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Heme/Onc/Endo > Endocrinology Exam 2 Cards > Flashcards

Endocrinology Exam 2 Cards Flashcards

1
Q

Role of FSH

A

Stimulates Sertoli cells to regulate spermatogenesis and produce inhibin B to cause negative feedback

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2
Q

Role of LH

A

Stimulates testosterone synthesis in the Leydig cells of the testes, testosterone give negative feedback and encourages spermatogenesis

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3
Q

2 things that testosterone can be converted into

A

DHT dihydrotestosterone) and Estradiol

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4
Q

2 proteins that bind systemic testosterone

A

Sex-hormone binding globulin
Hepatic metabolism, Renal excretion

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5
Q

Adrenarche

A

At 6-8 years of age - the zona reticularis produces greater amounts of androgens

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6
Q

Gonadarche

A

Around age 9 - activation of the HPG axis occurs allowing for the production of GnRH, LH, FSH, and Testosterone

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7
Q

Tanner stages

A

5 stages of male sexual characteristic development
Begins with testicular growth and sparse pubic hair, followed by phallic growth (length then width) and thicker pubic hair as the testes continue to grow

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8
Q

Measuring tool for testicular size

A

Prader orchidometer

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9
Q

Prepubertal
Pubertal
and
Adult
Testicular sizes

A

Prepubertal - 1-3mL
Pubertal - 4-12 mL
Adult - 12-25 mL

Greater than 2.5 cm long = Puberty

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10
Q

Precocious male puberty

A

Evidence of puberty in boys under the age of 9

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11
Q

Isosexual precocious puberty

A

Premature development of APPROPRIATE characteristics

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12
Q

Heterosexual precocious puberty

A

Development of secondary sexual characteristics of the opposite sex

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13
Q

Precocious puberty that results from premature release of GnRH

A

Gonadotropin dependent or central precocious puberty

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14
Q

Precocious puberty that results from increased secretion of androgens from the testes of adrenal cortex

A

Gonadotropin independent or peripheral precocious puberty

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15
Q

Cause of central precocious puberty

A

Often a CNS lesion or idiopathic - need to do a neurologic workup

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16
Q

3 things that may cause peripheral precocious puberty

A

hCG secreting tumor
Adrenal androgen secreting tumor
Congenital Adrenal hyperplasia

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17
Q

2 enzymes usually deficient in CAH

A

21 hydroxylase and 11beta hydroxylase

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18
Q

McCune-Albright syndrome

A

Acquired mutation of the Gsalpha subunit resulting in steroidogenesis
More common in females

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19
Q

McCune-Albright syndrome triad

A

Bone dysplasia
Cafe-au-lait skin pigmentation
Precocious puberty

Can be associated with stimulation of other endocrine systems

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20
Q

Familial male limited precocious puberty

A

Autosomal dominant disorder caused by LH receptor mutations

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21
Q

Non-biologic source of peripheral precocious puberty

A

Exposure to exogenous androgens such as testosterone creams, etc.

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22
Q

5 historical things to know for a precocious puberty patient

A

Onset, Progression, Associated symptoms (Neuro), Exposures, When family members went through puberty

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23
Q

Physical exam difference between central and peripheral precocious puberty

A

Central - Enlarged testicles
Peripheral - Testicles remain small

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24
Q

Testicular tumor presentation

A

Asymmetrical enlargement

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25
Q

Bone age assesment for precocious male puberty

A

X-ray of the left wrist and hand

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26
Q

Assesment of bone age X-ray and other measurements of PP

A

Compare data over six months rapid growth indicates a central or peripheral problem, slow growth is often more benign

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27
Q

Initial lab tests for precocious puberty (3)

A

Serum testosterone
LH and FSH (elevated in central, low in peripheral)

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28
Q

Lab to detect and hCG tumor

A

Serum hCG

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29
Q

2 Labs to detect CAH

A

DHEA (also could be adrenal tumor) and 17a-hydroxyprogesterone

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30
Q

Lab test that distinguishes CPP from peripheral

A

GnRH stimulation test

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31
Q

GnRH stimulation test interpretation

A

LH rise = CPP
No LH rise = Peripheral

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32
Q

3 places an hCG secreting tumor might be located with imaging modalities for each

A

Brain (MRI), Abdomen (CT), Testicles (US)

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33
Q

Central precocious puberty management

A

Refer tumor to neurosurgery
Use long acting GnRH agonists

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34
Q

How do long acting GnRH agonists help with central precocious puberty

A

GnRH agonists lead to desensitization of receptors and lower secretion of LH and FSH

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35
Q

2 GnRH agonist options

A

Histrelin acetate SQ implant
Leuprolide IM 1,3, or 6 month formulations

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36
Q

Treatment for peripheral precocious puberty

A

Depends on source:
Surgery for tumors. Androgen suppression for CAH
Goal is to halt sexual development and premature epiphyseal plate closure

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37
Q

Steroid synthesis inhibitor for precocious male puberty

A

Ketoconazole at high dosing - can be hepatotoxic

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38
Q

Delayed male puberty

A

Lack of testicular enlargement by 14 or incomplete genital growth with five years of initial puberty onset

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39
Q

Primary hypogonadism

A

Gonads fail, leading to a hypergonadotrpic state

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40
Q

Secondary hypogonadism cause

A

Often a constitutional delay of puberty can also be dues to illness or genetics

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41
Q

History factors that point to hypogonadism/delayed puberty

A

Failure to grow
Nutrition
Congenital abnormalities
Neurologic symptoms
Family history

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42
Q

Physical exam findings of hypogonadism

A

Arm span exceeding height by 5cm
Small testicular size (1-3 mL is prepubescent)
Low tanner stage

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43
Q

Finding that suggests CDGP as reason for puberty delay

A

Bone is younger than chronological age and growth pattern is normal

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44
Q

LH/FSH levels in primary and secondary hypogonadism

A

elevated in primary
decreased in secondary

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45
Q

Cryptorchidism

A

Testicles have not descended to the scrotum by 12 months of age - increases cancer risk

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46
Q

Management of constitutional delay of growth and puberty

A

Reassure patient, consider testosterone in patients whos self esteem is impacted

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47
Q

Testosterone replacement therapy for primary and secondary hypogonadism

A

Indefinite therapy for primary
Interrupt after 6 months for secondary to determine whether LH and FSH have been stimulated

Adding an aromatase inhibitor might allow for greater adult height

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48
Q

Effect of hypogonadism onset in the beginning of male fetal development

A

Ambiguous genitalia

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49
Q

Effect of hypogonadism in third trimester of fetal development

A

Cryptorchidism and micropenis

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50
Q

Clinical presentation of hypogonadism after puberty

A

Decreased energy
Loss of libido and morning erections
Loss of body hair
Increased fat mass

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51
Q

3 goals of a clinical evaluation of hypogonadism

A

Determine if it was before/after puberty
Determine state of genitalia
Determine if primary or secondary

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52
Q

Testosterone therapy indications

A

Lack of puberty onset by age 14
Primary testicular failure
Testosterone levels under 150 ng/mL

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53
Q

Andropause

A

Decrease in testosterone production between 4th and 6th decades of life
More common in those who are obese or have chronic illness

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54
Q

Testosterone therapy and screening for adult males recommendations

A

Routine screening not recommended

Replacement therapy indicated if 3 symptoms are present and testosterone is under 200ng/dL

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55
Q

5 symtpoms of low testosterone/hypogonadism

A

Poor morning erection, Depression, Fat gain, fatigue, low libido

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56
Q

Diurnal variation of testosterone

A

Highest at 8AM lowest at 8PM
Take a fasting specimen at 8-10 am

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57
Q

Next step after a low testosterone lab

A

Take a confirmatory sample

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58
Q

Lifespan testosterone levels

A

75-400 for first six months
Peaks in puberty at areound 1200
240-950 thereafter
Steady decline with age

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59
Q

When might you want to obtain a sex hormone binding globulin assay (2)

A

Suspected comorbid abnormality in testosterone binding

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60
Q

Indication to check LH/FSH levels

A

When further evaluation of testosterone levels is needed

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61
Q

Side effect of decreased sex hormone binding globulin

A

Increased estrogen

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62
Q

Indication for and meaning of inhibin B assay

A

Tests for damage to the sertoli cells
Decreased when there is damage

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63
Q

1 thing that can increase and 1 thing that can decrease Sex Hormone Binding Globulin

A

Age increases
Obestity decreases

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64
Q

3 hormones bound by sex hormone binding globulin

A

Testosterone
DHT
Estradiol

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65
Q

Semen analysis

A

Used for infertility, a normal sample excludes gonadal dysfunction
3 samples over 2-3 months

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66
Q

Use of a testicular biopsy

A

Distinguish between spermatogenic failure and ductal obstruction

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67
Q

True gynecomastia

A

Growth of glandular breast tissue (Not just fat) that is greater than 4cm in diameter and tender

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68
Q

3 normal places to see gynecomastia

A

New borns (from their mom)
Puberty
Aging with increased fat

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69
Q

4 things that can cause pathologic gynecomastia

A

hCG secreting tumors, Liver disease, Malnutrition, Hyperthyroidism

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70
Q

Historical findings for gynecomastia

A

Pain/Tenderness, Nipple sensitivity, Careful drug history

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71
Q

How will a breast malignancy feel

A

Unilateral, nontender, offset from the areola

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72
Q

Where will glandular tissue in gynecomastia be located

A

Symetric distribution below the areola

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73
Q

Causes of gynecomastia to assess for

A

Pubertal, Drug induced, Androgen deficiency, Tumor, Aromatization

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74
Q

Indications for testosterone replacement

A

Low testosterone and features of androgen deficiency - NOT helpful for infertility

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75
Q

Schedule of testosterone

A

Schedule III

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76
Q

Testosterone administration

A

IM followed by bimonthly regimen resulting in peaks and throughs
Injectable - long lasting - undecanoate
Gel - needs to be applied in an area that will not be touched (back?)

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77
Q

Testosterone therapy management

A

Monitor levels every 3-6 months

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78
Q

3 other things to check in testosterone management

A

Hematocrit
Bone mineral density
PSA, for men over 40

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79
Q

Testosterone contraindications (2)

A

CANCER - esp. prostate
CHF

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80
Q

Cholesterol

A

essential element of all animal cell membranes, precursor to steroid hormones and bile acids

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81
Q

Apolipoproteins

A

Protein required for the structure, function and metabolism of lipoproteins
KEY for lipids to move in and out of cells

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82
Q

Function of lipoproteins

A

Transport cholesterol, tryglycerides

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83
Q

Progression of lipoproteins

A

Become denser as deposit tryglycerides into the peripheral tissues
VLDL to IDL to LDL

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84
Q

Lipoprotein composition

A

Core of triglycerides and hydrophobic lipids
Shell of hydrophillic lipids and apolipoproteins

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85
Q

What changes as lipoproteins get denser

A

Less lipids, more apoprotein

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86
Q

Exogenous lipid pathway

A

Absorption of dietary lipids and formation of chylomicrons

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87
Q

Endogenous lipid pathway

A

Secretion of VLDL in the livier and its transformation to IDL and LDL

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88
Q

Transport of exogenous/dietary lipids

A

Broken down to chylomicrons in the GI tract
Absorbed and used via ApoCs
Broken down by LPL
Remnants travel to the liver to be taken up by LDL

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89
Q

Transport of hepatic or exogenous lipids

A

VLDL is derived in the liver and acquires ApoE and apoC from HDL
VLDLs are borken down by LPL for use

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90
Q

What happens to IDL that is formed from LDL after LPL activity

A

Taken up by the liver and systemically reduced to LDL. LDL May be removed from circulation for use in the bile

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91
Q

Synthesis of HDL

A

Reverse cholesterol transport, synthesized in the liver and intestines and recruits cholesterol

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92
Q

Role of HDL

A

Sweeps cholesterol out of circulation

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93
Q

Dyslipidemia

A

Disorder that results in increased plasma cholesterol and triglycerides along with low HDL - Often genetic

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94
Q

4 pathways to dyslipidemia

A

Excess hepatic secretion of VLDL
Impaired lipolysis of triglyceride rich proteins
Impaired hepatic uptake of ApoB contining lipoproteins
Inherited low levels of HDL-C

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95
Q

How does impaired lipolysis of triglyceride rich lipoproteins occur

A

Dysfunction of LPL

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96
Q

How does impaired hepatic uptake of apo-B containing lipoproteins usually occur

A

Down regulation of the hepatic LDL receptor

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97
Q

Pathophys of low HDL

A

Accelerated breakdown

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98
Q

Clinical presentation of dyslipidemia

A

Often asymptomatic
May present with eruptive xanthomas (pruritic patches on the skin, most commonly the buttocks)

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99
Q

Tendinous xanthomas

A

Lipid deposit nodules in the tendons of the hands, feet and heels
Seen with high LDL

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100
Q

Lipemia retinalis

A

Milky appearance of the veins on fundoscopic examination

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101
Q

Serum change of dyslipidemia

A

Serum may appear milky and opaque

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102
Q

Recommendation for lipid screenings

A

All adults beginning at age 20
Some suggest screening children at 9-11

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103
Q

6 ASCVD risk factors

A

Tobacco use
DM
HTN
Obesity (30+ BMI)
Family hx
Personal history of Atherosclerosis or Coronary artery disease

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104
Q

Non-fasting lipid labs we can take

A

Total cholesterol and HDL

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105
Q

Fasting labs for lipids and indication we need to take them

A

Non-fasting TC over 250 or HDL under 40
Full lipid panel - TC, LDL, HDL, TGs (9-12 hour fast)

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106
Q

HDL level that is cardioprotective

A

over 60 mg/dL

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107
Q

Screening schedule for lipids

A

Every 5 years for healthy adults
Every three years for those who may need therapy
65 is the suggested cutoff for screening

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108
Q

Four secondary causes of dyslipidemia to rule out

A

Hyperglycemia
Renal insufficiency
Hepatitis
Hypothyroidism

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109
Q

Four indications for statin therapy

A

Clinical ASCVD
DM
LDL over 190mg/dL
Primary prevention with ASCVD risk above 7.5%

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110
Q

Qualification for very high risk of ASVCVD

A

2 major events or 1 major event with 2+ high risk conditions

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111
Q

4 major ASCVD events

A

ACS within the past 12 months
History of MI
History of ischemic stroke
Symptomatic PAD

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112
Q

5 high risk conditions for ASCVD disease

A

Over 65
Smoking
Diabetes
LDL over 100 despite max statin use
CKD

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113
Q

Management of hyperlipidemia in those with ASCVD

A

High intensity statin if under 75 or very high risk
Moderate intensity statin if not very high risk or older than 75

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114
Q

2 high intensity statins

A

Atorvastatin
Rosuvastatin

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115
Q

Goal of hyperlipidemia management

A

50% reduction
V high risk - reduce to 55
Not V high risk - reduce to 70

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116
Q

Management of primary LDL over 190

A

High intensity statin reassessing every 4-12 weeks and then every 3-12 months

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117
Q

Goal of hyperlipidemia management with LDL over 190mg/dL

A

50% reduction or under 100mg/dL whichever is lower

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118
Q

Steps for 40-75 DM patient with LDL over 70-190

A

Calculate 10 year risk
Review diabetes high risk features

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119
Q

Management options and goals for Age 40-75 with DM and LDL 70-190

A

Those with >7.5%riskand 1 high risk factor need high intesnsity with 50% or <70mg/dL reduction
Otherwise - Moderate intensity with 30-49% reduction or under 100 mg/dL

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120
Q

Risk discussion for less than 5% risk of ASCVD

A

Emphasize lifestyle to reduce risk factors

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121
Q

Risk discussion for 5-7.5% risk of ASCVD

A

Consider moderate intensity statin therpay if risk enhancers are present

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122
Q

Risk discussion for 7.5-20% ASCVD risk

A

Moderate intensity statin with goal of 30-49% reduction

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123
Q

Risk discussion for 20+% ASCVD risk

A

Statin to reduce LDL to 50% or under 70mg/dL

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124
Q

3 risk enhancing factors for ASCVD

A

Metabolic syndrome
Family hx
CKD

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125
Q

CAC

A

Coronary artery calcium - low dose CT scan of the heart

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126
Q

Interpretation of CAC

A

Over 100 - add statin
1-99 - add statin if over 55
0 - Focus on lifestyle and reassess in 5-10 years

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127
Q

Assessment for patients initiated on statin therapy

A

Lipid panel every 4-12 weeks and then 3-12 months

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128
Q

Follow up for those with no therapy initiated

A

Recalculate ASCVD risk every 4-6 years

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129
Q

How long does it take for diet to impact hyperlipidemai

A

3-6 months

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130
Q

Mechanism of statins

A

HMG CoA reductase inhibitors - stimulate LDL catabolism
Reduction is dose dependent
Hepatic CYP450 metabolism

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131
Q

Side effects of statins

A

MYALGIA - less with pravastatin and fluvastatin
Hepatotoxicity
Hyperglycemia
Contraindicated in pregnancy

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132
Q

What to do when statin therapy is ineffective

A

Try adding another ststin or alternate regimen before trying a non-statin

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133
Q

Ezetimibe

A

Cholesterol absorption inhibitor - good choice because cheap - synergy with statin

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134
Q

2 PCSK-9 inhibitors

A

Alirocumab and Evolocumab

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135
Q

MOA and route of PCSK-9 inhibitors

A

Decrease LDL receptor degradation and increase LDL metabolism
SQ only

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136
Q

Bempedoic acid

A

ACL inhibitor that has some efficacy on treating hyperlipidemia - inhibits cholesterol synthesis - less effective with a statin more effective with absorption inhibitor

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137
Q

Side effects of bempedoic acid

A

Gout/Hyperuricemia - 70% urine excretion

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138
Q

Indication for bempedoic acid

A

Need LDL reduction while on max statin

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139
Q

Inclisiran

A

PCSK-9 small interfering agent day 1, 3 months, and then q 6 month dosing can cause arthralgia
better than other PCSK-9 inhibitors

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140
Q

3rd line treatment for hyperlipidemia

A

Bile acid sequestrants - Welchol
Safe in pregnancy
Impair absorption of other drugs taken 1 hr before or 4 hrs after

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141
Q

SEs of bile acid sequestrants

A

GI - nausea, bloating, etc.

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142
Q

Complication of hypertriglyceridemia

A

Pancreatitis
Casually related to CV disease

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143
Q

Indication for hypertriglyceridemia management of lifestyle modifications

A

Over 20 with TGs 175-499

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144
Q

Indication for statin therapy in hypertriglyceridemia

A

40-75, Over 7.5% ASCVD risk, TGs over 500

or TGs over 1,000 alone

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145
Q

Fibrates

A

Treat hypertriglyceridemia by stimulating LPL activity and apo-C III synthesis
Gemfibrozil, and fenofibrate

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146
Q

SEs of Fibrates

A

Dyspepsia, gallstones, myopathy
Caution in CKD can be hepatotoxic

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147
Q

Omega 3 FAs for hypertriglyceridemia

A

Need up to 4 grams/day
Can cause diarrhea or bleeding

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148
Q

Hicotinic acid (Niacin) for hypertriglyceridemia

A

Can cause flushing and increases LPL activity

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149
Q

MC inheritance pattern for metabolic mineral disorders

A

Autosomal dominant - often an enzyme deficiency

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150
Q

Sorbitol

A

Fructose alcohol

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151
Q

Glycogen storage disorder

A

Glycogen is stored excessively in the liver and the muscles and cannot be broken down leading to hypoglycemia during fasting

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152
Q

Clinical presentation of GSD

A

Lack of energy for exercise
Hypoglycemia with fasting
Delayed growth

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153
Q

3 things to evaluate for for GSD

A

Hypoglycemia
Elevated LFT
CPK for muscles
Genetic test - may be a replacement we can give

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154
Q

Fructosemia

A

Inability to break down fructose

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155
Q

Fructose 1,6 biphosphatase

A

Required for gluconeogenesis
Hypoglycemia during fasting when deficient
FDpase

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156
Q

Clinical presentation of 1,6 biphosphatase deficiency

A

Leads to hypoglycemia and acidosis
Avoid fructose and prolonged fasting

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157
Q

Aldolase B

A

In the initial breakdown of fructose

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158
Q

Aldolase B deficiency

A

Fructose 1 phosphate is deposited in the tissues and then causes organ damage
Jaundice, hepatomegaly, hypoglycemia

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159
Q

3 places fructose collects in an aldolase B deficiency

A

Intestines, Liver, Kidney

160
Q

Essential fructosuria

A

No fructose kinase = no by products
Fructose in urine

161
Q

Galactosemia

A

Inability to process galactose

162
Q

3 enzymes that may be deficient in galactocemia

A

GALT, GALK, GALE

163
Q

GALT deficiency

A

Decreased appetite, vomiting, jaundice - occurs right away because breast milk
Can develop cataracts due to galactitol deposition in the eye

164
Q

GALK deficiency

A

Mainly cataracts with no other issues

165
Q

GALE deficiency

A

Presentation depends on severity of deficiency

166
Q

GALT deficiency screening and management

A

Often done on newborns
RBC galactose 1 phosphate
Avoid all dairy products
soy based baby formula

167
Q

Mainainance for galactosemia

A

Take CBC and LFT yearly, Ophthalmology, Measure pubescent female hormones

168
Q

Phenylketoneuria

A

Phenylalanine cannot be converted to tyrosine and it builds up in the brain causing myelin toxicity

169
Q

Common ancestries of PKU pts

A

White or native american

170
Q

Manifestation of PKU

A

Lighter hair and skin, loss of apatite, weakness, vomiting

171
Q

4 things to avoid in PKU

A

Meat/Fish
Aspartame
Dairy
Nuts

172
Q

2 drugs that treat PKU

A

Break down Phenylalanine
Sapropterin - Ped and adults
Pegvaliase - Adult only

173
Q

Maple Syrup Urine disease

A

Can’t break down branch chain amino acids
Leucine, isoleucine and valine

174
Q

Leucine buildup in the body

A

Neurologic issues

175
Q

Isoleucine buildup in the body

A

Burnt sugary smell to urine

176
Q

Clinical presentation of severe MSUD

A

Irritability, Rapid onset, Seizures and death

177
Q

Clinical presentation of moderate MSUD

A

GI, muscle weakness, Eye symptoms, Hyperactivity

178
Q

Management of MSUD

A

Specific branch-chain-controlled formula
Try a trial of thiamine for 4 weeks before formulation

179
Q

Complication of MSUD

A

Metabolic decompensation - too much leucine
Hemodialysis, glucose, liver transplant last resort

180
Q

Homocysteinuria

A

Interrupted breakdown of Methionine

181
Q

Clinical presentation of homocystinuria

A

Dislocated optic lenses
retardation
Marfanoid
Pes excavatum
Genu valgum
Thromboembolic issues

182
Q

Management of homocysteinuria

A

Give folate and B12 supplements
Limit protein intake

183
Q

Lysosomal storage disorders

A

Abnormality in the biosynthesis or function of the lysosome

184
Q

Tay-Sachs disease

A

Lysosomal storage disorder
Hexoaminidase buildup causes neurological damage

185
Q

Infantile Tay Sachs

A

First 3-6 months
Abnormal startle reflex seen first - does not subside
Cheery red spot on fovea with gross motor delays
Lack of appropriate muscle tone

186
Q

Common cause of death in infantile Tay Sachs

A

Pneumonia due to diaphragm weakness

187
Q

Juvenile onset Tay Sachs

A

2-5 years
Respiratory infections and behavioral issues
Slow decline

188
Q

Adult onset Tay Sachs

A

Report a hx of clumsiness in childhood
Weakness and dysarthria
Intelligence declines slowly

189
Q

Treatment of Tay Sachs

A

Supportive care
Can diagnose via genetic testing
OT/PT

190
Q

Gaucher (Go-Shay) Disease

A

Deficiency of Gcase leads to buildup of glucocerebrosides in Macrophages
Stuffed macrophages lead to tissue fibrosis

191
Q

G1 Gaucher disease

A

Bone involvement - osteopenia and osteoporosis. No CNS involvement

192
Q

G1&2

A

G2 most aggressive
G3 more insidious
Both cause neurological issues

193
Q

Bone crisis

A

Gaucher cells cause clot and necrosis of bones - severe bone pain, sudden onset

194
Q

Diagnostic for Gaucher disease

A

Low beta glucosidase enzyme activity - only screened in 4 states

195
Q

Management of Gaucher disease

A

Recombinant enzyme replacement -won’t help neuro
Substrate reduction therapy - Eleglustat and miglustat

196
Q

Fabry disease

A

Alpha galactosidase A (GLA) is deficient
X-linked recessive
Fat buildup on capillary wall prevents oxygen transfer

197
Q

3Clinical presentation of Fabry disease

A

Small, non-blanchin lesions on umbilicus down
Decrease in sweating
Opaque cornea/lens from fatty deposits
Small vessel disease
Burning pain in extremities

198
Q

Management for Fabry disease

A

Enzyme replacement with Fabrazyme
Can aso use migalastat
Consider statin therapy

199
Q

Niemann-pick disease

A

Sphingomyelin cannot be broken down, fills macrophages causing cell death and tissue damage - FOAM cells

200
Q

NP-A

A

Most aggressive niemann-pick - failure to thrive
Lung scarring
Hepatosplenomegaly
Die at 2

201
Q

NP-B

A

Less serious
Lung issues, cirrhosis
Die in late adolescence

202
Q

NP-C

A

CNS disease, Liver spleen and lung issues
Aspiration and muscle problems

203
Q

Management of NP disease

A

NOT tested for in WV
PT/OT
Feeding tube
O2 therapy

204
Q

Pompe disease

A

Deficiency of acid alpha glucosidase - can’t break glycogen into glucose - tissue destruction

205
Q

Classic infantile Pompe disease

A

Few months after birth - progressive weakness - die before 1 year

206
Q

Non-classic Pompe disease

A

Delayed motor skills - onset around 1 usually don’t make it past early childhood

207
Q

Late onset Pompe disease

A

Less severe, often have respiratory failure as adults

208
Q

Management of Pompe disease

A

Lunizyme - enzyme replacement therapy
Watch for sleep apnea, aspiration

209
Q

3 things that can lead to hyperphosphatemia

A

Too much intake
Lack of excretion
Shift of phosphate from the inside to the outside of the cells (muscle or tumor breakdown)

210
Q

Clinical presentation of hyperphosphatemia

A

Hypocalcemia or underlying condition
May need to diurese or dialyze
Phosphate binders also possible
Treat cause

211
Q

Calcium acetate

A

Phosphate binder
for ESRD
Can cause GI side effects and cardiac arrhythmias
Compare risk/benefit for pregnancy

212
Q

Lanthanum carbonate

A

Phosphate binder NOT preferred for pregnancy - binds in gut

213
Q

Renagel

A

Phosphate that does not interfere with bicarb or calcium - may reduce vitamin uptake in pregnant patients - careful

214
Q

3 things that can cause hypophosphatemia

A

Inadequate intake, increased excretion, shift of phosphate into cells

215
Q

3 things that may caus inadequate intake of phosphate

A

Intestinal malabsorption
Antacids
Vitamin D deficiency

216
Q

Cause of increase secretion of phosphate

A

Saline diuresis
Hyperparathyroidism
Fanconi

217
Q

Cause of phosphate shifting into cells

A

Refeeding syndrome
DKA - when giving insulin
Increase in calcium due to bone disease

218
Q

Level for severe hypophosphatemia

A

Under 2 mg/dL

219
Q

Treatment for hypophosphatemia

A

Diet, supplements
Supplements can cause weakness, arrhythmia
Safe during pregnancy

220
Q

Magnesium role

A

Energy transfer, storage, metabolism, PTH regulation

221
Q

Source of magnesium

A

Green vegetables - low in alcohol abuse to TPN, Hungry bone syndrome, GI loss, NOT in a chamistry panel

222
Q

Clinical presentation of hypomangacemia

A

Usually hypocalcemia symptoms and hypokalemia
Nystagmus horizontal and verticle

223
Q

Management of hypomagnesemia

A

Dietary/supplement if mild
IV if severe

224
Q

Pagets disease

A

Breakdown of bone followed by inappropriate reformation of bone

225
Q

Clinical presentation of Pagets disease

A

Large vascular bones that get bent
Bone pain - deep and worse whn pt sleeps
Deformity
Compression of spinal nerves

226
Q

Evaluation for Pagets disease

A

Elevated alkaline phosphatase
Non-uniform bones on X-ray (lytic lesion)
Can use a radionuclide scan to determine where the disease is active

227
Q

Complications and management of Pagets

A
  • neoplasms joint, and neuromuscular issues
    Bisphosphonates to prevent osteoclastic activity
    NSAIDS for joint pain
    Calcium and Vitamin D
228
Q

4 Bisphosphonates

A

Alendronate
Ibandronate
Risedronate
Zoledronic acid

229
Q

Gene that is often suppressed in type 1 endocrine neoplasias

A

Menin encoded by the MEN1 gene

230
Q

3 P’s of MEN-1

A

MC organs effected
Parathyroid
Pancreas
Posterior pituitary

231
Q

Most common tumor types in MEN-2

A

Medullary thyroid
Parathyroid
Pheochromocytoma

232
Q

3 most common tumor types in MEN-3

A

Medullary thyroid cancer, pheochromocytoma, Mucosal and GI ganglioneuromas

233
Q

Presentation of MEN1 parathyroid tumor

A

Elevated PTH with asymptomatic mild hypercalcemia - use a nuclear scan to confirm

234
Q

Treatment for MEN1 parathyroid tumor

A

Surgical PT gland removal
Cinacalcet

235
Q

GEP-NET

A

Gastro-entero-pancreatic NeuroEndocrine Tumor

236
Q

5 types of GEP-NETs

A

Gastrinoma
Insulinoma
Glucagonoma
VIPoma
Ppoma

237
Q

Gastrinoma

A

A gastrin secreting tumor causing hypersecretion of gastric acid and peptic ulcers

238
Q

Clinical presentation of a gastrinoma

A

GERD, Peptic ulcer disease, Hypercalcemia, Diarrhea

239
Q

Gastric acid physiology 4 steps

A

Stimulation of gastrin by secretin
Gastrin secretion results in acid production
Gastric acid is released and travels to the duodenum where it…
Trigger secretin to be relased

240
Q

Lab evaluation for gastrinoma

A

Fasting serum gastrin with 1000 pg/mL being diagnostic
if 150-1000 also do a secretin stimulation test

241
Q

Management of gastrinoma

A

Convervative treatment:
PPIs - Omeprazole or Esomeprazole
H2 blockers - Cimetidine or famotidine

Surgery is controversial

242
Q

Insulinoma

A

Beta cell tumor usually in the second to 4th decade of life

243
Q

Clinical presentation of an insulinoma

A

Hypoglycemia with fasting - tremors, sweating, shaking, weakness

244
Q

Lab evaluation for an insulinoma

A

72-hour inpatient fast while monitoring insulin levels
Should check for C-peptide to r/o factitious disorder

245
Q

Management for insulinoma

A

Frequent Carb intake while waiting for surgery
Diazoxide (k+ channels) and Octreotide (somatostatin analogue) can help
Surgery is 1st line

246
Q

Clinical presentation of glucagonoma

A

Hyperglycemia
Weight loss
Necrolytic migratory erythema around orifices

247
Q

Lab evaluation for glucagonoma

A

Elevated blood glucose and elevated fasting glucose
Control BS, Octreotide, Excise IF one lesion can be identified

248
Q

VIPoma

A

Pancreatic tumor that secretes vasoactive intestinal polypeptide

249
Q

Clinical presentation of VIPoma

A

Severe tea colored diarrhea
Flushing
Inhibition of gastric acid secretion
Bone resorption
Hyperglycemia

250
Q

Lab evaluation for VIPoma

A

Serum VIP over 75 pg/mL confirmed by repeat testing

251
Q

Management of VIPoma

A

Correct fluid electrolyte and vitamin imbalances - B12 can’t be oral
Octreotide to inhibit VIP
Surgical excision if no mets

252
Q

2 types of nonfunctioning pancreatic tumors

A

Ppomas (polypeptide secreting)
Non-functioning NETs

253
Q

Progression of nonfunctional pancreatic tumors

A

May metastasize to the liver as they are not symptomatic

254
Q

Management of non-functioning pancreatic tumors

A

Surgery is controversial - evaluate for metastasis - don’t operate w/ mets!!
Iatrogenic diabetes, steatorrhea, dumping syndrome may result

255
Q

MC secretions of pituitary adenomas

A

60% prolactin
25% GH
5% ACTH
10-20% Non-secretory

256
Q

Lab evaluation and management of pituitary adenoma

A

Hypothalamic-pituitary testing
Transsphenoidal surgery for removal
Cabergoline for prolactinoma
Octreotide for GH secreting
Pasireotide for ACTH secreting

257
Q

Adrenal adenoma management

A

Excise if over 4cm

258
Q

Carcinoid tumor

A

Slow growing tumor of the bronchi or GI tract - asymptomatic until late in disease - excise

259
Q

Meningioma

A

Tumor of the meninges that should be referred to a neurosurgeon

260
Q

3 other possible MEN-1 tumors

A

Lipoma, Angiofibroma of face, Thyroid tumor

261
Q

When to screen for MEN-1

A

Two or more associated tumors
First degree relatives have it even if asymptomatic

262
Q

Wermer syndrome

A

MEN-1 from menin gene issue

263
Q

MEN-2

A

Mutation in RET-proto oncogenes causing thyroid, parathyroid, and adrenal cancers

264
Q

3 subtypes of MEN-2

A

MEN-2A
MEN-2B (MEN 3)
Familial medullary thyroid cancer

265
Q

Clinical presentation of medullary thyroid cancer

A

Increased secretion of calcitonin may include nodules and hoarseness

266
Q

Diagnostics for medullary thyroid cancer

A

Serum calcitonin and FNA biopsy

267
Q

Treatment for medullary thyroid cancer

A

Total thyroidectomy

268
Q

Treatment for pheochromocytoma

A

Surgical resection w/ alpha blockade while waiting

269
Q

Additional symptoms of MEN-2B

A

High arched palate, Pectus excavatum, High arched feet, scoliosis

270
Q

What should be done before removing any tumors

A

Remove a pheochromocytoma FIRST

271
Q

Neuroma

A

Tumor of the tip of the nerves - seen in MEN2B along with lip hypertrophy

272
Q

Screening guidlines for MEN2/3

A

All patients with Medullary thyroid cancer
MTC and hx of family tumors
MTC and pheochromocytoma
Unilateral pheo and increased calcitonin

273
Q

MEN-4

A

Rare and autosomal dominant
Tumors are similar to MEN1

274
Q

Autoimmune Polyendocrine syndrome

A

Rare immune endocrinopathies characterized by combined gland insufficiencies

275
Q

Clinical presentation of APS 1 -3 key symptoms

A

Chronic mucocutaneous candadiasis
Acquired hypoparathyroidism
Adrenal failure

Pretty much everything gets attacked

276
Q

Management of APS type 1

A

Always treat addisions FIRST can use ketoconazole for candidiasis

277
Q

APS 2

A

HLA gene mutation

278
Q

APS 1

A

AIRE gene mutation

279
Q

4 criteria for APS-II

A

Primary adrenal failure, Autoimmune thyroid disease, T1DM, Primary hypogonadism

280
Q

Diagnostics and monitoring for APS-II

A

No specific genetic test, monitor every 1-3 years

281
Q

Condition to treat before treating other endocrine conditions

A

Addison’s disease

282
Q

Storage of glycogen

A

In the liver and muscles

283
Q

Metabolism of glycerol and fatty acids

A

Glycerol becomes glucose
Fatty acids become ketones cannot become glucose

284
Q

Cell that secretes insulin

A

Beta cell

285
Q

Part of insulin that is cleaved off duing production

A

C-peptide

286
Q

GLUT-2 receptors

A

Transport glucose into body cells - insulin independant

287
Q

GLUT-4 receptors

A

Insulin dependent transport of glucose into adipose and muscle tissue

288
Q

How does glucose signal the pancreas to secrete insulin

A

It enters the beta cell, goes through glycolysis to form ATP which inhibits at K+ channel causing depolarization and insulin release

289
Q

How does insulin work in the body

A

Increases transport of macronutrients into the body cells and their synthesis except for gluconeogenesis

290
Q

Cells that secrete glucagon

A

Alpha cells

291
Q

Action of glucagon

A

Increased breakdown and gluconeogenesis

292
Q

Action of amylin

A

Secreted with insulin and C-peptide
Works with insulin and increases satiety

293
Q

Somatostatin

A

Secreted by delta cells
Suppresses insulin, glucagon and other hormones

294
Q

Incretins

A

Gut derived hormones that promote insulin release after an oral nutrient load leading to slowed gastric emptying and increased satiety

295
Q

3 counter-regulatory hormones to insulin

A

Epinephrine
Growth Hormone
Glucocorticoids

296
Q

Two types of Type I DM

A

IA - Autoimmune (most of cases)
IB - Idiopathic

297
Q

Pathogenesis of T1DM

A

Genetic with an immune trigger

298
Q

Use of immunosupressabts in T1DM

A

No beneift noted

299
Q

T1DM immune markers

A

Anti-GAD65 is the main one - markers decrease as beta cells are destroyed

300
Q

Pathogenesis of T2DM

A

Resisitance of the tissues to insulin, leading to inadequate insulin secretion
Environmental with obesity being the number 1 factor

301
Q

What happens in the liver during T2DM

A

The liver continues to make glucose leading to increased hyperglycemia

302
Q

T2DM Ominous Octet

A

Decreased insulin secretion
Increased hepatic glucose production
Decreased peripheral glucose uptake
Increased lipolysis
Decreased incretin effect
Increased glucagon secretion
Decreased neurotransmitter function
Increased renal glucose reabsorption

303
Q

Fasting and postprandial glucose levels that makr diabetes

A

126 fasting
200 postprandial

304
Q

A1c for diabetes

A

6.5+

305
Q

A1c for prediabetes

A

5.6-6.4

306
Q

Criteria for metabolic syndrome

A

3+ of five criteria
Fasting TG over 150
HDL under 40
BP over 130/85
Fasting Glucose over 100
Waist circumference over 40(M) 35(F)
If they are on meds for any of these conditions that counts

307
Q

2 ethnic groups at the highest risk for Metabolic syndrome

A

Mexican Americans, blacks

308
Q

Insulin effect on sdium, blood vessels and lipolysis

A

Retains sodium, dilates blood vessels, leads to FFAs in blood stream
In insulin resistance it still retains sodium but DOES NOT dilate blood vessels

309
Q

Adiponectin

A

Anti-inflammatory cytokine produced by fat cells that is reduced in patients with metabolic syndrome

310
Q

3 conditions commonly associated with metabolic syndrome

A

Hyperuricemia, PCOS, Obstructive sleep apnea

311
Q

Suggested calorie restriction for MetS

A

about 500 per day

312
Q

Physical activity suggested for MetS

A

at least 30 minutes per day - more for weight loss

313
Q

3 poly’s of a general diabetes presentation

A

Polyuria
Polydipsia
Polyphagia

314
Q

How does T1DM cause blurry vision

A

Hyperosmolar tears blur the vision

315
Q

Dual peak of T1DM incidence

A

4-7 or 10-14

316
Q

4 potential exam findings for T2DM

A

Poorly healing footh ulcer, Balanoposthitis, Rash in intertriginous fold, Acanthosis nigricans

317
Q

Clinical presentation of hypoglycemia

A

Trembling, Diaphoresis, Feeling faint, Tachycardia, confusion

318
Q

Who should be screened for diabetes

A

All adults at 45
Any patient who is obese or has 1+ DM risk factors
1st prenatal visit
HIV+

319
Q

Prediabetic fasting and postprandial glucose

A

Fasting - 100-125
Postprandial - 140-199

320
Q

How many tests do we need to confirm a diabetic diagnosis

A

Abnormal blood sugar must be repeated once

321
Q

Best location for glucometry

A

Finger tip - other areas can be behind in the reading

322
Q

What does A1c indicate

A

Glycemic state over the past 8-12 weeks - more heavily weighted to the last 4 weeks

323
Q

False low A1c readings

A

High levels of HbF
Shortened erythrocyte survival (hemolytic anemia)
IV drugs or iron

324
Q

False elevations in A1C

A

Splenectomy leading to decreased turnover
Stress over a long time

325
Q

3 interpretations for a low A1c

A

Hemolytic anemia, chronic blood loss, chronic renal failure

326
Q

Special education for glucose tolerance testing

A

Eat at least 150g of carbs daily three days before test
Avoid physical activity and smoking until test is complete

327
Q

Use of C-peptide testing

A

Determines beta cell function, causes of hypoglycemia, evaluation of insulinomas

328
Q

Normal C-peptide:Insulin ratio

A

5-10

329
Q

Indication for ketone testing

A

Evaluation for ketosis - can test serum or urine

330
Q

3 ketone bodies and which is predominant in DKA

A

Acetone, Acetoacetate, beta-hydroxybutyrate (BHB is most common in DKA)

331
Q

Ketone level that is concerning

A

Greater than 3

332
Q

Which ketone test is more reliable

A

Serum ketones because it picks up beta-hydroxybuterate

333
Q

3 general goals of DM treatment

A

Glycemic control
Reduction or elimination of complications
Maintain quality of life

334
Q

Fasting BS
Postrprandial BS
A1c
Desired for patients who are diabetic for glycemic control to be acheived

A

A1c - Under 7%
Fasting BS - 80-130
Postprandial BS - Under 180

335
Q

Targets for pediatric patients with DM

A

A1c under 7.5
Fasting BS 90-130
Postprandial BS 90-150

336
Q

Hypoglycemia management in conscious patient

A

Give 15-20g glucose orally
Eat a snack or meal when glucose returns to normal

337
Q

Hypoglycemia management in an unconscious patient

A

IV glucose with nasal glucagon

338
Q

DM nutrition guidelines

A

Low carb, T1 shoudl eat consistently, Dietary fiber prevents glucose absorption
Encourage weight loss in type 2

339
Q

DM exercise recommendations

A

150min/week min
Resistance training
no more than 2 days w/o exercise

340
Q

BMI at which to consider pharmacotherapy

A

27

341
Q

BMI at which to consider bariatric surgery

A

30 (27.5 for asian americans)

342
Q

2 best antihypertensives for DM

A

ACE or ARB ~Pril or ~Sartan

343
Q

Management of hyperlipidemia in DM

A

Yearly lipid profile recommended

344
Q

Management of ASCVD in DM

A

Consider aspirin if risk greater than 5%

345
Q

Management of diabetic nephropathy

A

Yearly check of urine albumin and eGFR for diabetics who have been for over 5 years

346
Q

Management of DM retinopathy and feet

A

Dilated eye exam at time of diagnosis for T2
After 5 years for T1
Preform yearly
Same for feet

347
Q

Screening for diabetic neuropathy

A

Monofilament and one other test (ie. vibration)
Educate patients on foot care

348
Q

5 Exams DM patients need once a year at least

A

Eye exam
Foot exam
BP (every visit)
Psych eval
Check on ASA therapy

349
Q

4 labs DM patients should get taken yearly

A

eGFR
Urine albumin
Lipid profile
A1c (twice per year)

350
Q

Where to put moisturizer on diabetic feet

A

Everywhere but NOT between toes

351
Q

Side effects of insulin injection

A

Hypoglycemia
Lipohypertrophy or lipoatrophy at injection site

352
Q

Alcohol effect on the insulin dependant

A

Causes hypoglycemia (liver stops doing gluconeogenesis)

353
Q

Common dosing for insulins

A

U100 (100units/mL)

354
Q

Basal insulin

A

50% of insulin given, long acting background

355
Q

Bolus insulin

A

Other 50% covers meals

356
Q

5 bolus insulins

A

Lispro
Aspart
Glulisine
Technosphere (IN)
Human REGULAR

357
Q

5 Basal insulins

A

Human NPH
Detemir
Glargine (U300 is ultra long)
Tresiba (ultra long)

358
Q

Pro/Con of inhaled insulin

A

Rapid acting
Not for smokers and can cause cough and lung cancer

359
Q

Pro/Con of premixed insulins

A

Fewer injections but less easy to control dose

360
Q

Insulin needle guage

A

31 or 33

361
Q

4 insulin injection sites

A

Upper outer arms
Abdomen
Buttocks
Upper outer thighs

362
Q

Proper injection regimen for insulin

A

Choose 1 site but rotate spots within that site

363
Q

Guidelines for Males and Females for DM carb counting

A

M - 60g per meal 30g per snack
F - 45g per meal 15g per snack

364
Q

Dawn phenomenon

A

Hyperglycemia that occurs in the morning due to the body naturally countering the effects of insulin

365
Q

Somogyi effect

A

Hyperglycemia that occurs because of excessive nocturnal insulin - high BS is a rebound reaction

366
Q

2 ways to differentiate between Dawn and Somogyi

A

Check BS at 3 am Low=Somyogi, Med/High=Dawn

Decrease bedtime insulin improves with somyogi, gets worse with Dawn

367
Q

Slow absorption and fast absorption insulin injection sites

A

Abdomen and buttocks are fast
Legs and arms are slow

368
Q

Physiologic insulin regimen

A

4 injections per day 3 rapid and 1 long basal
half basal, half for boluses
or 1 unite per 15 g of carbs
ACHS

369
Q

How to use Blood sugar readings in adjusting insulin dose

A

Adjust insulin dose taken at the meal BEFORE the one for which you are checking glucose

370
Q

Dose adjustments for high or low sugars

A

Under 80 (or 125 before bed) subtract 2 units
Over 130 (or 150 before bed) add 2 units
Under 70 eat something sugary

371
Q

Best insulins for basal doses

A

Long acting (ie. lantus) better than NHP
Toujeo and Tresiba have less hyperglycemia

372
Q

BID premixed dosing insulin regimen

A

2 injections per day
2-3 checks per day

373
Q

Starting dose for premixed insulin

A

10% of the patients weight in units

374
Q

Sliding scale insulin

A

Usually used in inpatient settings
uses a reactive approach to control and can result in wide swings

375
Q

Metformin

A

Biguanide - FIRST LINE
Inhibits hepatic gluconeogenesis
Decreases glucose absorption
Slightly improves insulin sensitivity

376
Q

Pro/Con of metformin

A

Cheap, weight loss, good lipid profile
GI side effects, metallic taste, B12 deficiency, can cause lactic acidosis

377
Q

A1c reduction with Metformin

A

1-2%

378
Q

TZDs

A

Rosiglitazone and Pioglitazone
Unlock muscle and fat cells and improve insulin sensitivity

379
Q

A1c increase from TZDs

A

.5-1.4%

380
Q

TZD MOA

A

Bind to PPAR gamma cause an increase in adipogenesis

381
Q

TZD pro/con

A

improves fasting and postprandial glucose like metformin
Improves TG requirements and lowers insulin needs
Weight gain edema, BBW for CHF

382
Q

3 Sulfonylureas and 2 Meglitinides

A

Glimepiride
Glipizide
Glyburide
Lower A1c by 1-2%

Repaglinide
Nateglinide
Lower A1C by .5-1%

383
Q

Pro/Con of sulfonylureas/meglitinides

A

Cheap, Short onset, improves XFBG and PPBG
Hypoglycemia, Weight gain, liver/renal disease, TID

384
Q

Alpha glucosidase inhibitors

A

Block breakdown of starches in the intestine and delay carb absorption
Acarbose and Miglitol
Reduce A1c by .5-.8

385
Q

Pro/Con of alpha glucosidase inhibitors

A

Improve PPBG without hypoglycemia
Flatulence, TID, May increase hypoglycemia in combo with SFUs or insulin

386
Q

SGLT2 inhibitors

A

Halt renal glucose absorption in the PCT
(sugar flows in the toilet instead)
Canagliflozin
Dapagliflozin
Empagliflozin
Ertugliflozin

387
Q

Pro/Con of SGLT2 inhibitors

A

Weight loss, CKD improvement, Lower BP
UTIs, increases LDL, May mask DKA

388
Q

GLP-1 receptor agonists

A

Mimic GLP-1 increase insulin, decrease glucagon, decrease gastric emptying end in TIDE - Incretin related

389
Q

Oral GLP agonist

A

Rybelsus/Semaglutide

390
Q

Pro/Con to GLP-1 receptor agonists

A

Improves FBG and PPBG without hypoglycemia, weight loss
Mostly SC, BBW thyroid cancer, GI effects

391
Q

DPP-4 inhibitors

A

Extend effects of Incretin by inhibiting its degradation
END in Liptin

392
Q

Pro/Con of DDP-4 inhibitors

A

Improves FBG and PPBG
Pancreatitis, GI but less than GLP-1 aggies
May cause increased risk of heart failure

393
Q

Amylin analogs

A

Pramlitide
decrease glucagon and gastric emptying while increasing satiety A1c increase of .25-.5%

394
Q

Pro/Con of amylin analogues

A

Glucose and weight improvement
Can help with Type 1 OR 2 diabetes
Must be SC, can cause hypoglycemia - BBW

395
Q

Covesevelam

A

Bile acid qequestrant lowers A1c by .3-.5% and reduces LDL
GI effects of Constipation and Dysipepsia

396
Q

Bromocriptine

A

Dopamine receptor agonist that lowers A1c by .1%-.5%, N/V, dizziness, HA

Heme/Onc/Endo (5 decks)

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