ca <8.5
Ionized serum Ca <4.6

Mg, PTH, Vit D

190
Q

What is happening in the body during HypoCa w/ inc PTH?

What bone changes are seen due to inc PTH?

A

Defected renal PTH receptors
Inc Ca excreted in urine

Cystic lesions
Pathologic Fxs
Demineralization

191
Q

Define Albrights Hereditary Osteodystrophy

What can cause Vit D induced HypoCa, Inc PTH

A 
HypoCa, Inc PTH
PTH resistance (pseudohypoparathyroid)
Short, round face, short 4th/5th metacarpals

Defective supply
Malabsorption: Sprue, Crohns
Meds: Rifampin INH Phenytoin
Rickets

192
Q

Define Osteomalacia

How do PTs present and what X-ray finding is seen?

A

Adult Vit D deficiency

Bone pain
Radiolucent lines perpendicular to cortex- Loosers Lines
Pseudo Fxs- pathognomonic for Rickets/Osteomalacia

193
Q

How is ASx Hypocalcemia from any origin Tx?

Define Hypoparathyroid Tetany

A

PO supplements, Vit D, Sunlight

Acute Hypocalcemia
Medical emergency- dec PTH circulating causes dec Ca level

194
Q

How is Hypoparathyroid Tetany Tx on inpatient status?

What maintenance Tx are they placed on after emergent Tx?

A

Airway
Tx HypoMg first w/ Mg Sulfate
Tx low Ca w/ Ca Gluconate

1-3g PO Ca/Vit D w/ meals per day

195
Q

How often are post-Acute Hypocalcemia Tetany PTs monitored?

What is given it PT presents w/ hypercalciuria

A

Q3mon for Ca levels w/ Spot urine Ca

HCTZ- keeps Ca in blood

196
Q

Define Osteitis Deformans

What happens in this Dz?

A

Paget’s Dz
Autosomal dominant Dz

Bone lysis replaced by vascular fibrous CT tissue leading to bone formation that’s more likely to Fx

197
Q

What is the first Sx of Paget’s Dz?

Why do these PTs go deaf?

A

Pain, constant and worse at night, not relieved w/ rest
Inc warmth over bones
Leads to HOutput HF

Middle/inner ear cavities lay w/in petrous portion of temporal bone

198
Q

What is the name of Fx that occurs in Paget’s PTs?

What will be seen on labs?

A

Chalk stick

Inc alkaline phosphatase (ALP)
Normal Ca, Phosph, PTH
Inc Ca if PT is immobile

199
Q

What would a bone scan of Paget’s show?

What x-ray finding can be seen?

A

Inc uptake in skull, spine and long bones

Pic frame vertebrae

200
Q

How is ASx Paget’s Tx?

What is the DOC for Sx Tx?

A

Annual ALP checks/x-rays

Bisphosphantes- IV Zoledronate

201
Q

Vit D is controlled by ?

A

Intestines

IPAP (212 decks)

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