Endo Block II Flashcards
What is the MOST COMMON medical d/o
Obesity
A BMI of 18.5 or less is…
Underweight
What is a normal BMI
18.5-24.9
What is an overwieght BMI
25-29.9
What is Class I obesity BMI
30-34.9
What is class II obesity BMI
35-39.9
What is the class III obesity BMI
Any BMI greater than 40
What are the wiast measurments for high risk metabolic syndrome
Men greater than 40 in or women greater than 35
What two cancers are highly assoiated with obestity
Breast cancer and Uterine Cancer
What is prader-willi syndrome
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
An infant presents with almond shaped eyes, norrowed bifrontal diameter and a thin upper lip with difficult feeding
Think
Early Stage of Prader-Willi syndrome
What is the key to wt loss
Behavior modification
When can pharmicological intervention be indicated in pt with obestity
BMI >30
Or
BMI> 27 with HTN, DM2, or CVD
What is orlistat
GI agent wt loss mediaction
inhibits intestinal lipase & reduces dietary fat absorption
Common SE: oily stools, diarrhea, fecal incontinence, reduced fat-soluble vitamin absorption
What is the relationship between orlistat and vitmains ADEK
Decreaded absoption of fat soluable vitamins
What is phentermine
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
What is buproprion/ naltrexone
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
What is liraglutide
-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
What are the general C/I for the use of wt loss medications
Uncontrolled cardiovascular disease
Pregnancy and/or lactation
History of psychiatric disease
Age < 18 years
Use of certain incompatible medications (monoamine oxidase inhibitors - MAOIs)
What is the indication for bariatric surgery
BMI greater than 40, or BMI greater than 35 with HTN, DM2, or CVD
What is a Roux-en-Y surgery
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
What are the cells in the testes than make sperm
Sertoli cells
When should free testosterone be measured
First thing in the MORNING when they are NOT fasting
What testosterone level is hypogonadism
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)
Failure to enter puberty before what age…. Is hypogonadism
14
What is the difference between early and late prenatal testosterone deficiency
In early, they have ambigious genitellia and in late prenatal they have micropenis or cryptorchidism
What does eunichoidal porpotions mean
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
What is the most common autosomal abnm in males
Klinefelters (47XXY)
Assoc with seminiferous tubule dysgenesis
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
Klinefelter Syndrome
If testes are left undecended in cryptorchidsm.. what is the pt at an increased rsk of
Infertiliy and testicular cancer
When should T levels be checked after initiating Test treatment
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
What is the most common form of congenital hypogonadism
Kallmann Syndrome ( X linked inheritance)
A pt presents with anosmia and an impaired sense of smell, is a male and has low T and FH and LSH
Think
Kallmann Syndrome
A pt presents with well developed breast without a period, think of..
Complete androgen insufficiency or a 46XY male
What are the major endocrine hormones of the pancreas
Insulin, glucagon, somatastatin, gherlin
A pt presents with frequent vag candida.. think
DM2
What is C-peptide
Fragment of pro insulin, should mimic insulin levels
What does a serum fructonase measure
A 1-2 week look at the “A1c”
MNT can decrease A1C by
1-1.9% for DM1
Or 0.3-2% for DM2
How do you admin insulin to a DM2
Continue oral agents at same dose except Stop sulfonylureas,
Add single bed time dose, if not at target at daytime at day time dose.,
What is the difference between dawn and somogyi phenomenon
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
What is the most common complication in DM pts treated with insulin
Hypoglycemia ( BG less than 60)
Drinking ETOH triggers what physiological glucose responce
Gluconeogenesis ( this can be a problem for T1DM)
A pt presents with irratability and confusion, diploploa, fatigue, HA, and aphasia
What is the BG
Below 50
Anything below 50 can lead to LOC and SZR
What is the best Tx for hypoglycemia
PREVENTION!
What is the Tx approach to mild hypoglycemia
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
What is the Tx approach to severe hypoglycemia
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
What is often the initial presentation of T1DM
DKA
What are the RSK fxs to developing DKA
MC in T1DM
Recent infex
Lapse in insulin dosage
Truma, ETOH, steroids (glucocorticoids)
Idiopathic (WE DONT KNOW)
What are the sick day guidlines for prevention of DKA
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
What is a typical BG in DKA
350-900 with postive ketones (uring and serum)
What is typical BG in DKA
250-900 with postive ketones
What is the 1st step in the treatment of DKA
FLUIDS!
What is the lab that can test for microalbuminiuria
Morning spot urin albumin.creatine ratio
What is the most common type of DM neuropathy
Distal symmetric polyneuropathy
Charcot joint is specific to what kind of neuropthay
Distal symmetric
What type of neuropathy is associated with CN III palsy
Isolated
ED is a DM pt is what kind of neuropathy
Autonomic
What is papaverine used for
Erectile dysfunction
What is the leading cause of death in DM pts
HEART DISEASE/ MI
Does a diabetic female have the “female advantage” of reduced heart disease risk ?
NO! DM pts have 3-5x increased risk of HDz
What is the BP goal for DM pts
Less than 140/90
What is the MGMT for PVD in a DM pts
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.
What is the minimum requiirment for foot checks on DM
Annually
What does a DM consult require at every visit
BP, Pulse, H/W, Foot exam !
What is the Fasting CMP goal for gl
110-120
When should microalbumin be checked in a DM1 and DM2
DM1 after five years then annually
DM2 at Dx and then annually
What all do DM pts need at encounter appointment
Statin, Glycemic meds, Baseline ECG, ACE or ARB, BG checking kit, Med bracelets +/- glucagon rescue kits
What is the role Ca2+
Muscle contraction and nerve function
What stimulates and suppresses PTH
Fallin free Ca2+ levels stimulate and high levels inhibit
Hypo magnesium stimulates PTH and hypermag inhibits
A pt presetns with hypercalcemia and VERY high PTH levels
Think ..
Parathyroid Cancer
What is a autosomal dominant hypercalcemia disorder assoc with lifelong hypercalcemia with hypocalcuria
Familillia hypocalciuric hypercalcemia
What kind of parathyroid substance do malignant pts/ tumors secrete
PTH related protein, presents with severe hypercalcemia
A pt with severe hypercalcemia and a low PTH, that should prompt what other lab
PTHrP
Find the cancer
What is the most concerning reason for low PTH
Cancer (SQUAMOUS cell of the lungs, not small cell)
What is the triad of milk alkali syndrome
Hypercalcemia, Met alki , and AKI
Due to large amounts of calcuim ingestions
Pt presents with LOW pth
How does thyrotoxicos effect bone growth
High bone turn over/. Resorbtion
What is the tx approach to Hypercalcemia
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
What is the role of IV bisphosphate
Used to treat hyperCa2+
Temp inhibits bone resorption
Used for prolonged immobilization, malignancy, or hyperparathyroid
How often should pts with hypercalcemia have thier levels checked
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
What is the most common cuase of hypoCa2+
CKD
Elderly pts with hypoCa2+ and an elevated PTH has what common vitamin deficiency
Vit D
What is a corrected serioum calcium level
Serum Ca +0.8(4-serum albumin)
A pt presents with parasthesias, muscle cramps, irratabilty, confusion, anxiety, depression , SZR, tetany
Think
Hypocalcemia
What is chvosteks sign
Hypocalcemia
Tapping on the facial nerve causes a spasm
What is trousseuas phenomenon
Hypocalcemia
Carpal spasm when BP cuff is inflated above SBP for 3 minutes
What does the Mnemonic CATS go numb
Stand for
Hypocalcemia
Convulsions
Arrythmias
Teatny
SZR
Nubness
What is the testing approach to Hypocalcemia
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
A pt presents with hypocalcemia, with short stature, round faceis, and short 4th and 5th metacarslas.. think
Albrights heriditary osteodystrophy
May have both PTH resistnace, and TSH, FSH and LH resistnace
What are the two types of Vit D deficiency
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’)
What are two causes of hypomag
ETOH abuse or malabsorption
Both can lead to hypoparathyroidism
What is the tx approach to inpt hypocalcemia tetany (severe)
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
Each year, the metabolic drive decreases by what percent?
2%
What provides the most convenient population-level measure of overweight and obesity currently available
BMI
What the NML hip to waist ratio in men and women
Less than 1 in men , and less than 0.85 in women
Obese pts underestimate the amount of food eaten by..
30-40%
What are the later in life complications on prader-will syndrome
Short Stature, OSA, morbid obestity
What is the W/ for obestity
Good FMHx
Age of onset
Ocupation Hx
Previous wt loss attempts and methods
Eating/ Behaviour
ETOH/ Smoking Hx
Depression/ Eating D/O?
What is a common cause of 2ndary obestity
Hypothyroidism! (TSH/T4)
Cushing Syndrome
Suspect with rapid onset in an otherwise health pt
What effect does semistarvation have on wt gain
Semi starvation can cause wt gain fue to basal energy expendeture decrease ( Famine and Fasting States)
What is the proper exercise regiment for obestity
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
Why should you not use lorcaserin for wt loss
Pulled from the market in 2020 due to assoc cancer
A pt is taking phentermine for 4 weeks and has seen no wt loss, what is the next step
D/c the medication and attempt a new approach
If a pt is taking a MAO-I should they be started on wt loss drugs
NO or use caution
What is the ADE of Sleeve gastrectomy
Ghrelin levels may be decreased for up to 1 year post srgry
What are the typical complications of bariatric srgry
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
When should obestity pts be referred
BMI > 30 (or >27 with weight-related comorbidities)
—Obesity medicine specialist
BMI > 40 (or >35 with weight-related comorbidities)
—Bariatric surgeon
What are the levels of the adrenal cortex from outer most layer to inner most layer
GFR COR
Glomerulus
Fasciculata
Reticularis
Cortex
What is the pathphsy of hirsutism
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
Half of women with hirsutism have what underlying condition
hyperandrogenism
What are the two types of Hirsutism
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
What is the Ferriman-Gallwey score
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
A score of greater than 8 on the Ferriman-Gallway score=
Hirsutism
Greater than 15 is severe
What are the major androgens in females that cause Hirsutism
DHEA, Androstenedione (from the Ovaries/ Adrenals), Testosterone
Peripheral conversion of androstenedione leads to what
Terstosterone
Free testosterone is converted to DHT by what in the skin
5a-reductase
What does DHT stimulate in the skin
Hair follice growth
What are the 5 causes of Hirsutism
Idiopathic/ Familial
Polycystic Ovarian Syndrome
Steroidgenic enzyme defects
Neoplastic D/o
Pharmecologic
Familial Hirsutism is most common in what demographic
medeterrainan and Middle eastern
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
Familial
What is the most common cause of Hirsutism in women
Polycystic ovarian syndrome
Its often familial and is transmitted bu an autosomal dominatant trait
What is the triad of criteria that must be meat to dx polycystic ovarian syndrome
- 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)
What are the two etiologies of steriodgenic Hirsutism
Congenital adrenal hyperplasia (21-hydroxylase deficiency)
Cortisol def=increase ACTH=hyperplasia
What is classic vs nonclassic steroidgenic hisrutism
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
What are the three causes of neoplastic Hirstism
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)
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
neoplastic (investigate for a tumor or cancer)
What are 5 drugs that can cause hirsutism
Minoxadil
Cyclosporine
Phynetoin
Anabolic steroids
Norethindrone (contraceptive)
What is virilizzation
Frontal balding (androgenic alopecia)
Increased muscularity
Clitoromegaly
Deepening of voice
Consider a NEOPLASMIC source
What are the imporatant labs in Hirsutism
Labs: serum androgen testing is mostly useful to find the adrenal/ovarian neoplasms
Free and total testosterone—most important!!!
Androstenedione
DHEA-S
If a female pt have a Total T above 200 or a Free T above 40, what exam must be performed
Pelvic exam and US !
If both are negative then order a bilateral adrenal CT scan
A pt with a serum androstenedione of greater than 10000 suggest what…
Ovarian adrenal neoplasm
(Perfrom a pelvic exam AND bilateral adreanl CT
A pt with a serum DHEA S greaer than 700mcg/dl suggest what
An adreanl source of excess androgens (hirsutism)
(Perform bilat adrenal ct scan)
What is a NML androstenedione level
0.7-3.5
What is a NML DHEA S level
Less than 10
What is the Tx approach to Hirsutim
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
OCP are C/I in what pts
smokers, migraine with aura, age 39+, HTN, Hx of DVT
What is vaniqa cream
Vaniqa cream (eflornithine HCl)
Topical which reduces hair growth
4-8 week until improvement…sxs return when d/c
Works well with laser tx
What are the two things that convert testosterone
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
What is the pathway that secretes the negative feedback inhibin molecule
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
LH woks on the leydig cells to make what
Testosterone
If a male pt is over 70 years old, what is the cutoff for hypogonadism
Less than 30 on a free T test
What is HYPERgonadatrophic Hypogonadism
Low test with elevated LH and FSH
Primary hypogonadsim
What is HYPOgonadatropic hypogonadism
Low test and low FSH/LH
Secondary Hypogonadism
A pt with a normal T level and elevated LH and FSH, think
LH and FSH should go down if the Test is normal or elevated, so think of a defect in androgen resistance
A male pt presents with delayed puberty, an deminished libido./erections
+fatigue, depression, and reducced excercise tolerance
May have small or NML testes
Think
Hypogonadsim
Order a Free T level and A LH/FSH level
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?
T deficieny at puberty onset
What is the effect o testosterone on growth plates
Normally testosterone closes epiphyses
lack of testosterone causes increased long bone growth
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
Post-pubertal testosterone deficiency
What are the 3 cuases of congenital primary hypogonadism
Klinefelter syndrome
Cryptorchidism
Bilateral anorchia
What are the 4 causes of aquired primary hypogonadism
Infection (mumps etc)
Aging
Trauma
Chemotherapy/ radiation therapy
A pt has seminiferous tubule dysgenesis
Think
Klinefetlers
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
Klinefelters
Breast cancer—increased incidence Chronic pulmonary disease Varicosities of legs Diabetes mellitus/impaired glucose tolerance (27% of patients) Osteoporosis
What is the PE appraoch to testing for cryptorchidism
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!
What is the Tx approach to Cryptorchism and what do we no longer do..
Orchiolexy is the tx at 12-24 months
We no longer do a hCG injection.
Does orchioplexy eliminate the risk of testicular cancer in cryptorchid pts
No 2-3 fold risk still remains
If you were to give a pt with bilateral anorchia a hCG test (no longer used) what would happen
You would see no increase in the testosterone level
An increase would mean they have undescended testes
You are testing a pt for hypogonadism and the labs show a low T and low FSH/LH
Think
Hypothalamic Pituitary abnml
(2nd dary cause)
Order a prolactin level and Pit MRI
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
THink Primary test abnomrality
No testes= hCG stimulation
Increased Test= Cryptorshidsm
No Test response= Anorchia
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
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)
How should Test replacement be admin’d
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)
What are the ADE of testosterone replacement
Acne Decreased HDL levels Gynecomastia—IM Erythrocytosis—IM OSA
If a pt has active prostate cancer, can they get T replacement Tx
NO!
What is the age cut off for T replacemnt Tx
Cant be younger than 13
Avoid due to premature epiphyseal closure and short stature
A pt presetns with Eunuchoid proportions, gyno, and prepubertal testes are small and rubery
Think
Kallmans
What is the MC cause of hyperprolactinemia
Pituitary adenomas
Inhibits normal GnRH release
Inhibits the action of testosterone
Decreases the effectiveness of LH
WHat are some common causes of secondary hypogonadism
Obestiy (BMI>40)
Renal failure, CHF
Aging ETOH use Marijuana Cushings Hypothyroid Cancer AIDS
A female pt presetns with eleveated levels of FSH/LH and elevated T
Think
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
IF testosterone is not recognized in the receptor, what is it converted to
Testosterone is not recognized so it is converted to estradiol by aromatase in adipose tissue
Happens in complete androgen insensitivity
What is the approach to Tx for Complete or Incomplete Androgen Insensitivity Syndrome - Testicular Feminization
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
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
Androgen Insentisty syndrome
Testes are in the abdomin, but the pt developed as a girl
What is needed of rmasculinization of external genitalia in utero
DHT
Which required 5-a-reductase
At what week gestation is 5-a-reductase needed for development of target organs
8-12
A female child pt has a penis development at age 12 has what condition
5-alpha reductase deficiency
What is a NML serus Ca2+ level
8.5-10.5
What is the function of PTH
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
What is the role of VIT D on calcium and phosphate
Vitamin D increases calcium and phosphate absorption from the intestines
What is the role of calcitonin
Inhibits osteoclaast activity, (decreasing calcium breakdown from bones)
Increases calcium storage in bones
increase renal excrteion of Calcium
What is the most common cause of HyperCa2+
Primary hyperparathyroidism – most common cause
—Parathyroid adenoma (80%),
—parathyroid hyperplasia (20%) or —parathyroid cancer (less than 1%)
A pt presents with hyperCa2+ and a low PTH
Think
Secondary malignancy (not parathyroid CA)
A calcium level above 14 is an indication of
MAlignancy
What effect does hypercalcemia have on the EKG
short QTi
What is Stones, bones, groans, moans, and overtones
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
If a pt presents with an increased PTH think
Parathyroid adenoma
Hyperplasia
Or CA
A pt presents with High serum calcium
High urine calcium and a high PTH
Think
Parathyroid adenoma (MCC)
What is the imaging approach to parathyroid ademonas
Imaging not necessary
May be used prior to surgery
U/S can be used or CT/MRI if negative US
What are the indications for SRGYRY in a pt with Hypercalcemia and aparathyroid adenoma
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
A pt has elevated Calcium levels with an elevated PTH, BUT is aS/s
What is the f/u criteria
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
What is the Tx approach to Parathyroid hyperplasia
Subtotal parathyroid removal
What is the Tx for PArathyroid Cancer
Tumor resection along with the affected thyroid lobe
What is the MOA of PTHrP
PTH related protein
Causes bone resorption and hypercalcemia similar to the action of PTH
Taking too much vitamin D can do what to PTH
Suppress it
What are some common causes of excess endogenous Vit D production
Lymphomas Sarcoidosis TB Histoiplasmosis Coccidiomycosis
Immobilization in the ICU has waht effect on calcium
Marked resorption of calcium from bone
Seen in ICU patients
Suppresses the PTH with a HIGH calcium level
What is the TxOC in malignancy associated hypercalcemia
IV bisphosphonates
How does hypoalbunimeia effect serum calcium
Hypoalbuminemia is a common cause of low total serum calcium
Hypocalcemia due to hypoalbuminemia is not clinically significant, if ionized Calcium is normal
Severe hypocalcemia requires what intervention
IV calcium gluconate
A pt presents with hypocalcemia yet an elevated PTH
Think
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
What are three medications what can decrease Vit D processing
Isoniazid, rifampin, phenytoin
Can lead to hypocalcemia with elevated PTH
Sprue and Chorns Dz effects vit d how
They are bot malabsorption issues that can lead to hypocalcemia with elevated PTH
If a pt presents with hypocalcemia , and low PTH and a elevated VIt D level
Think
VitD resistance (Genetic defects in VIT D metabolism)
What is the aS/s tx to hypocalcemia
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
What is the most common fx of osteoporosis
Vertebral fx
In pts older than 50 or hypogonadism pts … alwasy look for what bone problem
Osteoporosis
What does a T score (DEXA) of -1.0 to -2.5
Osteopenia
What does a T score (DEXA) of -2.5 tell you
Osteoporosis
A T score of -2.5 with a fracture means
Severe Osteoporosis
Can also just be a Tscore below -3.5
When can bisphophonate be used for osteoporosis
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%
Drugs that end in -Dronate
Bisphophonates
What are the ADE of bisphosphonates
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%)
If a pt has Barretts esophagus and osteoporosis
What is the Tx approapriate
IV!!! Bisphosphonates
Do not use oral meds
What do Beta cells of the pancreas secrete
Insulin
What do alpha cells of the pancrease secrete
Glucagon
What do delta cells of the pancreas secrete
Somatastatin
What is MODY DM
Non-insulin dependent DM Age of onset: <25 yrs Non-obese Due to impaired glucose-induced secretion of insulin Autosomal dominant inheritance
A pt presents with elevated TGs, Low HDL, and elevated LDL, HTN, and Elevated CRP, has hyperruecemia, and abdonmial obesity
Think
metabollic syndrome
A pt presents with blurred vision , and poly dypsna, polyuria, and poly phagia, and recent wt loss
+/- postural HOTN, parasthesia, Ketoacidosis
Think
T1DM
What are 3 chronic skin infections associteed with DM2
Candida, General Pruritis, and Vaginitis
What is Acanthosis Nigricans
Darking of skin folds seen in type 2 DM
From insulin resisstnace
What is the criterai to screen for DM is aS/s adults
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
If a pt has ketonuria greater than 3.0..
they need..
ADMIT!
What can cause falsely low A1C
Acute blood loss, anemia, hemolysuis, recent transfusion
Heavy bleeding
What can cause falsely high A1C
Iron, B12, or folate deficiency
Liver/Kidney Failure
What is the tx approach to a pt with pre diabetes
Diet and excercise
What is the approtiate counselling to DM pts and ETOH consumption
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
When should DM pts receive thier vax
Influenza—annually
Pneumococcal vaccine
At diagnosis
Repeat at age 65 (if initially given prior to 65)
All Dm pts should receive what medication to prevent ASCVD
ASA and statins And ACE/ARBS
What is the effect of metformin on HOgl and wt
HOgl neutral
With slight wt loss
What is the MOA of metfromin
Suppresses hepatic gluconeogenesis;
increases hepatic insulin sensitivity
Metformin (Glucophage) –1st line therapy for new DM2
What is the HOgl and Wt effects of DPP-4s
Neutral to both
What is the major ADE of DDP-4
Pancrreatitis
What are the HOgl and Wt effects of GLP-1
HOgl neutral
Wt loss!
How should GLP-1 be used as part of DM2 tx
Add on tx ONLY!
With either metformin or a SU
What is the major ADE of GLP-1
Thyroid Cancer
What is the HOgl and wt effects of SGLT-2
HOgl neutral
Wt loss!
What SGLT-2 has been approved for reducing CV risk in DM2 pts
Empaglaflozin
What is the HOgl effect and wt effect of TZDs
HOgl neutral and WT GAIN!
What are the major ADE of TZDs
Heart problems, edema, Osteoposris, angina and WT GAIN!
What are the HOgl and wt effects of SUs and Meglitinides
Severe HOgl and WT GAIN!
DO not use glyburide becasue it is long acting and has the most HOgl of the SUs
What are the glucose goals in DM
preprandial 90-130
Postprandial less than 150
Ave. Bedtime gl 110-150
A1C less than 7 ( or 8 in eldery)
What type of insulin is used for DKA tx
Regular (short acting)
What is Lente insulin
intemediate acting ( NPH is aslo in this class)
When should T1DM pts be referred
When to refer: Patients with type 1 diabetes should be referred to an endocrinologist for co-management with a primary care provider.
Where can you NOT inject insulin
Within 2inch of the navel/ umbilicus
What is the insulin of choice in an insulin pump
Lispro
How should weekly insulin adjumstmens be titrated in type2DM
Increase insulin dose weekly
Increase 4U if FBG >180mg/dl
Increase 2U if FBG 120-180mg/dl
Addisons pts with DM are at an increased rsk of
HOgl
Due to ortisol deficiency
Remember BB mask the effects of HOgl
tachyardia (bb block this)
Palpatatoins (bb prevent this)
Tremors (bb symopathetic tone)
Sweating
DKA Pathogenesis
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.
What is the mainstay of tx for dka
IV fluids, insulin, potassium, bicarb +/-, ABX +/-
What is the serum gl goal in a DKA pt
250-300
If a pt has DKA with a pH less than 7.0
What adjunct should be considered
Bicarb
What are the 2 Rx that can precipitate HHS
Thiazide diuretics and glucocorticoids
What is the BUN level in HHS
Greater than 100
What is the major cause of death of T1dm and T2dm
T1: Major cause of death – complications from end stage renal disease
T2: Major cause of death – macrovascular disease leading to MI and stroke
What are the major ocular complications of DM
Cataracts, reinopathy, Gluacoma
What is the MC cause of visual impariment in DM2
Non proliferative Retinopathy
Microaneurysms
Dot hemorrhages
Exudates
Retinal edema
What are cotton wool spots in the retina
Growth of new capillaries due to retinal hypoxia
Increased risk of macular edema & retinal detachment
What is the tx approach to DM retinopathy
BLOOD gl control and smoking cessation
Laser tx are available, and bevacizumab
When should you refer a pt with Retinopathy
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
What is the MC cause of ESRF (CKD)
DM nephropathy
What is the assay of choice for microalbuniimia
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
What is the tx approach to microalbunima
STRICT gl controll (6.5)
ACE or ARBs
Low protein diet
Monitor Albumin/Cr ration q 6 months
Can DM pts get contrast
Avoid in pts with CrCl above 3
What are the Rx options to distal symetric polyneuropathy
Nortriptyline Gabapentin (Neurontin) Pregabalin (Lyrica) Duloxetine (Cymbalta) Capsaicin cream Lidocaine patches
What are the MC envolved nerves of Isolated Peripheral Neuropathy
Femoral or Cranial nerves
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
painful DM neuropathy
Tx: amitriptyline (TCAs)
gabapentin (anticonvulsants)
duloxetine (SNRI) (Cymbalta)
Capsaicin cream
What is a Rx option for GI system neuropathy in DM pts
Metoclopramide
What is the treatment option for postmenopausual women with hirsutism
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
What is the recommendation of using OCPS in pts with hirsutism
Use low dose estradiaol
