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IPAP JUNIOR SEM. > Endo Block II > Flashcards

Endo Block II Flashcards

1
Q

What is the MOST COMMON medical d/o

A

Obesity

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2
Q

A BMI of 18.5 or less is…

A

Underweight

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3
Q

What is a normal BMI

A

18.5-24.9

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4
Q

What is an overwieght BMI

A

25-29.9

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5
Q

What is Class I obesity BMI

A

30-34.9

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6
Q

What is class II obesity BMI

A

35-39.9

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7
Q

What is the class III obesity BMI

A

Any BMI greater than 40

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8
Q

What are the wiast measurments for high risk metabolic syndrome

A

Men greater than 40 in or women greater than 35

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9
Q

What two cancers are highly assoiated with obestity

A

Breast cancer and Uterine Cancer

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10
Q

What is prader-willi syndrome

A

The most common cause of marked genetic obesity

Presents with hypotonia, feeding difficulities with subsequent hyperphagia and wt gain, almond shaped eyes, narrowed bifrontal diameter, and a thin upper lip, developmental delays, hypogonadism

Short development, OSA, and morbid obesity

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11
Q

An infant presents with almond shaped eyes, norrowed bifrontal diameter and a thin upper lip with difficult feeding

Think

A

Early Stage of Prader-Willi syndrome

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12
Q

What is the key to wt loss

A

Behavior modification

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13
Q

When can pharmicological intervention be indicated in pt with obestity

A

BMI >30
Or
BMI> 27 with HTN, DM2, or CVD

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14
Q

What is orlistat

A

GI agent wt loss mediaction

inhibits intestinal lipase & reduces dietary fat absorption

Common SE: oily stools, diarrhea, fecal incontinence, reduced fat-soluble vitamin absorption

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15
Q

What is the relationship between orlistat and vitmains ADEK

A

Decreaded absoption of fat soluable vitamins

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16
Q

What is phentermine

A

CNS stimulatnt

Increases reuptake of norepi & dopamine to suppress appetite

Schedule IV drug with abuse potential

Common SE: mood changes, fatigue, insomnia

C/I hyperthyroidism, glaucoma

D/c if no weigth loss in 4 weeks

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17
Q

What is buproprion/ naltrexone

A

Regulates activity in dopamine reward system
Controls cravings & overeating behaviors
May assist with quitting smoking/ETOH

Antidepressant/ opiod antagonist

Only use in pts with simple pych d/o

SE: GI upset

Caution with history of psychiatric disorders

Contraindicated in seizures, eating disorders, hypertension, opioid use

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18
Q

What is liraglutide

A

-TIDE (GLP-1) (can cause wt loss)

increases glucose dependent insulin secretion, decreases inappropriate glucagon, slows gastric emptying

Common SE: GI upset, HA, hypoglycemia

Contraindicated in patients with history of medullary thyroid cancer and MEN 2

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19
Q

What are the general C/I for the use of wt loss medications

A

Uncontrolled cardiovascular disease

Pregnancy and/or lactation

History of psychiatric disease

Age < 18 years

Use of certain incompatible medications (monoamine oxidase inhibitors - MAOIs)

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20
Q

What is the indication for bariatric surgery

A

BMI greater than 40, or BMI greater than 35 with HTN, DM2, or CVD

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21
Q

What is a Roux-en-Y surgery

A

Basically bipass srgry

Combination restrictive and malabsorptive surgery

Distal stomach is resected

Remaining gastric pouch is anastomosed to a retro-colic
Roux-en-Y segment of jejunum

Gastric remnant capacity – 30-50 ml

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22
Q

What are the cells in the testes than make sperm

A

Sertoli cells

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23
Q

When should free testosterone be measured

A

First thing in the MORNING when they are NOT fasting

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24
Q

What testosterone level is hypogonadism

A

A serum less than 291 (240) or (150-300)
or
a free T less than 70 (or less than 30 in a pt over 70 y/o)

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25
Q

Failure to enter puberty before what age…. Is hypogonadism

A

14

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26
Q

What is the difference between early and late prenatal testosterone deficiency

A

In early, they have ambigious genitellia and in late prenatal they have micropenis or cryptorchidism

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27
Q

What does eunichoidal porpotions mean

A

Arm span is greater than hieght by 5+ cm and the crown of the pubis < than the pubis floor

From long bones continuing to grow under the influence of growth hormone in hypogonadism

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28
Q

What is the most common autosomal abnm in males

A

Klinefelters (47XXY)

Assoc with seminiferous tubule dysgenesis

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29
Q

A male pt presents with gyno at puberty, Testes normal during childhood, but during adolescence the testes become firm, fibrotic, nontender to palpation, and small <2cm (>3.5 nl), Tall in stature, with decrease facial and pubic hair

A

Klinefelter Syndrome

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30
Q

If testes are left undecended in cryptorchidsm.. what is the pt at an increased rsk of

A

Infertiliy and testicular cancer

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31
Q

When should T levels be checked after initiating Test treatment

A

14 days after initiation and then 6 months at a minimum

Also should have lipids, LFTs, and H/h along with a DRE every 6-12 months

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32
Q

What is the most common form of congenital hypogonadism

A

Kallmann Syndrome ( X linked inheritance)

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33
Q

A pt presents with anosmia and an impaired sense of smell, is a male and has low T and FH and LSH

Think

A

Kallmann Syndrome

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34
Q

A pt presents with well developed breast without a period, think of..

A

Complete androgen insufficiency or a 46XY male

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35
Q

What are the major endocrine hormones of the pancreas

A

Insulin, glucagon, somatastatin, gherlin

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36
Q

A pt presents with frequent vag candida.. think

A

DM2

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37
Q

What is C-peptide

A

Fragment of pro insulin, should mimic insulin levels

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38
Q

What does a serum fructonase measure

A

A 1-2 week look at the “A1c”

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39
Q

MNT can decrease A1C by

A

1-1.9% for DM1

Or 0.3-2% for DM2

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40
Q

How do you admin insulin to a DM2

A

Continue oral agents at same dose except Stop sulfonylureas,
Add single bed time dose, if not at target at daytime at day time dose.,

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41
Q

What is the difference between dawn and somogyi phenomenon

A

Dawn will be elevated at 0200 and somogyi will by hypoglycemic at 0200

Dawn you increase the insulin at bedtime and somogyi you decrease the bed time insulin

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42
Q

What is the most common complication in DM pts treated with insulin

A

Hypoglycemia ( BG less than 60)

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43
Q

Drinking ETOH triggers what physiological glucose responce

A

Gluconeogenesis ( this can be a problem for T1DM)

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44
Q

A pt presents with irratability and confusion, diploploa, fatigue, HA, and aphasia

What is the BG

A

Below 50

Anything below 50 can lead to LOC and SZR

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45
Q

What is the best Tx for hypoglycemia

A

PREVENTION!

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46
Q

What is the Tx approach to mild hypoglycemia

A

Eat or drink
Like 2-3 glucose tabs, 6oz of OJ, regular soda, 1/3 cup of raisins, or 5 lifesaver candies

Check glucose in 15 min, treat again if below a BG of 60

Aka 15-15-15

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47
Q

What is the Tx approach to severe hypoglycemia

A

If at home: Glucagon rescue kit

Inpt: 
IV glucose ( 50 ml of 50% glucose solution)

If IV glucose is not avail. Then use glucagon 1 mg injection

If no glucagon is avial,. Small amounts of honey, syrup, or glucose in a buccal pouch

Once pt is conscious then oral glucose should be given

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48
Q

What is often the initial presentation of T1DM

A

DKA

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49
Q

What are the RSK fxs to developing DKA

A

MC in T1DM

Recent infex
Lapse in insulin dosage
Truma, ETOH, steroids (glucocorticoids)
Idiopathic (WE DONT KNOW)

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50
Q

What are the sick day guidlines for prevention of DKA

A

Test urine ketones every 2-4 hours
Pts is to call if urine ketones for more than 6 hours

Test BG regularly
At least 4x a day
Pt is to call if BG is greater than 250 for more than 6 hrs

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51
Q

What is a typical BG in DKA

A

350-900 with postive ketones (uring and serum)

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52
Q

What is typical BG in DKA

A

250-900 with postive ketones

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53
Q

What is the 1st step in the treatment of DKA

A

FLUIDS!

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54
Q

What is the lab that can test for microalbuminiuria

A

Morning spot urin albumin.creatine ratio

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55
Q

What is the most common type of DM neuropathy

A

Distal symmetric polyneuropathy

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56
Q

Charcot joint is specific to what kind of neuropthay

A

Distal symmetric

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57
Q

What type of neuropathy is associated with CN III palsy

A

Isolated

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58
Q

ED is a DM pt is what kind of neuropathy

A

Autonomic

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59
Q

What is papaverine used for

A

Erectile dysfunction

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60
Q

What is the leading cause of death in DM pts

A

HEART DISEASE/ MI

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61
Q

Does a diabetic female have the “female advantage” of reduced heart disease risk ?

A

NO! DM pts have 3-5x increased risk of HDz

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62
Q

What is the BP goal for DM pts

A

Less than 140/90

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63
Q

What is the MGMT for PVD in a DM pts

A 
Keep BP below 140/90 (ACE, ARB) 
(Remember BB mask glyccemia) 
Low dose Asprin (81mg) 
Stop smoking 
STATINS! (LDL less than 100 or 70 2nd prevention, HDL greater than 40, TG less than 150)

Regular excercise program.

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64
Q

What is the minimum requiirment for foot checks on DM

A

Annually

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65
Q

What does a DM consult require at every visit

A

BP, Pulse, H/W, Foot exam !

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66
Q

What is the Fasting CMP goal for gl

A

110-120

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67
Q

When should microalbumin be checked in a DM1 and DM2

A

DM1 after five years then annually

DM2 at Dx and then annually

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68
Q

What all do DM pts need at encounter appointment

A

Statin, Glycemic meds, Baseline ECG, ACE or ARB, BG checking kit, Med bracelets +/- glucagon rescue kits

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69
Q

What is the role Ca2+

A

Muscle contraction and nerve function

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70
Q

What stimulates and suppresses PTH

A

Fallin free Ca2+ levels stimulate and high levels inhibit

Hypo magnesium stimulates PTH and hypermag inhibits

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71
Q

A pt presetns with hypercalcemia and VERY high PTH levels

Think ..

A

Parathyroid Cancer

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72
Q

What is a autosomal dominant hypercalcemia disorder assoc with lifelong hypercalcemia with hypocalcuria

A

Familillia hypocalciuric hypercalcemia

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73
Q

What kind of parathyroid substance do malignant pts/ tumors secrete

A

PTH related protein, presents with severe hypercalcemia

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74
Q

A pt with severe hypercalcemia and a low PTH, that should prompt what other lab

A

PTHrP

Find the cancer

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75
Q

What is the most concerning reason for low PTH

A

Cancer (SQUAMOUS cell of the lungs, not small cell)

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76
Q

What is the triad of milk alkali syndrome

A

Hypercalcemia, Met alki , and AKI

Due to large amounts of calcuim ingestions

Pt presents with LOW pth

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77
Q

How does thyrotoxicos effect bone growth

A

High bone turn over/. Resorbtion

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78
Q

What is the tx approach to Hypercalcemia

A

Mobilaztion, fluid maintenance

Furosemide- produces caluresis

Avoid thiazid diuretics

Avoid vitamins A and D ( Fat soluable and can lead to AKI)

Avoid Antacids- vitamin rich

Dialysis may be benificial for CHF, HyperK, or renal failure pts

Parathyroid ectomy

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79
Q

What is the role of IV bisphosphate

A

Used to treat hyperCa2+

Temp inhibits bone resorption

Used for prolonged immobilization, malignancy, or hyperparathyroid

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80
Q

How often should pts with hypercalcemia have thier levels checked

A

AS/s pts calcium and albumin 2x per year

Check renal function 1x year

Check bone denisty q1-2 years

Consider estrogen replacement in post menopausual

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81
Q

What is the most common cuase of hypoCa2+

A

CKD

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82
Q

Elderly pts with hypoCa2+ and an elevated PTH has what common vitamin deficiency

A

Vit D

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83
Q

What is a corrected serioum calcium level

A

Serum Ca +0.8(4-serum albumin)

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84
Q

A pt presents with parasthesias, muscle cramps, irratabilty, confusion, anxiety, depression , SZR, tetany
Think

A

Hypocalcemia

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85
Q

What is chvosteks sign

A

Hypocalcemia

Tapping on the facial nerve causes a spasm

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86
Q

What is trousseuas phenomenon

A

Hypocalcemia

Carpal spasm when BP cuff is inflated above SBP for 3 minutes

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87
Q

What does the Mnemonic CATS go numb

Stand for

A

Hypocalcemia

Convulsions
Arrythmias
Teatny
SZR

Nubness

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88
Q

What is the testing approach to Hypocalcemia

A

1 check serum calcium
2 in true hypocalcemia scheck ionized CA is also low
3 Check mag levels, correct if necessary
4. Check pTH level
5. Check vit D level

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89
Q

A pt presents with hypocalcemia, with short stature, round faceis, and short 4th and 5th metacarslas.. think

A

Albrights heriditary osteodystrophy

May have both PTH resistnace, and TSH, FSH and LH resistnace

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90
Q

What are the two types of Vit D deficiency

A

Child: rickets
(Prro bone formation at growth plates)

Adult: osteomalacia
(Abnormal bone mineralization
Major clinical finding: bone pain
X-rays of long bones may reveal thin radiolucent lines perpendicular to the cortex (‘Looser’s lines’)

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91
Q

What are two causes of hypomag

A

ETOH abuse or malabsorption

Both can lead to hypoparathyroidism

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92
Q

What is the tx approach to inpt hypocalcemia tetany (severe)

A

Airway MGMT

Correct the mag 1st with IV mag sulfate

Then correct hypocalcemia with calcium gluconate

Follow up with oral calcium and vit d ASAP with 1-2 g per day with meals

Transplantation of cryopreserved parathyroid tissue removed during prior surgery restores normocalcemia in about ¼ of patients

IT IS IMPORTANT to maintain Seurm Ca level lightly low (8.0-8.6)

F/u monitor CA levels q 3months

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93
Q

Each year, the metabolic drive decreases by what percent?

A

2%

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94
Q

What provides the most convenient population-level measure of overweight and obesity currently available

A

BMI

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95
Q

What the NML hip to waist ratio in men and women

A

Less than 1 in men , and less than 0.85 in women

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96
Q

Obese pts underestimate the amount of food eaten by..

A

30-40%

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97
Q

What are the later in life complications on prader-will syndrome

A

Short Stature, OSA, morbid obestity

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98
Q

What is the W/ for obestity

A

Good FMHx

Age of onset

Ocupation Hx

Previous wt loss attempts and methods

Eating/ Behaviour

ETOH/ Smoking Hx

Depression/ Eating D/O?

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99
Q

What is a common cause of 2ndary obestity

A

Hypothyroidism! (TSH/T4)

Cushing Syndrome
Suspect with rapid onset in an otherwise health pt

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100
Q

What effect does semistarvation have on wt gain

A

Semi starvation can cause wt gain fue to basal energy expendeture decrease ( Famine and Fasting States)

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101
Q

What is the proper exercise regiment for obestity

A

150 minutes of moderate intensity exercise (tennis or brisk walking)

75 minutes of vigorous (high) intensity exercise (jogging or swimming laps) OR
An equivalent combination of moderate and vigorous exercise, with each episode lasting more than 10 minutes

Weight resistance is recommended at least twice per week

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102
Q

Why should you not use lorcaserin for wt loss

A

Pulled from the market in 2020 due to assoc cancer

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103
Q

A pt is taking phentermine for 4 weeks and has seen no wt loss, what is the next step

A

D/c the medication and attempt a new approach

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104
Q

If a pt is taking a MAO-I should they be started on wt loss drugs

A

NO or use caution

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105
Q

What is the ADE of Sleeve gastrectomy

A

Ghrelin levels may be decreased for up to 1 year post srgry

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106
Q

What are the typical complications of bariatric srgry

A

Peptic ulcers
Outlet stenosis
Leakage leading to spesis
Staple disruption

Needs for surgical revision 
Wound problems 
Abdominal wall hernias 
Gallstone common 
Pulmonary Edema 
Dumping syndrome
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107
Q

When should obestity pts be referred

A

BMI > 30 (or >27 with weight-related comorbidities)
—Obesity medicine specialist

BMI > 40 (or >35 with weight-related comorbidities)
—Bariatric surgeon

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108
Q

What are the levels of the adrenal cortex from outer most layer to inner most layer

A

GFR COR

Glomerulus
Fasciculata
Reticularis

Cortex

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109
Q

What is the pathphsy of hirsutism

A

Androgen production acts on sex hormone responsive hair follicles. Converting vellus hairs to terminal hairs

Androgens also increase sebaceous gland activy, which leads to excess acne and oily skin

110
Q

Half of women with hirsutism have what underlying condition

A

hyperandrogenism

111
Q

What are the two types of Hirsutism

A

Elevated levels of circulating androgens (pathology) – will have elevated labs

OR

Increased sensitivity of hair follicles to normal levels of androgens (familial/genetic) – will have normal labs

112
Q

What is the Ferriman-Gallwey score

A

Hirsutism Can be quantitated using Ferriman-Gallwey score

Hirsutism is graded from 0 to 4 in 9 areas of the body

Max score = 36

Score of ≥8 defines hirsutism!!!!

Severe: >15

Moderate: 8-15

113
Q

A score of greater than 8 on the Ferriman-Gallway score=

A

Hirsutism

Greater than 15 is severe

114
Q

What are the major androgens in females that cause Hirsutism

A

DHEA, Androstenedione (from the Ovaries/ Adrenals), Testosterone

115
Q

Peripheral conversion of androstenedione leads to what

A

Terstosterone

116
Q

Free testosterone is converted to DHT by what in the skin

A

5a-reductase

117
Q

What does DHT stimulate in the skin

A

Hair follice growth

118
Q

What are the 5 causes of Hirsutism

A

Idiopathic/ Familial

Polycystic Ovarian Syndrome

Steroidgenic enzyme defects

Neoplastic D/o

Pharmecologic

119
Q

Familial Hirsutism is most common in what demographic

A

medeterrainan and Middle eastern

120
Q

A female pt from the middle east presents with normal androgen levels, with slow progression of hair growth at the onset of puberty
NML menses,

What is this type of hirsutism

A

Familial

121
Q

What is the most common cause of Hirsutism in women

A

Polycystic ovarian syndrome

Its often familial and is transmitted bu an autosomal dominatant trait

122
Q

What is the triad of criteria that must be meat to dx polycystic ovarian syndrome

A
  1. androgen excess with clinical hyperandrogenism or elevated testosterone

2 - ovarian dysfunction or polycystic ovary morphology
—Oligomenorrhea/amenorrhea with anovulation (50%)
—Infertility

3 - absence of other causes of testosterone excess
(Pregnancy, Thyroid D/o, Cushings)

123
Q

What are the two etiologies of steriodgenic Hirsutism

A

Congenital adrenal hyperplasia (21-hydroxylase deficiency)

Cortisol def=increase ACTH=hyperplasia

124
Q

What is classic vs nonclassic steroidgenic hisrutism

A

Classic: (complete deficiency of 21-h) ambiguous genitalia, may become virilized unless treated with corticosteroids

Non-Classic: (Partial 21-hydroxylase deficiency)
2% of women with adult-onset hirsutism
—PCOS and adrenal adenomas are more likely to develop in these women
—Features (non-classic CAH): Irregular menses since menarche, Gradual onset of hirsutism

125
Q

What are the three causes of neoplastic Hirstism

A 
Ovarian tumors 
(Arrhenoblastomas, Sertoli-Leydig cell tumors, dysgerminomas, and hilar cell tumors)

Adrenal Carcinoma leading to cushings or hypogonadism!

Pure androgen secreting tumors (rare)
(50% are malignant)

126
Q

A female pt presents with Hirsutism, onset was outside to perimenarchal periodm, and they have rapid and severe hair growth, the have recent onset of menstral irregularity

What kind of hirsitsm is this

A

neoplastic (investigate for a tumor or cancer)

127
Q

What are 5 drugs that can cause hirsutism

A

Minoxadil

Cyclosporine

Phynetoin

Anabolic steroids

Norethindrone (contraceptive)

128
Q

What is virilizzation

A

Frontal balding (androgenic alopecia)
Increased muscularity
Clitoromegaly
Deepening of voice

Consider a NEOPLASMIC source

129
Q

What are the imporatant labs in Hirsutism

A

Labs: serum androgen testing is mostly useful to find the adrenal/ovarian neoplasms

Free and total testosterone—most important!!!

Androstenedione

DHEA-S

130
Q

If a female pt have a Total T above 200 or a Free T above 40, what exam must be performed

A

Pelvic exam and US !

If both are negative then order a bilateral adrenal CT scan

131
Q

A pt with a serum androstenedione of greater than 10000 suggest what…

A

Ovarian adrenal neoplasm

(Perfrom a pelvic exam AND bilateral adreanl CT

132
Q

A pt with a serum DHEA S greaer than 700mcg/dl suggest what

A

An adreanl source of excess androgens (hirsutism)

(Perform bilat adrenal ct scan)

133
Q

What is a NML androstenedione level

A

0.7-3.5

134
Q

What is a NML DHEA S level

A

Less than 10

135
Q

What is the Tx approach to Hirsutim

A

If its neoplastic then cut it out
(Think postmenopuasal women with severe hirsutsim)

Spirinolactone can reduce Hirsutism (often combined with OCPS)

Flutamide (combined with OCPS) (nonsteroidal antiandrogen)

Finasteride (5a-reductase inhibitor)
(Use only in postmenopausal women)
(Can cause genitalia problems in fetuses)

Oral contraceptives (estradiol) (progesterone) 
(DVT RSK!)

Metformin (if PCOS) (use with spirinolcatone)

Simvastatin (use with OCPs)

Clomiphene- Used in PCOS for infertitlity

136
Q

OCP are C/I in what pts

A

smokers, migraine with aura, age 39+, HTN, Hx of DVT

137
Q

What is vaniqa cream

A

Vaniqa cream (eflornithine HCl)

Topical which reduces hair growth
4-8 week until improvement…sxs return when d/c
Works well with laser tx

138
Q

What are the two things that convert testosterone

A

Testosterone exerts effects directly on androgen receptors, and is also converted to either
1) estradiol by the aromatase enzyme
0r
2)to DHT by the 5 alpha reductase enzyme

139
Q

What is the pathway that secretes the negative feedback inhibin molecule

A

GnRH (hypothalmus) goes to the AntPit, FSH is released which goes to the sertoli cells, whcih secrete Inhibin, that then shuts off the Hypothalmus and AntPit

140
Q

LH woks on the leydig cells to make what

A

Testosterone

141
Q

If a male pt is over 70 years old, what is the cutoff for hypogonadism

A

Less than 30 on a free T test

142
Q

What is HYPERgonadatrophic Hypogonadism

A

Low test with elevated LH and FSH

Primary hypogonadsim

143
Q

What is HYPOgonadatropic hypogonadism

A

Low test and low FSH/LH

Secondary Hypogonadism

144
Q

A pt with a normal T level and elevated LH and FSH, think

A

LH and FSH should go down if the Test is normal or elevated, so think of a defect in androgen resistance

145
Q

A male pt presents with delayed puberty, an deminished libido./erections

+fatigue, depression, and reducced excercise tolerance

May have small or NML testes

Think

A

Hypogonadsim

Order a Free T level and A LH/FSH level

146
Q

A pt presnts at around age 14-15 with poor muscel development, high pitched voice, and sparse axiallary and pubic hair
With lack of sexual differentiation

Think?

A

T deficieny at puberty onset

147
Q

What is the effect o testosterone on growth plates

A

Normally testosterone closes epiphyses

lack of testosterone causes increased long bone growth

148
Q

A 30 year old male presents with decreased libido, impotence, low energy, with fine wrinkilin around the eyes and mouth

Testes may be nomral or small in size

Think

A

Post-pubertal testosterone deficiency

149
Q

What are the 3 cuases of congenital primary hypogonadism

A

Klinefelter syndrome

Cryptorchidism

Bilateral anorchia

150
Q

What are the 4 causes of aquired primary hypogonadism

A

Infection (mumps etc)

Aging

Trauma

Chemotherapy/ radiation therapy

151
Q

A pt has seminiferous tubule dysgenesis

Think

A

Klinefetlers

152
Q

A pt has recently had a child with a 47XXY deficinecy but cant remember the name, what is this child at risk of developing and what is the condition

A

Klinefelters

Breast cancer—increased incidence
Chronic pulmonary disease
Varicosities of legs
Diabetes mellitus/impaired glucose tolerance (27% of patients)
Osteoporosis
153
Q

What is the PE appraoch to testing for cryptorchidism

A

Must be distinguished from retractile testes

Examine in warm, relaxed environment

Begin exam at inguinal canal & move downward

Look for asymmetry & contralateral hypertrophy

L side affected more!

154
Q

What is the Tx approach to Cryptorchism and what do we no longer do..

A

Orchiolexy is the tx at 12-24 months

We no longer do a hCG injection.

155
Q

Does orchioplexy eliminate the risk of testicular cancer in cryptorchid pts

A

No 2-3 fold risk still remains

156
Q

If you were to give a pt with bilateral anorchia a hCG test (no longer used) what would happen

A

You would see no increase in the testosterone level

An increase would mean they have undescended testes

157
Q

You are testing a pt for hypogonadism and the labs show a low T and low FSH/LH

Think

A

Hypothalamic Pituitary abnml
(2nd dary cause)

Order a prolactin level and Pit MRI

158
Q

You order a LH/FSH level and a T level and it comes back with low FSH/LH and Low/NML Test

On PE you do not find testes in the scrotum

What is your appraoch

A

THink Primary test abnomrality

No testes= hCG stimulation

Increased Test= Cryptorshidsm
No Test response= Anorchia

159
Q

You order a LH/FSH level and a T level and it comes back with an elevated FSH/LH and Low/NML Test

On PE you DO find testes in the scrotum

What is your appraoch

A

Primary Test abmnormality

Testes present, so check size and consistency

Small and firm= possible klinefelters ( order a karyotype)

NML or Soft= Acquired primary hypogonadims ( mumps, ect)

160
Q

How should Test replacement be admin’d

A

IM injections q 2-3 weeks

Or transdemral patches

Can use topical on the thighs, but caution with transfer to females

Can also be admin’d buccal q12 hrs
(Do not hcew or swallow)

Intranasal and oral are also available
(I/N has severe URI s/s)

161
Q

What are the ADE of testosterone replacement

A 
Acne
Decreased HDL levels
Gynecomastia—IM 
Erythrocytosis—IM 
OSA
162
Q

If a pt has active prostate cancer, can they get T replacement Tx

A

NO!

163
Q

What is the age cut off for T replacemnt Tx

A

Cant be younger than 13

Avoid due to premature epiphyseal closure and short stature

164
Q

A pt presetns with Eunuchoid proportions, gyno, and prepubertal testes are small and rubery

Think

A

Kallmans

165
Q

What is the MC cause of hyperprolactinemia

A

Pituitary adenomas

Inhibits normal GnRH release
Inhibits the action of testosterone
Decreases the effectiveness of LH

166
Q

WHat are some common causes of secondary hypogonadism

A

Obestiy (BMI>40)
Renal failure, CHF

Aging 
ETOH use 
Marijuana 
Cushings 
Hypothyroid 
Cancer 
AIDS
167
Q

A female pt presetns with eleveated levels of FSH/LH and elevated T

Think

A

Complete androgen insensitivity

External female genitalia is observed—appears a normal pre-pubertal GIRL

There is no uterus or fallopian tubes
There are no male accessory sex organs, testes are cryptorchid

Abnormal receptors in the pituitary gland do not recognize testosterone so development proceeds as if there is a lack of testosterone

168
Q

IF testosterone is not recognized in the receptor, what is it converted to

A

Testosterone is not recognized so it is converted to estradiol by aromatase in adipose tissue

Happens in complete androgen insensitivity

169
Q

What is the approach to Tx for Complete or Incomplete Androgen Insensitivity Syndrome - Testicular Feminization

A

There are no Tx to restore androgen receptors

Removal of intra-abdomial testes to reduce malignancy rsk

Estrogen tx if desired

Family counselling for gender

170
Q

A pt presents with blind vaginal pounch, amenorrhea, and an absent uterus, has well breast development

You order a panel and it comes back with high FSH/LH and HIGH T

Think

A

Androgen Insentisty syndrome

Testes are in the abdomin, but the pt developed as a girl

171
Q

What is needed of rmasculinization of external genitalia in utero

A

DHT

Which required 5-a-reductase

172
Q

At what week gestation is 5-a-reductase needed for development of target organs

A

8-12

173
Q

A female child pt has a penis development at age 12 has what condition

A

5-alpha reductase deficiency

174
Q

What is a NML serus Ca2+ level

A

8.5-10.5

175
Q

What is the function of PTH

A

Stimulates resorption (or dissolution) of bone to increase calcium and phosphorus in circulation in the blood

Stimulates renal tubular reabsorption of calcium and inhibits phosphate reabsorption (increases serum calcium)

Indirectly stimulates intestinal activation of vitamin D (Increases calcium absoprtion)

Vitamin D enhances intestinal absorption of calcium

176
Q

What is the role of VIT D on calcium and phosphate

A

Vitamin D increases calcium and phosphate absorption from the intestines

177
Q

What is the role of calcitonin

A

Inhibits osteoclaast activity, (decreasing calcium breakdown from bones)

Increases calcium storage in bones

increase renal excrteion of Calcium

178
Q

What is the most common cause of HyperCa2+

A

Primary hyperparathyroidism – most common cause

—Parathyroid adenoma (80%),
—parathyroid hyperplasia (20%) or —parathyroid cancer (less than 1%)

179
Q

A pt presents with hyperCa2+ and a low PTH

Think

A

Secondary malignancy (not parathyroid CA)

180
Q

A calcium level above 14 is an indication of

A

MAlignancy

181
Q

What effect does hypercalcemia have on the EKG

A

short QTi

182
Q

What is Stones, bones, groans, moans, and overtones

A

HYPERcalcemia

Stones: kidney stones, nephrocalcinosis, thirst, polyuria, metabolic acidosis

Bones: bone pain and fractures – osteitis fibrosa cystica

Groans: anorexia, dyspepsia, constipation

Moans: myalgia, proximal muscle weakness, joint pain

Overtones: depression, memory loss, confusion, lethargy, coma

183
Q

If a pt presents with an increased PTH think

A

Parathyroid adenoma
Hyperplasia
Or CA

184
Q

A pt presents with High serum calcium
High urine calcium and a high PTH

Think

A

Parathyroid adenoma (MCC)

185
Q

What is the imaging approach to parathyroid ademonas

A

Imaging not necessary
May be used prior to surgery

U/S can be used or CT/MRI if negative US

186
Q

What are the indications for SRGYRY in a pt with Hypercalcemia and aparathyroid adenoma

A

If + stones, bones, groans, overtoans

Or if Ca2+ level is above 11.5 
Urine Ca level greater than 400 
CrCl is less than 60 
Nephrolithiasis 
Severe Osteoporosis 
IF the pt is level than 50 y.o 
Pregnant pts with CA >11
187
Q

A pt has elevated Calcium levels with an elevated PTH, BUT is aS/s

What is the f/u criteria

A

Observation:
Follow-up every 6 months
BP every 6 months
Serum Calcium every 6 months

Urine Calcium yearly
Kidney function yearly

Bone density every 2 years

188
Q

What is the Tx approach to Parathyroid hyperplasia

A

Subtotal parathyroid removal

189
Q

What is the Tx for PArathyroid Cancer

A

Tumor resection along with the affected thyroid lobe

190
Q

What is the MOA of PTHrP

A

PTH related protein

Causes bone resorption and hypercalcemia similar to the action of PTH

191
Q

Taking too much vitamin D can do what to PTH

A

Suppress it

192
Q

What are some common causes of excess endogenous Vit D production

A 
Lymphomas 
Sarcoidosis 
TB 
Histoiplasmosis 
Coccidiomycosis
193
Q

Immobilization in the ICU has waht effect on calcium

A

Marked resorption of calcium from bone
Seen in ICU patients

Suppresses the PTH with a HIGH calcium level

194
Q

What is the TxOC in malignancy associated hypercalcemia

A

IV bisphosphonates

195
Q

How does hypoalbunimeia effect serum calcium

A

Hypoalbuminemia is a common cause of low total serum calcium

Hypocalcemia due to hypoalbuminemia is not clinically significant, if ionized Calcium is normal

196
Q

Severe hypocalcemia requires what intervention

A

IV calcium gluconate

197
Q

A pt presents with hypocalcemia yet an elevated PTH

Think

A

PTH resistance

The receptors are not working in the renal receptors

Bone breakdown continues to happen by the renal system pees out the calcium

Leasd to patho fxs, cyctis lesions in the bones

198
Q

What are three medications what can decrease Vit D processing

A

Isoniazid, rifampin, phenytoin

Can lead to hypocalcemia with elevated PTH

199
Q

Sprue and Chorns Dz effects vit d how

A

They are bot malabsorption issues that can lead to hypocalcemia with elevated PTH

200
Q

If a pt presents with hypocalcemia , and low PTH and a elevated VIt D level

Think

A 
VitD resistance 
(Genetic defects in VIT D metabolism)
201
Q

What is the aS/s tx to hypocalcemia

A

Oral calcium supplements (800-1000mg)

Oral vitamin D supplements (1000-5000IU)
(Individuals resistant to vitamin D will not benefit)

Increase exposure to sunlight

Goal of treatment is to keep the serum calcium level in the low-normal range

202
Q

What is the most common fx of osteoporosis

A

Vertebral fx

203
Q

In pts older than 50 or hypogonadism pts … alwasy look for what bone problem

A

Osteoporosis

204
Q

What does a T score (DEXA) of -1.0 to -2.5

A

Osteopenia

205
Q

What does a T score (DEXA) of -2.5 tell you

A

Osteoporosis

206
Q

A T score of -2.5 with a fracture means

A

Severe Osteoporosis

Can also just be a Tscore below -3.5

207
Q

When can bisphophonate be used for osteoporosis

A

Is a pt has a DEXA T score from -1.5 to -2.5

Or a 10 year hip fx risk greater than 3%

Or major fx risk greater than 20%

208
Q

Drugs that end in -Dronate

A

Bisphophonates

209
Q

What are the ADE of bisphosphonates

A

Oral: nausea, CP, hoarseness
(Don’t use oral if pt has Barrett esophagus)

IV: acute-phase response lasting several days
Fever, chills, flushing (20%)
MSK pain(20%)
—Loratidine helps
N/V/D (8%)
Fatigue, dyspnea, edema, HA, dizziness (22%)

210
Q

If a pt has Barretts esophagus and osteoporosis

What is the Tx approapriate

A

IV!!! Bisphosphonates

Do not use oral meds

211
Q

What do Beta cells of the pancreas secrete

A

Insulin

212
Q

What do alpha cells of the pancrease secrete

A

Glucagon

213
Q

What do delta cells of the pancreas secrete

A

Somatastatin

214
Q

What is MODY DM

A 
Non-insulin dependent DM
Age of onset: <25 yrs 
Non-obese
Due to impaired glucose-induced secretion of insulin
Autosomal dominant inheritance
215
Q

A pt presents with elevated TGs, Low HDL, and elevated LDL, HTN, and Elevated CRP, has hyperruecemia, and abdonmial obesity

Think

A

metabollic syndrome

216
Q

A pt presents with blurred vision , and poly dypsna, polyuria, and poly phagia, and recent wt loss

+/- postural HOTN, parasthesia, Ketoacidosis
Think

A

T1DM

217
Q

What are 3 chronic skin infections associteed with DM2

A

Candida, General Pruritis, and Vaginitis

218
Q

What is Acanthosis Nigricans

A

Darking of skin folds seen in type 2 DM

From insulin resisstnace

219
Q

What is the criterai to screen for DM is aS/s adults

A 
Any pt that is overwt or obese 
African america, latino, or native america 
History of CVD 
HTN 
HDL less than 35 
TriGs over 250

Women with polycyctic ovarian syndrome

Any pt with prediabetes should be screened annually

Women with GDM q 3 years

220
Q

If a pt has ketonuria greater than 3.0..

they need..

A

ADMIT!

221
Q

What can cause falsely low A1C

A

Acute blood loss, anemia, hemolysuis, recent transfusion

Heavy bleeding

222
Q

What can cause falsely high A1C

A

Iron, B12, or folate deficiency

Liver/Kidney Failure

223
Q

What is the tx approach to a pt with pre diabetes

A

Diet and excercise

224
Q

What is the approtiate counselling to DM pts and ETOH consumption

A

Alcohol use in moderation:

Men: not more than 2 drinks/day

Women: not more than 1 drink/day

Drink = 12 oz. beer, 5 oz. wine, or 1 ½ oz. spirits = 2 fat exchanges

Warn patient about hypoglycemia

225
Q

When should DM pts receive thier vax

A

Influenza—annually

Pneumococcal vaccine
At diagnosis

Repeat at age 65 (if initially given prior to 65)

226
Q

All Dm pts should receive what medication to prevent ASCVD

A

ASA and statins And ACE/ARBS

227
Q

What is the effect of metformin on HOgl and wt

A

HOgl neutral

With slight wt loss

228
Q

What is the MOA of metfromin

A

Suppresses hepatic gluconeogenesis;

increases hepatic insulin sensitivity

Metformin (Glucophage) –1st line therapy for new DM2

229
Q

What is the HOgl and Wt effects of DPP-4s

A

Neutral to both

230
Q

What is the major ADE of DDP-4

A

Pancrreatitis

231
Q

What are the HOgl and Wt effects of GLP-1

A

HOgl neutral

Wt loss!

232
Q

How should GLP-1 be used as part of DM2 tx

A

Add on tx ONLY!

With either metformin or a SU

233
Q

What is the major ADE of GLP-1

A

Thyroid Cancer

234
Q

What is the HOgl and wt effects of SGLT-2

A

HOgl neutral

Wt loss!

235
Q

What SGLT-2 has been approved for reducing CV risk in DM2 pts

A

Empaglaflozin

236
Q

What is the HOgl effect and wt effect of TZDs

A

HOgl neutral and WT GAIN!

237
Q

What are the major ADE of TZDs

A

Heart problems, edema, Osteoposris, angina and WT GAIN!

238
Q

What are the HOgl and wt effects of SUs and Meglitinides

A

Severe HOgl and WT GAIN!

239
Q

DO not use glyburide becasue it is long acting and has the most HOgl of the SUs

A
240
Q

What are the glucose goals in DM

A

preprandial 90-130

Postprandial less than 150

Ave. Bedtime gl 110-150

A1C less than 7 ( or 8 in eldery)

241
Q

What type of insulin is used for DKA tx

A

Regular (short acting)

242
Q

What is Lente insulin

A

intemediate acting ( NPH is aslo in this class)

243
Q

When should T1DM pts be referred

A

When to refer: Patients with type 1 diabetes should be referred to an endocrinologist for co-management with a primary care provider.

244
Q

Where can you NOT inject insulin

A

Within 2inch of the navel/ umbilicus

245
Q

What is the insulin of choice in an insulin pump

A

Lispro

246
Q

How should weekly insulin adjumstmens be titrated in type2DM

A

Increase insulin dose weekly

Increase 4U if FBG >180mg/dl
Increase 2U if FBG 120-180mg/dl

247
Q

Addisons pts with DM are at an increased rsk of

A

HOgl

Due to ortisol deficiency

248
Q

Remember BB mask the effects of HOgl

tachyardia (bb block this)
Palpatatoins (bb prevent this)
Tremors (bb symopathetic tone)
Sweating

A
249
Q

DKA Pathogenesis

A

Insulin deficiency

glucose cannot enter cells for use

rapid mobilization of energy stores in muscle/fat

Increased flux to the liver of: amino acids for conversion to glucose and fatty acids to ketones.

250
Q

What is the mainstay of tx for dka

A

IV fluids, insulin, potassium, bicarb +/-, ABX +/-

251
Q

What is the serum gl goal in a DKA pt

A

250-300

252
Q

If a pt has DKA with a pH less than 7.0

What adjunct should be considered

A

Bicarb

253
Q

What are the 2 Rx that can precipitate HHS

A

Thiazide diuretics and glucocorticoids

254
Q

What is the BUN level in HHS

A

Greater than 100

255
Q

What is the major cause of death of T1dm and T2dm

A

T1: Major cause of death – complications from end stage renal disease

T2: Major cause of death – macrovascular disease leading to MI and stroke

256
Q

What are the major ocular complications of DM

A

Cataracts, reinopathy, Gluacoma

257
Q

What is the MC cause of visual impariment in DM2

A

Non proliferative Retinopathy

Microaneurysms
Dot hemorrhages
Exudates
Retinal edema

258
Q

What are cotton wool spots in the retina

A

Growth of new capillaries due to retinal hypoxia

Increased risk of macular edema & retinal detachment

259
Q

What is the tx approach to DM retinopathy

A

BLOOD gl control and smoking cessation

Laser tx are available, and bevacizumab

260
Q

When should you refer a pt with Retinopathy

A

DM pt with sudden loss of vision or retinal detachment
—Emergent to ophthalmologist

Proliferative retinopathy or macular involvement
—Urgent to ophthalmologist

Severe nonproliferative retinopathy
—Early referral to ophthalmologist

261
Q

What is the MC cause of ESRF (CKD)

A

DM nephropathy

262
Q

What is the assay of choice for microalbuniimia

A

A morning spot urine screen for the albumin/creatinine ratio is the assay of choice

If albumin/creatinine ratio is 30-300 mcg/mg, confirm with at least 2 of 3 positive collections performed within 3-6 months before diagnosing

263
Q

What is the tx approach to microalbunima

A

STRICT gl controll (6.5)

ACE or ARBs

Low protein diet

Monitor Albumin/Cr ration q 6 months

264
Q

Can DM pts get contrast

A

Avoid in pts with CrCl above 3

265
Q

What are the Rx options to distal symetric polyneuropathy

A 
Nortriptyline 
Gabapentin (Neurontin)
Pregabalin (Lyrica)
Duloxetine (Cymbalta)
Capsaicin cream
Lidocaine patches
266
Q

What are the MC envolved nerves of Isolated Peripheral Neuropathy

A

Femoral or Cranial nerves

267
Q

A pt presetns with hyperseniticity to light touch, and a severe burning pain at night

What kind of neuropathy is this and what is the Tx approach

A

painful DM neuropathy

Tx: amitriptyline (TCAs)
gabapentin (anticonvulsants)
duloxetine (SNRI) (Cymbalta)
Capsaicin cream

268
Q

What is a Rx option for GI system neuropathy in DM pts

A

Metoclopramide

269
Q

What is the treatment option for postmenopausual women with hirsutism

A

If severe then surgery

Rx option: Finasteride

Risk of ambiguous genitalia in 1st trimester exposure
So only use it in women that cant get pregnant

270
Q

What is the recommendation of using OCPS in pts with hirsutism

A

Use low dose estradiaol

IPAP JUNIOR SEM. (43 decks)

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