7 ⼀ENDOCRINE/OPHTHO Flashcards

(350 cards)

1
Q

how are pregnant patients screened for hyperthyroidism? (3)

torn

A

TSH

(low TSH) ➜ [free T4]

(normal [free T4]) ➜ [Total T3]

use trimester-specific norms

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2
Q

management? (2)

A

eye shield

+

[hospital admit (strict bed rest + 30° bed + serial intraocular pressures+ [prevent rebleeding and intraocular HTN → vision loss])]

HYPHEMA

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3
Q

Stress Hyperglycemia occurs when ⬜. This presents very similarly to ⬜
_________________

how do you differentiate the two? (2)

Stress Hyperglycemia is a/w ⇪ morbiditiy

A

[STRESS (severe illness > 39C)] ➜ [CortisolGlucocorticoid] secretion➜ ⇪ Insulin resistance ➜ hyperglycemia ;

DKA
_________________

DKA has [hgbA1C ≥6.5%] +[“FUDGe” DM classic s/s]

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4
Q

patient newly diagnosed with Papillary Thyroid Cancer

What’s 1st step after this?
_________________

What are the treatments? (2)​

A

[Neck & Cervical lymph node US for initial staging]
_________________

  • [< 1 cm = lobectomy]
  • [TOTAL THYROIDECTOMY if: ≥1cm ​​| extension outside thyroid ​| distant metz ​| hx head/neck radiation exposure]
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5
Q

Which antiDM are a/w weight gain? (3)

A

Insulin

[Thiazolidinediones (pioglitazone)]

Sulfonylurea

Insulin Tops Scales”

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6
Q

What is Euthyroid Sick Syndrome? (4)
_________________

mgmt? (3)

A

⭐acute illness ➜ [⬇︎ peripheral conversion of T4➜ T3] → forces peripheral T4 to be converted to ®T3 instead
but causes no other change to the thyroid →[nml TSH, nml T4 ]
with
⭐[low T3io\normal TSH and normal T4]
and
⭐[HIGH ®T3io\normal TSH and normal T4]

[ ✔︎TSH, ✔︎T4, , ⬇︎T3, ⇪®T3 ] = Euthyroid Sick Syndrome

should resolve once acute illness is resolved
_________________
Repeat Thyroid Function Test after acute illness is resolved –(if persist)–> give [Liothyronine T3] supplement

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7
Q

What is [reverse ®T3]?

_________________

what is it used for?

A

rT3 = [inactive metabolite of​ unconverted T4]
_________________

[rT3] Differentiates …

Euthyroid Sick Syndrome (illness ⬇︎ peripheral conversion of T4 ➜ T3 = [⬇︎T3] but [⇪ rT3 (from INC unconverted T4)])

_________from________

central hypOthyroidism (low TSH ➜ ⬇︎T4 ➜ [⬇︎T3] AND [⬇︎rT3])

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8
Q

How do you workup a patient with suspected [central hypOpituitarism] (5)

A
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9
Q

patients with [classic Congenital Adrenal Hyperplasia] require prompt therapy with ⬜ and chronic tx with ⬜

Why ? (3)

A

[high dose hydrocortisone] ; glucocorticoid and mineralocorticoid replacement
_________________

avoid adrenal crisis by maintaining BP / growth/ suppress adrenal androgens​

classic CAH = 21hydroxylase deficiency CAH

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10
Q

Recite the Adrenal Gland blueprint for

Zona Glomerulosa (13)

A

*

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11
Q

Recite the Adrenal Gland blueprint for

Zona Fasciculata -7

A
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12
Q

Recite the Adrenal Gland blueprint for

Zona Reticularis-6

A
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13
Q

The most common enzyme deficiency for [Congenital Adrenal Hyperplasia] is

________________

cp?-3

A

21 hydroxylase

[(complete=CLASSIC CAH (C)] | [(reduced=NONClassic CAH (NC)]

🅶

C[⬇︎AldosteroneMineralocorticoid] → [Salt Wasting( losing Na+ / gaining K+)] → hypOtension + vomiting

🅵

C[⬇︎CortisolGlucocorticoid]

🆁

NC & C[⇪Testosterone] ← [⇪ 17HydroxyProgesterone]

= Virilization = [Ambiguous genitalia in females] + (acne, premature adrenarche/pubarche)

MC=MineraloCorticoid/GC=GlucoCorticoid

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14
Q

The 2nd most common enzyme deficiency for [Congenital Adrenal Hyperplasia] is

________________

cp?-5

A

11βhydroxylase

🅶

▶ [⇪ 11DOCSMC] = weak Mineralocorticoid → Salt RetentionFluid Retention = HTN

▶[⬇︎AldosteroneMineralocorticoid]

🅵

▶[⇪11dcGC]

▶[⬇︎CortisolGlucocorticoid]

🆁

▶[⇪ ⇪Testosterone] ← [⇪⇪ 17HydroxyProgesterone] ← {[⇪11DOCSMC]🅶 & [⇪11dcGC]🅵}

= Virilization = [Ambiguous genitalia in females] + (acne, premature adrenarche/pubarche)

[11dc =11deoxycortisol] | [11DOCS =11DeOxyCorticoSterone] | MC=MineraloCorticoid/GC=GlucoCorticoid

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15
Q

The least common enzyme deficiency for [Congenital Adrenal Hyperplasia] is

________________

cp?-2

A

17 αhydroxylase

🅶

▶[⇪ ⇪ AldosteroneMineralocorticoid] ← [⇪⇪ 11DOCSMC]

= Salt RetentionFluid Retention = HTN

🅵

▶[⬇︎CortisolGlucocorticoid]

🆁

▶[⬇︎Testosterone]

= ALL PATIENTS PHENOTYPICALLY FEMALE

[11dc =11deoxycortisol] | [11DOCS =11DeOxyCorticoSterone] | MC=MineraloCorticoid/GC=GlucoCorticoid

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16
Q

The most common enzyme deficiency for Congenital Adrenal Hyperplasia is ⬜

Which lab value is diagnostic for this deficiency?

A

21 hydroxylase (complete = classic CAH | reduced=nonClassic CAH)

⬆︎17 HydroxyPROGESTERONE

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17
Q

What benefits does maintaining Tight Glucose Control in DM pts give?

A

⬇︎ microvascular complications (retinopathy/nephropathy)

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18
Q

What are all the functions of [CortisolGlucocorticoid] - 6

A

BIG ⬇︎FIB

  1. Blood pressure (⬆︎a1 receptors)
  2. Insulin resistance –> DM
  3. Gluconeogenesis
    _________________
  4. ⬇︎Fibroblast –> striae
  5. ⬇︎Immune system (WHITE)
  6. ⬇︎Bone formation by ⬇︎osteoBlast
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19
Q

what is Apathetic Thyrotoxicosis ? (4)

A
  1. [atypical elderly HYPERthyroidism] =
  2. [APATHY (lack of enthusiasm/interest), mimics DEPRESSION, lethargy, confusion, wt loss]
  3. (misdiagnosed as depression or dementia),
  4. likely NO thyromegaly
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20
Q

S/S of hypOthyroidism is mostly opposite of Hyperthyroidism sx

What are 9 symptoms specific to only hypOthyroidism?

A

Mostly opposite of TT Feels ARCHED but specifically causes {med}3

menorrhagia

macroglossia

myalgia/arthralgia

[edema ([Myxedema nonpitting] / pedal)]

[eval labs (HLD, Macrocytosis & hypOnatremia in elderly)]

[eerie (HOARSE) voice]

diastolic HF

depression

dry coarse skin

BOTH HAVE FATIGUE AND HTN

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21
Q

Clinical definition of Diabetic Ketoacidosis (DKA) -2

A

[metabolic acidosis (HCO3<15 or pH<7.3)]

in the setting of [hyperglycemia > 200]

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22
Q

how do you manage HHONKS-6?

[HHONKS (Hyperglycemia HyperOsmolar NON Ketone State)]

A

FIPAAR control

  1. Fluid control : (NS) < [Blood Sodium 135] < (1/2 NS)
    _________________
  2. Insulin control:
    🍭[Continuous infusion until BG 200]]
    🍭➜ [when BG ≤ 200 ⬇︎ infusion and add dextrose5%]
    🍭➜ [on G.A.P.E.Resolution = start (subQ mealtime + basal insulin)] ➜ DC insulin infusion 2h later]
    _________________
  3. Potassium control: [✳]
    _________________
  4. Acid control: give HCO3 for [pH< 6.9 or HCO3< 15]
    _________________
  5. ANION GAP CONTROL: [correct to 10-14]
    _________________
  6. G.A.P.E.RESOLUTION = {[Glucose< 200] + [Anion Gap 10-14] + [pH>6.9 and HCO3 ≥15] + [Eating tolerated → ICU admitted]}
    _________________

(monitor phosphate and Ca+ also)

[✳] : {serum K+: [(hold insulin) < –3.3–(give IV K+)– 5.2–> ✔︎]}

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23
Q

how do you manage DKA-6?

DKA:Diabetic Ketoacidosis

A

FIPAAR control

  1. Fluid control : (NS) < [Blood Sodium 135] < (1/2 NS)
    _________________
  2. Insulin control:
    🍭[Continuous infusion until BG 200]]
    🍭➜ [when BG ≤ 200 ⬇︎ infusion and add dextrose5%]
    🍭➜ [on G.A.P.E.Resolution = start (subQ mealtime + basal insulin)] ➜ DC insulin infusion 2h later]
    _________________
  3. Potassium control: [✳]
    _________________
  4. Acid control: give HCO3 for [pH< 6.9 or HCO3< 15]
    _________________
  5. ANION GAP CONTROL: [correct to 10-14]
    _________________
  6. G.A.P.E.RESOLUTION = {[Glucose< 200] + [Anion Gap 10-14] + [pH>6.9 and HCO3 ≥15] + [Eating tolerated → ICU admitted]}
    _________________

(monitor phosphate and Ca+ also)

[✳] : {serum K+: [(hold insulin) < –3.3–(give IV K+)– 5.2–> ✔︎]}

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24
Q

[HHONKS (Hyperglycemia HyperOsmolar NON Ketonic State)**] is a complication of DM

What Blood Glucose precipitates this?

A

Blood Glucose > 600

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25
How does DKA and HHONKS affect total body K+ levels?
⬇︎**total body** K+ (REGARDLESS OF WHAT SERUM VALUE SAYS) ## Footnote DKA & HHONK causes severe osmotic diuresis --\> ⬇︎total body K+ stores even though serum K+ level may be elevated = [maintain > 5.3*K+* ✳]
26
In DKA and HHONKS management, when do you hold the insulin?
serumK \<3.3 *Remember that ALL DKA and HHONKS pts are Total Body K+ depleted due to osmotic diuresis regardless of what serum values say*
27
In DKA and HHONKS management, when do you consider using Sodium Bicarbonate?
pH\<6.9
28
You suspect a pt has Cushing *Syndrome* How do you work this up?-3
1st: .Determine if pt has ⇪ [CortisolGC]([Overnight low-dose dexamethasone suppression test] | [late night salivary cortisol assay] | [24 hr urine free cortisol]) 2nd. If [CortisolGC] ⇪ = ⊕Cushing Syndrome 3rd: If ⊕Cushing Syndrome → perform ACTH workup(image) to determine if Cushing Syndrome [ACTH-*dependent*] or [ACTH-*INdependent*]
29
You suspect a pt has Cushing *Syndrome* *After completing step 1 and step 2 of Cushing Syndrome workup, your attending ask you to perform the [3rd step ⼀ACTH workup] to determine \_\_\_\_\_\_\_* What is the ACTH workup? -3
3rd: If ⊕Cushing Syndrome → perform ACTH workup(image) to determine if Cushing Syndrome [ACTH-*dependent*] or [ACTH-*INdependent*]
30
Name the characteristics of Cushing Syndrome - 7
"**F**at **H**eavy **P**eople **M**ay **HOG** *the Cushing*" 1. **F**at reDistribution (central obesity, Moon face) 2. **H**yperpigmentation (from excess ACTH activating [Melanocyte MC1 R]) 3. **P**urple striae with skin atrophy and bruisability 4. **M**uscle atrophy 5. **H**TN 6. **O**steoporosis 7. **G**lucose intolerance \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *Cushing **SYNDROME** is caused by ⇪ [CortisolGlucocorticoid](which may be ACTH-INdependent or ACTH-dependent)*
31
autoimmune adrenalitis is known as _____ disease etx?
[Addison's Primary Adrenal Insufficiency] disease **Autoimmune** Primary Adrenal Insufficiency (suspect this in pts with other Autoimmune diseases - pernicious anemia, vitiligo, hypothyroid!) *Sx = HYPERKalelmia, hypOnatremia, wt loss, fatigue*
32
What are the main causes of [Addison's Primary Adrenal Insufficiency]? - 4
1. TB 2. Autoimmune adrenalitis 3. CA 4. Adrenal Hemorrhage
33
Main sx for [Addison's Primary Adrenal Insufficiency] - 8
“*Addison was a* **SNAP FHAG**” 1. [**S**odium ⬇︎ DEC] 2. [**N**AHA (Normal AG Hyperchloremic metabolic acidosis)] 3. **A**norexiaWT LOSS 4. [**P**otassium ⇪ INC] 5. **F**atigue 6. [**H**yperpigmentation(ACTH and MSH)] 7. [**A**ndrogen deficiency(⬇︎axillary/pubic hair)] 8. **G**I Sx
34
What is Cosyntropin? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Describe how it used to workup ⬜
ACTH analog ⼀*used for ACTH stimulation test -- when [basal morning plasma cortisol] and [basal morning plasma ACTH] are equivocal* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [Addison's Primary Adrenal Insufficiency]
35
What test should you order to diagnose [Addison's Primary Adrenal Insufficiency]? (3)
1. **basal morning plasma cortisol ⼀(*****dx = low cortisol*****)** 2. **basal morning plasma ACTH ⼀(*****dx = HIGH ACTH*****)** 3. [Cosyntropin ACTH stimulation test] ⼀(*use if 1 and 2 are equivocal*)
36
Which 5 drugs cause Drug-Induced Lupus? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ How is Drug-Induced Lupus diagnosed?​ (2)
**HEMPI** to *DIL* **H**ydralazine [**E**tanercept (TNFα R Blocker)] **M**inocycline **P**rocainamide [**I**nfliximab (TNFα R Blocker)] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ +ANA and **+antiHistone**
37
Why are frequent ophthalmologic exams necessary for prolonged CTS users?
CTS changes lens epithelial gene transcription ➜ **CATARACTS**
38
In addition to ⇪ glucose urinary excretion , how do SGLT2 inhibitors delay the progression of DM nephropathy?
inhibiting Na+/Glucose transporter ➜ [⇪ urinary glucose] AND [⇪ urinary Na+] and the [⇪ urinary Na+] travels to macula densa where it causes ⬇︎renin secretion ➜ [⬇︎Angiotensin II] ➜ ⬇︎efferent arteriole constriction ➜ ⬇︎GFR = delays DM nephropathy
39
*pt p/w eye pain with foreign body sensation* what's your workup? (4)
40
Both preseptal cellulitis and orbital cellulitis present with (⬜3) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ How are they differentiated? (3)​
[eyelid swelling-redness] ​/ fever ​/ conjunctivitis \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ **orbit**al = **orbit** eye pain with movement + proptosis + ophthalmoplegia​
41
How do you treat Orbital cellulitis? (2)
IVAbx ➜ [Surgical debridement (if fluid collection/abscess present)]
42
How do you workup Hyperthyroidism? -5
43
*Exogenous* thyrotoxicosis MOD
[OTC Thyroid supplement vs surreptitious prescription thyroid med] ➜ supressess [ANT Pit TSH] ➜ ⬇︎thyroid gland synthesis ( ⬇︎RAIU and ⬇︎thyroglobulin)
44
Common s/s of HYPERthyroidism -9
**TT** **F**eels **ARCHED** 1. **T**remor 2. **T**achycardia 3. [**F**atigue*(+/- Apathy in Elderly)*] 4. **A**ppetite ⬆︎ but Wt ⬇︎ 5. **R**eflexes ⬆︎ 6. **C**ardio* (Tachycardia, Palpitations,Exertional SOB, ⇪Myocontractility→HTN)* 7. **H**eat intolerance --\> SWEATING 8. [**E**xophthalmos with lid lag = GRAVES DISEASE] 9. **D**iarrhea +/- dyspepsia *Older pts may only have Fatigue, Cardio, or Apathetic!*
45
For patients taking CTS, which patients need their dose regimens *tapered down* at the end?
[CTS \> 3 Weeks] = TAPER DOWN *(taper allows for return of adequate endogenous cortisolglucocorticoid*)
46
How do you workup Hypercalcemia? -4
MEASURE PTH!
47
*Hypercalcemia can either be PTH-dependent or PTH-INdependent* What are the causes of [PTH-**dependent**Hypercalcemia]? (4)
- Primary HyperParathyroidism - Tertiary HyperParathyroidism(Intractable Hypercalcemia 2/2 Autonomous Parathyroid) - [Familial hypOcalciuric Hypercalcemia] - Lithium
48
*Hypercalcemia can either be PTH-dependent or PTH-INdependent* What are the causes of [PTH-**INdependent**Hypercalcemia]? (8)
1. **MALIGNANCY** 2. [VitD toxicity] 3. [VitA toxicity] 4. Granulomatous disease 5. [*LCD-TV* Rx] 6. Milk-alkali syndrome 7. Thyrotoxicosis*(Thyroid hormone causes bone resorption → ⇪ Ca+)* 8. Immobilization
49
normal range for PTH
10-60
50
*After working up Hypercalcemia, you determine cause is Malignancy* List the 3 Causes of [Hypercalcemia of Malignancy] , which Cancers cause them and their MOD
51
Which Rx cause Hypercalcemia (5) *NormalCa+ = 8.4-10.2*
“**LCD**-**TV** with too much Calcium!” **L**ithium **C**a+carbonate excess **D**Vitamin **T**hiazides **V**itamin*A*
52
# nml TSH: [0.4-4.0] which thyroid condition is a/w Thyroid Lymphoma? ​
**hCAT** [**h**ashimoto **C**hronic **A**utoimmune*(antiTPO)* **T**hyroiditis] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *hCAT can progresses to Thyroid Lymphoma | [hCAT+ Pemberton = Thyroid Lymphoma]* | *chronic [antiTPO Lymphocyte] infiltrate thyroid targeting TPO*
53
What is Pemberton's sign? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ What does it indicate? -2
facial plethora or neck vein distension when arms are raised ​ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ - obstructive **ENLARGED THYROID** - [Thyroid lymphoma (if ⊕ in the setting hCAT)]
54
Medullary thyroid cancer cp -2
1. [thyroid nodule iTSo MEN] 2. [Calcitonin ⇪ (from thyroid gland C cell neoplasia)] * MEN = Multiple Endocrine Neoplasia // iTSo = in The Setting of*
55
Describe MEN1 (3)
**P**ituitaryMacroAdenoma **P**arathyroid hyperplasia [**P**ancreatic-GI *GLIV* tumors ⼀*G*astrinoma/g*L*ucagonoma/*I*nsulinoma/*V*IPoma]
56
Describe MEN2A (3)
- Parathyroid Hyperplasia - Medullary Thyroid CA - Pheochromocytoma
57
# Pt with new diagnosis MEN2B Prior to thyroidectomy, patient must be 1st evaluated for coexisting tumors such as ⬜ and Pheochromocytoma. Name the dx labs for Pheochromocytoma (4) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Why is this important?
Parathyroid hyperplasia \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 1st: {[Plasma free metanephrines] --(confirm by)-- \> 2nd: - [24h urinary fractionated metanephrines] - catecholamines - abd imaging]} \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Undiagnosed Pheochromocytoma can cause fatal HDUS peri-thyroidectomy
58
# MEN2A and MEN2B share the same initial workup List the diagnostic workup for {new dx[MEN2A ] or new dx[MEN2B]} - (5)
1. Calcitonin 2. CEA 3. [Neck US (r/o regional metastasis)] 4. [Chromo10*RET* protooncogene] germline testing 5. [Coexisting tumor r/o *([Parathyroid hyperplasia], [Medullary Thyroid Hyperplasia], Pheochromocytoma,)*]
59
Describe MEN2B (4)
60
# Pt p/w the 3 P's of MEN1 ( _______ ) What's the next step in Management of MEN1?
**P**ituitaryMacroadenoma/**P**arathyroid hyperplasia/[**P**ancreatic-GI *GLIV* tumors] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [PARATHYROIDECTOMY with autotransplantation to muscle pocket]
61
# Pt p/w the 3 P's ( ⬜ ) of MEN1 Measurement of Gastrin is often used to diagnose ⬜, but Gastrin can only be measured in the setting of ⬜ serum Ca+ and No ⬜. Why is this?
[**P**rolactinoma]/[**P**arathyroid hyperplasia]/[**P**ancreatic&GI *GLIV* tumors] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [**P**ancreatic *G*astrinoma (Zollinger Ellison)] - normal Ca+ (*⇪ Ca+ ➜ falsely elevated gastrin*) - NO acid-reducing tx (*PPI ➜ falsely elevated gastrin*)
62
How are the **thyroid** and **Calcium** related?
[**T3/T4**thyroid hormone] causes bone resorption **➜ ⇪ serum Ca+/Hypercalcemia**
63
Candida Endophthalmitis ``` clinical features (4) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ``` Treatment?​ (3)
1. [fundoscopic fluffy yellow-white chorioretinal lesions] 2. [floaters + eye pain and ⬇︎acuity] 3. [hospitalized patients on Parenteral nutrition = RF1] 4. [s/p GI surgery or GI perforation = RF2] ​ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Tx = [Vorizonazole + Intravitreal antifungal + vitrectomy] ​ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *RF = Risk Factor*
64
What causes [Pancreatogenic DM]? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Which antiDM should be used to treat this? Which 3 should not? why?
Chronic pancreatitis (RF cystic fibrosis) ➜ islet cell damage ➜ ⬇︎insulin secretion then insulin deficiency ➜ glucose intolerance ➜ DM \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ✔︎ = INSULIN*-replace Insulin pt stopped producing* ❌❌= [GI peptide antiDM (DPP4 inhibitors / GLP1🟢)] - *since these target GI peptides ➜ slows gastric emptying and ⇪ risk for pancreatitis* or ❌= [insulin secretagogues (Glipizide)]*- impaired ability to secrete endogenous insulin from DEC islet beta cell reserve*
65
*Glipizide* MOA
insulin secretagogues
66
*GLP1 R agonist* MOA Name 3 examples \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *Glucagon-Like Peptide-1 R agonist*
Food → intestine [GLP1] secretion naturally ➜ GLP1**iLAGG** → GLP1 is then cleaved-inactivated by DPP4 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ⇪ **i**nsulin secretion and insulin sensitivity ⬇︎**L**iver glucose secretion ⬇︎**A**ppetite → wt loss ⬇︎**G**astric emptying*(⇪pancreatitis risk)* ⬇︎**G**lucagon secretion \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ so... [GLP1🟢] → ⇪GLP1**iLAGG** \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *liragluTIDE / exenaTIDE / dulagluTIDE*
67
*DPP4 inhibitors* MOA Give 2 examples
Targets GI peptides ➜ slows gastric emptying \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ## Footnote *linaGLIPtin* *sitaGLIPtin* *saxaGLIPtin*
68
Why are [Pioglitazone thiazolidinedione] contraindicated in CHF?
[Pioglitazone thiazolidinedione] ⇪ insulin sensitivity by stimulating [PPAR-γ] on liver/muscle/fat] BUT it also stimulates [PPAR-γ] on renal CD ➜ ⇪ Na+ reabsorption ➜ fluid retention ➜ precipitates CHF
69
What is Amaurosis fugax?
sudden **reversible** transient monocular blindness 2/2 carotid artery atherosclerotic disease
70
Amaurosis fugax tx?
carotid endarterectomy
71
Amaurosis fugax dx?
carotid doppler US
72
What is subclinical thyrotoxicosis? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ how is it managed?
mildly low TSH **but** [normal free T4, normal T3 and normal physiology (*normal HR, bone density*)] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ RECHECK Thyroid function test in 8WKS (*most TSH normalize on its own*)
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*a Patient with chronic hypOparathyroidism presents with low serum Ca+ but HIGH urinary Ca+ from their Ca+ supplement* How do you mitigate this?
HCTZ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *HCTZ [⇪ serum Ca+] while [⬇︎ urinary Ca+]*
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How is the thyroid system associated with Surgery?
[hypOthyroidism] ➜ [poor periOperative outcomes] ⼀BUT 911 surgeries are Ok if hypOthyroidism not severe (i.e. no myxedema coma)
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Why must Levothyroxine at first be titrated very slowly in CAD pts ?
[levothyroxine T4] ⇪ myocardial O2 demand which can ➜ Myocardial ischemia ➜ in CAD pts can cause MI or arrhythmia = slow gradual [levothyroxine T4] titration
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NPH is a ⬜ insulin that is sometimes used as ⬜. Why should it NOT be used in patients who've had hypOglycemic episodes?
intermediate-acting ; [basal insulin when injected BID] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ NPH has a pronounced peak which can ➜ hypOglycemia = bad for patients who already have hypOglycemic episodes
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When is it indicated to switch a T1DM pt from [manual SQ Basal/bolus insulin injection] to [automated SQ continuous infusion insulin pump]?
*Pump Indicated if T1DM pt (on current manual injection) has…* 1. hypOglycemic episodes 2. [suboptimal glycemic control HbA1C\>7] 3. highly variable BG readings
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# Patient presenting with new diagnosis T1DM. Tx requires exogenous insulin. Describe the [manual SQ Basal/bolus insulin injection] regimen the patient will start with
T1DM require a [(long basal) and (rapid bolusx3)] every day
79
Work up for Thyroid Nodule?
[Cancer RF = (\> 1cm), fam hx, radiation hx, cervical LAD, compressive sx, thyroid hormone ∆] [Suspicious US = hypOechoic, microcalcifications, internal vascularity]
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# After RF and US eval -- Any Thyroid Nodule > ⬜ cm needs work up with FNA List all the [High Risk Thyroid features] that warrant FNA for Thyroid Nodule (9)
> \> 1 cm > > \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [Cancer RF = (\> 1cm), fam hx, radiation hx, cervical LAD, compressive sx, thyroid hormone ∆] [Suspicious US = hypOechoic, microcalcifications, internal vascularity]
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Why are hypoglycemic episodes in _long standing_ DM1 pts even more serious than newly diagnosed DM1 pts? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ how is this mitigated?
✔︎ long standing DM1 pts overtime develop blunting of their autonomic feedback to [hypOglycemia (tremor, sweating, AMS)] = ⬇︎[*hypOglycemia awareness system (HAS)*] ✔︎ so this means… if _long_-standing DM1 present with hypOglycemia ⼀ it’s likely to be a SEVERE HYPOGLYCEMIA EPISODE (since , in a {blunted *HAS*} pt, only SEVERE HYPOGLYCEMIA can activate a {blunted *HAS*} to induce sx necessary to make pt aware/get help] **\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_** [Strict avoidance of **any** hypOglycemia x 2-3 weeks] restores patient’s *HAS*
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# nml TSH: [0.4-4.0] Name the 2 [DeTC (Differentiated epithelial Thyroid CA)] subtypes
1. [papillary thyroid cancer] 2. [follicular thyroid cancer] * * * DeTC target TSH : [**LR** =TSH(0.1-0.5)6mo(Ln)] | [**IR**=TSH(0.1-0.5)] | [**HR**=TSH(\<0.1)x yrs]
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# nml TSH: [0.4-4.0] Why is it important to [**prevent** ***elevated*** **TSH**] in pts with DeTC? * * * Considering this, how do you determine the ideal TSH level DeTC patients should be kept? (3) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *(DeTC=Differentiated epithelial Thyroid Cancer)*
in [DeTC s/p thyroidectomy] pts, ***elevated*** **TSH** actually **stimulates growth of residual thyroid cancer cells** = goal TSH depends on _Risk of Recurrence_ * * * [**LR** =*TSH* (0.1-0.5)6-12mothen → (low nml TSH range)] [**IR**=*TSH* (0.1-0.5)] [**HR**=*TSH* (\<0.1)]x years * * * TSH\*=DeTC TSH goal
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# nml TSH: [0.4-4.0] management for [DeTC (*papillary vs follicular*)] varies and is dependent on ⬜ and importantly ⬜ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *(DeTC=Differentiated epithelial Thyroid Cancer)*
[initial stage of CA] ; [Risk of Recurrence] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ DeTC target TSH : [**LR** =TSH(0.1-0.5)6mo(Ln)] | [**IR**=TSH(0.1-0.5)] | [**HR**=TSH(\<0.1)x yrs]
85
Name the 3 benefits to [STRICT blood glucose control] in DM pts
DECREASES… 1. [**micro**vascular complications ⼀*nephropathy, retinopathy*] 2. [peripheral neuropathy onset] 3. [peripheral neuropathy progression]
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Gastroparesis = ⬜ and is ultimately diagnosed with what test?
delayed gastric emptying (2/2 DM, drugs, postviral) ; [nuclear gastric emptying study]
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Clinical manifestations of gastroparesis? (5)
- [succussion splash] - [early satiety] - [Abd fullness postprandial] - [dysautonomia *(dizziness, diaphoresis)*] - [labile glucose control] | *BE SURE TO R/O MECHANICAL OBSTRUCTION*
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Name 2 promotility drugs used to treat gastroparesis
1. metoclopramide 2. erythromycin
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When is [screening for diabetic retinopathy and nephropathy] indicated ? (2)
[5y after T1DM dx] and [**AT TIME OF DX for T2DM**] * * * * give Statin if [age ≥40 with DM]*
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What is the preferred antiHTN for DM pts?
ACEk2 inhibitor \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *this improves diabetic nephropathy AND INC GFR*
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Patients with Graves disease have [⬜positive | negative] Thyroid Stimulating Immunoglobulins and ⬜ uptake on [(RadioActive Iodine Uptake) scintigraphy] * * * *Tx for hyperacute [symptomatic Hyperthyroidism] is Cardiac + Thyroid* [CardiacPLUS Thyroid[AntithyroidMed1st line or \_\_\_\_\_or \_\_\_\_\_] * * *
positive; diffuse * * * 1. propranolol 2. Thyroid Tx ([AntithyroidMed] vs [Radioactive iodine ablation] vs [Thyroidectomy]) ## Footnote tx = [**P**ropranolol] --\> [**P**TU ---(1 hr later)]--\> [**P**otassium Iodine and PrednisoneCTS]
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*Tx for hyperacute [symptomatic Hyperthyroidism] is Cardiac + Thyroid* [CardiacPLUS Thyroid[AntithyroidMed1st line or \_\_\_\_\_or \_\_\_\_\_] * * * Aside from being 1st line tx, when are AntithyroidMeds actually **preferred as 1st line** as *Thyroid* tx for [symptomatic Hyperthyroidism]? (4)
1. Cardiacpropranolol 2. Thyroid ([AntithyroidMed1st line] vs [Radioactive iodine ablation] vs [Thyroidectomysurgery]) * * * a. [*mild* hyperthyroidism] b. [Pregnancy (PTU→ MTZ → MTZ)] c. Elderly(older with limited life expectancy) d. Prep for [radioactive iodine ablation]
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Patients with Graves disease have [⬜positive | negative] Thyroid Stimulating Immunoglobulins and ⬜ uptake on radioiodine scintigraphy \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [RadioActive Iodi**_n_**e ablation] is contraindicated c❌d in pregnancy and lactation When is it indicated for Graves tx? (5)
positive; diffuse \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 1. alternative to **AntiThyroids**(if unable to tolerate) 2. alternative to [**ThyroidectomySurgery** ](if surgery not preferred) 3. [*SEVERE* hyperthyroidism +/- ophthalmopathy] 4. [*Moderate* hyperthyroidism +/- ophthalmopathy] 5. [*mild* hyperthyroidism +/- ophthalmopathy](* *PATIENT PREFERENCE* *) * * * *C❌D(pregnancy, lactation)* *| RAI ablation is useful in Graves/Toxic nodular thyroid since INC uptake concentrates Radioactive isotope in diseased thyroid*
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Patients with Graves disease have [⬜positive | negative] Thyroid Stimulating Immunoglobulins and ⬜ uptake on radioiodine scintigraphy \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ When is [ThyroidectomySurgery] indicated for Graves disease ? (5)
positive; diffuse \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ a.{Pregnant (and can't 1st tolerate [ThionamidesAntithyroid])} [b. GOITER(LARGE | Retrosternal_obstructive)] c. [Thyroid CA (suspicion|confirmed)] d. [1º Hyperparathyroidism superimposed] e. *SEVERE* OPHTHALMOPATHY
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What do you use to track thyroid function in pt who just started AntiThyroid Rx*(drugs vs Radioactive Iodine vs SURGERY)*? (3)
- [TSH*nml0.4 - 4* *(TSH q 4mo if Chronic Amiodarone Rx)*] - [**FREE** T4 *nml0.9 - 1.7*] - [total T3] ## Footnote *[Free T4 = 0.9 - 1.7]*
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# Identify and Explain the finding What diagnosis does this indicate?
Seidel Sign ⼀*concentrated fluorescein uptake (indicating corneal epithelial defect) with subsequent clearing in a waterfall pattern (indicating fluorescein is being washed out by inappropriately draining aqueous humor)* *\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_* Full Thickness Corneal laceration
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# Pt presents with positive Seidel sign a. Diagnosis? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ b. Management of this diagnosis?
a. Full thickness Corneal **LACERATION** \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ b. ⼀URGENT OPTHO CONSULT!! If laceration extends through the full thickness of cornea ➜ can create [perforated open globe injury] = STAT SURGICAL REPAIR \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *Seidel sign= concentrated fluorescein uptake with subsequent clearing (from draining aqueous humor) in waterfall pattern*
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How do you manage Corneal Abrasion? -3
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* Both insulinoma and [surreptitious med use**(Exogenous insulin vs Oral hypOglycemic agents)**] can present with hypOglycemia sx* * \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_* When is it clinically indicated to workup a patient with hypOglycemia?
**ONLY IF [⊕ WHIPPLE'S TRIAD\*]** = clinical hypOglycemia = workup indicated 1. low BG 2. [*SADHAT*hypOglycemia sx] 3. [*SADHAT*sx] resolve with glucose admin \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *\*Whipple's Triad is required because many people have low BG without hypOglycemia sx = not clinically significant hypoglycemia*
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* Both insulinoma and [surreptitious med use**(Exogenous insulin vs Oral hypOglycemic agents)**] can present with hypOglycemia sx* * \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_* clinical hypOglycemia is characterized by the presence of ⬜ How do you workup clinical hypOglycemia? -4
**[⊕ WHIPPLE'S TRIAD]** = clinical hypOglycemia = workup indicated 1. low BG 2. [*SADHAT*hypOglycemia sx] 3. [*SADHAT*hypOgluc sx] resolve with glucose admin
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* Both insulinoma and [surreptitious med use**(Exogenous insulin vs Oral hypOglycemic agents)**] can present with hypOglycemia sx* * \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_* Why is [HIGH or normal serum Insulin] in a patient p/w hypOglycemia sx concerning and require additional workup? (2)
1) Normally, hypOglycemia ➜ negative feedback ➜ suppression of release of [Insulin/CPeptide/ProInsulin] = [low serum Insulin ✅] 2) If Pt has sx hypOglycemia but [High or normal serum Insulin] there must be an abnormal additional source of Insulin (exogenous vs endogenous) = additional workup
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What is the [mixed meal challenge] used for?
evaluates Pts who only have hypOglycemia sx after eating
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What lab is ordered alongside C-Peptide to evaluate endogenous insulin production?
Proinsulin
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The most common cause of DEC vision in elderly patients are ⬜ with ⬜ . Why is the evaluation so critical for these conditions? (2)
▶([cortical cataracts] ; [AMD]) ▶Elderly Cataracts patients must be thoroughly evaluated for severity of [*cca*AMD] since they: 1.may require both [Cataract lens extraction Surgery] *AND [ccaAMD] tx (PO eye vitamin)]* or 2. may not benefit from [Cataract lens extraction Surgery] at all *(since opacified lens prevent* [*cca*AMD] *progression)* [*cca*AMD]*: (Cortical Cataract) associated -Age related Macular Degeneration*
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The most common cause of DEC vision in elderly patients are ⬜ with ⬜ . Describe each condition
([cortical cataracts] ; [*cca*AMD]) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ **[cortical cataracts]**: nonpainful *slow progressive lens opacification* ➜ *blurry vision but fields intact* with **[*****cca*****AMD]**:*(potentially irreversible)* ***loss of central vision** due to central retina degeneration ➜ poor reading, scotomas, dim vision, [dry AMD with Drusen], [wet AMD with choroidal neovascularization]* [*cca*AMD]*: (Cortical Cataract) associated -Age related Macular Degeneration*
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Similar to CROA amaurosis fugax ⬜ also usually presents with sudden uL nonpainful vision loss
Retinal Detachment
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Pt with sudden eye pain, has *Visualization of leukocytes in the anterior segment* of her eye Dx? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ What other 5 sx would you expect?
[IritisAnterior Uveitis] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 1. photophobia 2. pain 3. redness 4. vision loss 5. [irregular constricted pupil] * 6. [Leukocytes in ANT segment]*
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Infectious Keratitis sx (3)
1. **corneal opacity** 2. severe photophobia 3. difficulty keeping affected eye open
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*s/p coronary angiography, patient soon after develops palpitations, fatigue, heat intolerance, sweating* Diagnosis? Explain \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Which diagnostics support this dx? (3)
Iodine-induced hyperthyroidism; [pts with Nodular thyroid dz or Chronic iodine deficiency] have INC risk for thyrotoxicosis following [**iodine exposure** (*radiocontrast for Coronary angio or imaging /amiodarone)* . \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [DEC TSH], [⊝thyrotropin R Ab], [US: ⇪ vascularity +/- nodules]
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*s/p newly starting amiodarone, patient soon after develops palpitations, fatigue, heat intolerance, sweating* Diagnosis? Explain \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Tx for this? (2)
Iodine-induced hyperthyroidism; [pts with Nodular thyroid dz or Chronic iodine deficiency] have INC risk for thyrotoxicosis following [**iodine exposure** (*radiocontrast for Coronary angio or imaging /amiodarone)* . \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 1. [BBlocker Propranolol] 2. [Methimazole *(add if Severe hyperthyroidism vs elderly heart disease)*]
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[Lugol ⬜ solution] is a solution containing ⬜ that does what mechanistically? Indications? (2)
(**LARGE LOAD iodiNe**) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 👄 *(Wolff-Chaikoff phenomenon)* = _any_ [**LARGE LOAD iodiNe**] →actually *paradoxically* inhibits TPO (temporarily) → [⬇︎iodiNe organification and coupling] → [⬇︎thyroid hormone synthesis] 👄[Lugol (**LARGE LOAD iodiNe**) solution] = clinically activates (*Wolff-Chaikoff phenomenon*) → [⬇︎thyroid hormone synthesis] for: \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 1. [prethyroidectomy in Graves disease] 2. [acutethyroid storm tx]
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Prednisone is used to treat which 3 thyroid diseases?
1. [PDSGT-(Painful Dequervain Subacute Granulomatous Thyroiditis)] \* 2. [amiodarone *destructive Type 2* thyroiditis] \* 3. thyroid storm ⼀*DEC conversion of T4 ➜ [active T3]* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *\*used in thyroid when destruction of gland ➜ preformed thyroid hormone being released.*
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# [*normal* Retina] = (⬜-4) on fundoscopy describe how a [*Papilledema* Retina] looks on fundoscopy (4) | 🔎[*Papilledema* Retina] = [Retina io\Papilledema]
[*normal* Retina] = normal**DSLs**= [**D**isc margin defined/**S**mall veins *linear* /**L**arge veins defined]/ [**s**plinter hemorrhage] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ | "*my Retina loves **DSLs***" ## Footnote [*Papilledema* Retina*(Retina in the setting of Papilledema)*] = Papilledema⚠️**DSLs** = [**D**isc margin *OBSCURED* / **S**mall veins *SERPENTINE /* **L**arge veins *OBSCURED*] / [**s**plinter hemorrhage**⊕**]
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normal range for TSH
0.4 ⼀ 4.0
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normal range for [**free** thyroxine T4] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [Total Thyroxine T4]
**free** thyroxine T4**[0.9 ⼀ 1.7]** \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ## Footnote 5-12
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# "Thyroiditis" suggest ⬜2. And there's 3 types: PDSGT, hCAT, [NSLP-hCAT] *[NSLPhCAT]* *: [**N**onpainful(silent) **S**ubacute **L**ymphocytic **P**ostpartum]hCAT* ## Footnote Clinical Features (4) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Diagnostics (2)
[Lymphocyte infiltration [Transient HYPERthyroidism] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 1. variant of hCAT(dx = [⊕TPO antibody], [low RAIU]) 2. HYPERthyroid *transiently* → hypOthyroid (or sometimes Euthyroid) → spontaneous recovery 3. Goiter**Nonpainful**, small 4. includes postpartum thyroiditis (midaged Women postpartum) | *🔎TPO = ThyroPerOxidase* ## Footnote * * * *[NSLPhCAT] dx =same as hCAT dx:* a. ⊕TPO antibody b. low RAI uptake
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# "Thyroiditis" suggest ⬜2. And there's 3 types: PDSGT, hCAT, [NSLP-hCAT] *hCAT: [**hashimoto** Chronic Autoimmune Thyroiditis]* ## Footnote Diagnostics (2)
[Lymphocyte infiltration [Transient HYPERthyroidism] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ * * * - ⊕[Thyroid PerOxidase Ab] - [**low**RAI uptake]
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# "Thyroiditis" suggest ⬜2. And there's 3 types: PDSGT, hCAT, [NSLP-hCAT] *hCAT: [**hashimoto** Chronic Autoimmune Thyroiditis]* ## Footnote Clinical Features (5)
{[Lymphocyte infiltration [Transient HYPERthyroidism]} \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 1. [initial Transient HYPERthyroid[damage from *AntiTPO*Lymphocytes(= Lymphocytes that secrete **AntiTPO Abs**) → infiltrate thyroid follicles → [*preformed* T4/T3/TG] thyroid reservoir release] 2. **damage ultimately → hypOthyroid**(since damage impairs thyroid function) 3. GoiterDIFFUSE 4. daughter condition = [NSLPhCAT] 5. → CA*(hCAT can → Thyroid DLBL)*
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# "Thyroiditis" suggest ⬜2. And there's 3 types: PDSGT, hCAT, [NSLP-hCAT] *PDSGT: [**P**AINFUL **D**eQuervain **S**ubacute **G**ranulomatous **T**hyroiditis]* Clinical Features (5)
[Lymphocyte infiltration [Transient HYPERthyroidism] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 1. Postviral inflammatory process 2. self-limited 3. **PAINFUL** **DIFFUSE ENLARGED GOITER** 4. FEVER [from postviral inflammatory process(*etx: viral antigens provoke [CD8 cytotoxic T-lymphocytes] against Thyroid follicles → follicular injury → ****) 5. **_HYPER_**thyroid(TT Feels ARCHED) symptoms ## Footnote {PDSGT etx: *(Viral antigen cross rxn) → [**PAINFUL** autoimmune CD8 follicle infiltration( = **large painful goiter**, FEVER, ⇪ESR, ⇪CRP)] → [release of stored T4/T3 = **transient HYPERthyroid**] → DEC TSH → DEC iodine organification → DEC iodine demand = **DEC RAIU****}
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# "Thyroiditis" suggest ⬜2. And there's 3 types: PDSGT, hCAT, [NSLP-hCAT] *PDSGT: [**P**AINFUL **D**eQuervain **S**ubacute **G**ranulomatous **T**hyroiditis]* Dx labs (3)
[Lymphocyte infiltration [Transient HYPERthyroidism] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ - - ⇪ ESR - ⇪ CRP - [***low*** RadioActive Iodine Uptake]thyroid scintigraphy ## Footnote {PDSGT etx: *(Viral antigen cross rxn) → [**PAINFUL** autoimmune CD8 follicle infiltration( = **large painful goiter**, FEVER, ⇪ESR, ⇪CRP)] → [release of stored T4/T3 = **transient HYPERthyroid**] → DEC TSH → DEC iodine organification → DEC iodine demand = **DEC RAIU****}
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# "Thyroiditis" suggest ⬜2. And there's 3 types: PDSGT, hCAT, [NSLP-hCAT] *PDSGT: [**P**AINFUL **D**eQuervain **S**ubacute **G**ranulomatous **T**hyroiditis]* Explain Why does *PDSGT* have low RAIU??
[Lymphocyte infiltration [Transient HYPERthyroidism] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ -[Elevated ESR & CRP]labs -[***low*** RadioActive Iodine Uptake]thyroid scintigraphy * * * {*(Viral antigen cross rxn) → [**PAINFUL** autoimmune CD8 follicle infiltration( = **large painful goiter**, FEVER, ⇪ESR, ⇪CRP)] → [release of stored T4/T3 = **transient HYPERthyroid**] → DEC TSH → DEC iodine organification → DEC iodine demand = **DEC RAIU****}
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# "Thyroiditis" suggest ⬜2. And there's 3 types: PDSGT, hCAT, [NSLP-hCAT] *PDSGT: [**P**AINFUL **D**eQuervain **S**ubacute **G**ranulomatous **T**hyroiditis]* Tx (3)
[Lymphocyte infiltration [Transient HYPERthyroidism] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 1. [NSAIDs ➜ Prednisone*(refractory)*] 2. [Propranolol (or Atenolol)] 3. [self limited (viral infxn → [*PDSGT* HYPERthyroid]3w → hypOthyroid → Euthyroid)] * * * ## Footnote {PDSGT etx: *(Viral antigen cross rxn) → [**PAINFUL** autoimmune CD8 follicle infiltration( = **large painful goiter**, FEVER, ⇪ESR, ⇪CRP)] → [release of stored T4/T3 = **transient HYPERthyroid**] → DEC TSH → DEC iodine organification → DEC iodine demand = **DEC RAIU****}
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On Thyroid Scintigraphy, when do you see Patchy uptake? ## Footnote * * * Clinical features of this condition (3)
toxic multinodular goiter * * * 1. {HYPERthyroidthyrotoxicosis **(TT F**eels**ARCHED)**} 2. nodular enlargement 3. OLDER patients
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On Thyroid Scintigraphy, when do you see Diffuse uptake? * * * why do you see diffuse uptake in this condition?
[Graves*1º HYPERthyroidthyrotoxicosis*] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [thyrotropin R autoantibodies] stimulate thyroid *diffusely* to [INC iodine uptake] and [INC thyroid hormone synthesis]
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clinical features of Ocular melanoma (4)
★ [1º malignant melanocytes from uvea*(choroidal pigmented nevus)*] ★ [identified *incidentally* frequently] ⼀[gold standard dx = US] ★ {⊝**sx** or [small (diameter\<10mm) (thickness\<3mm) pigmented lesion] = [**observation** (repeat exam in 3 mo, then q6 mo)]} ★ {⊕SX or [LARGE (d ≥10mm)(t ≥3mm)] = XBRT --(*if VERY LARGE or extrascleral extension*)--\> Enucleation | *Enucleation: removal of entire globe and intraocular contents*
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In hospital setting, American Diabetes Association suggest maintaining inpatient glucose at ⬜
140-180
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▶Hospitalized* * [**⬜** DM1 | DM2] patients' basal insulin **must** be continued at all times in hospital. But because ⬜, inpatient basal insulin has to be DEC by ⬜% from prehospital dose ▶Describe the 3 basic components of Hospital Insulin administration
DM**1** (*inpatient basal insulin is req'd for ALL hospitalized DM1 patients and most DM2*) ; [hospitalized patients eat _less_ than normal = INC hypOglycemia risk] ; [25-50%] * * * **BNC** [**B**asalLA or IA]= controls glucose between meals*ALL DM1 (and most DM2)* [**N**utritional bolusSA] = controls postprandial glucose excursions*req'd only for patients eating obvi* [**C**orrectional bolus Sliding ScaleSA] = corrects random hyperglycemic excursions \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *L/I/SA: Long/Intermediate/Short-ACTING*
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When should you consider insulin infusion pump for IDDM pts (5)
1. critical illness 2. DKA 3. HHONKS 4. perioperation 5. [(SQ insulin) failure]
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# nml TSH: [0.4-4.0] TSH-secreting pituitary adenomas cause ⬜ with elevated ⬜ and ⬜ levels. How can this pituitary adenoma be differentiated from other (*FLAT PiG*) pituitary adenomas? (3)
central Hyperthyroidism; [TSH] & [T4/T3] * * * * * Although [mass effect (HA, visual ∆ )] = common pituitary adenoma sx…* * 85% [**TSH** pituitary adenoma] tumors secrete [**biologically inactive alpha subunit**] = * elevated [**(Bi)alpha subunit**]? = likely from ⊕[**TSH** pituitary adenoma] *tx = somatostatin analog vs transsphenoidal surgery*
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Dx?
[NMER]*Glucagonoma* | (necrolytic migratory erythematous rash) ## Footnote ***DAN** had a Glucagonoma!* Glucagonoma triad: DM, [NMER (necrolytic migratory erythematous rash)], [Anorexia weight loss] * * * *Glucagonoma is a rare but malignant pancreatic tumor of the [islet alpha cell] that secretes VIP, calcitonin, GLP1 / dx = high glucagon level / tx = surgical*
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Sulfonylurea MOA \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ List examples-5
closes {[pancreatic β islet cell] *ATP-sensitive*K+ Efflux channel*( which typically closes from ⇪ATP)*} → inner cell membrane depolarization → Ca+ INflux → **endogenous** insulin Efflux secretion = **insulin secretagogue** \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 1. 2GGlimepir_**ide** 2. 2GGlybur_**ide** 3. 2GGliPiz_**ide** 4.1G*Chlorpropam**ide*** 5.1G*Tolbutam**ide*** | G = Generation ## Footnote *[Megliti**Nide**s ("Repagli**Nide**, "Nategli**Nide**")] = same MOA as Sulfonylurea*
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Meglitinide MOA \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ List examples-2
**insulin secretagogue**= (*same as Sulfonylurea MOA*) stimulates **endogenous** insulin secretion \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 1. Nategli_nide_ 2. Repagli_nide_
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[Alpha glucosidase inhibitor] MOA \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ List examples-2
inhibits α-glucosidease ➜ inhibits intestinal carb digestion → ⬇︎postprandial HYPERglycemia \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 1. Acarbose 2. Miglitol
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[DPP-4 inhibitors] MOD \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ List examples-2
inhibits [DPP-4 GLP1 peptidase] --\> ⬆︎GLP1--\> ⬆︎Glucose-induced insulin release \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 1. SitaGliptin 2. SaxaGliptin
135
What are the GLP1 homologs?-2 ; What do they do?
1. ExenaTIDE 2. LiragluTIDE *These require Injections* | ⬆︎Glucose-induced insulin release ## Footnote "GLP1a says... "**iLAGG** behind food" [⇪**i**nsulin *secretion* & *sensitivity*⇪*[Glucose-induced Insulin Secretion]* [⬇︎**L**iver Glucose secretion] [⬇︎ **A**ppetite*(secreted after food intake)*] [⬇︎**G**astric emptying*(⚠️Pancreatitis risk)*] [⬇︎ **G**lucagon secretion]
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Classic Presentation for DM -5
**FUDge**
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# Clomiphene Citrate MOA \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Indication
[hypothalamic estrogen🟥]***SERM***; PCOS Infertility
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# Leuprolide MOA \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Indication
[GnRH🟢] ; endometriosis
139
How does respiratory rate affect Calcium levels?
Tachypnea causes ⬇︎CO2 acid --\> H+ ions dissociate from albumin so they can help maintain pH --\> ⬆︎free albumin which bind to free ionized Ca+ --\> overall ⬇︎ in ionized unbound calcium
140
# [Normal serumCa+: 8.4-10.2] *Pt presents with hypOcalcemia* How do you work this up? -5
141
# [Normal serumCa+: 8.4-10.2] *causes of hypOcalcemia can be categorized based on PTH level* What are the causes of [hypOcalcemia(**HIGH PTH**)]? -6
1. vitD deficiency 2. Chronic Kidney Disease 3. Pancreatitis 4. Sepsis 5. Tumor lysis syndrome 6. pseudohypOparathyroidism
142
# [Normal serumCa+: 8.4-10.2] *causes of hypOcalcemia can be categorized based on PTH level* What are the causes of [hypOcalcemia(**low/normal PTH**)]? -9
1. a. Parathyroidectomy 2. b. Thyroidectomy 3. c. radical neck surgery 4. d. [Polyglandular autoimmune syndrome] 5. e. Metastatic CA 6. f. Wilson disease 7. g. hemochromatosis 8. h. [(*PTH R*) gene mutation] 9. i. [(*Calcium-sensing R*) gene mutation]
143
cp for Glucagonoma - 3
***DAN** had a Glucagonoma!* 1. **D**M 2. **A**norexia weight loss 3. **N**ecrotic Migratory Erythema (perioral, extremities, perineum)
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dx for Glucagonoma ## Footnote ***DAN** had a Glucagonoma!*
Glucagon \>500 ## Footnote Look for **N**ecrotic Migratory Erythema!
145
Pt w hx Graves disease s/p [RadioActive iodine ablation], now with iatrogenic hypOthyroidism. You've just learned, pt *may* also have Celiac disease. * * * How is Celiac disease related to Thyroid disease? (3)
★ [Celiacmalabsorption] is common with autoimmune thyroid disease = frequent cause of levothyroxine malabsorption ★ Pt now with iatrogenic hypOthyroidism needs Levothyroxine replacement , but potential [Celiacmalabsorption] will → [**constant escalating dose requirements of Levothyroxine**] ★ Celiac dx = (elevated serum anti-**TED** → endoscopy). If ⊕Celiac → gluten-free diet → restores nml Levothyroxine absorption * * * * Take Levothyroxine [on empty stomach30-60m ac] and [4h before other drugs]*
146
Pt w hx Graves disease s/p [RadioActive iodine ablation], now with iatrogenic hypOthyroidism. You've just learned, pt *may* also have Celiac disease. * * * In pts with hypOthyroidism, name 6 co-conditions that will cause INC requirement for Levothyroxine replacement
1. [Malabsorption\_Disease (Celiac)] 2. [Malabsorption\_Rx (iron, Ca+)] 3. [catabolic Thyroxine-T4\_Rx (*INC Thyroxine metabolism:* phenytoin, carbamazepine, Rifampin)] 4. Obesity 5. Pregnancy 6. overt prOteinuria * * * *Take Levothyroxine [on empty stomach30-60m ac] and [4h before other drugs]*
147
Explain how patients should take Levothyroxine? (2)
Take Levothyroxine [on empty stomach30-60m ac] *--and ---* Take Levothyroxine [4h before other drugs]
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# Pts with hypOthyroidism will require a [Levothyroxine replacement regimen] Describe the 3-part [Levothyroxine replacement regimen] for pts with hypOthyroidism
**IBM** **I**: { **I**nitial[75-125mcg/day]*(or 25-50 for elderly | CVD) *} ⬇ **B**:{ [**B**oost/INC Dose q6w until TSH nml0.4-4 } ⬇ **M**: {**M**aintain & Monitor TSH q6-12months] * * * * note: elevated TSH despite constant escalating levothyroxine doses = levothyroxine malabsorption (c/s Celiac)*
149
How is an ovarian tumor related to thyroid regulation?
[Struma Ovarii ovarian teratoma] = *rare* ovary tumor that ectopically secretes thyroid hormone → [*rare* ectopicHYPERthyroidism with low TSH]
150
# nml TSH: [0.4-4.0] clinical features of [**NSLPhCAT**] (5)
[Nonpainful Subacute Lymphocytic Postpartum Thyroiditis]hCAT = [(transienthyper*T*) → ( transienthypO*T* ) → normal*T*] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 1. **within ≤1 year postpartum** {[TPO Ab inflammation] → [release of preformed T4 + preformed Thyroglobulin] → [nonpainful goiter + transienthyper*T*] } 2. {[transienthyper*T*] → [transienthypO*T* *with ⬇︎RAIU*due to positive feedback's_⬇︎TSH] ) → normal*T*] (PDSGT also)} 3. [variant of *hCAT*] (PDSGT also) 4. [⊕TPO Ab] ⼀(PDSGT also) 5. [⇪T4, ⇪Thyroglobulin, ⬇︎TSH, ⬇︎RAIU]
151
What is Thyroglobulin? (2)
used to build thyroid hormone in thyroid follicle, and then **co-secreted with endogenous thyroid hormone secretion** ## Footnote * * * = *in* *pts exogenously taking thyroid hormone → [⇪ T4 but ⬇︎Thyroglobulin]* * = Graves disease → [⇪ T4, ⇪ Thyroglobulin]* * =hCAT (PST, PT) → [⇪ T4, ⇪ Thyroglobulin] (2/2 inflammatory release of preformed T4 and preformed Thyroglobulin)*
152
Diabetic retinopathy requires years to develop and occurs 2/2 ⬜3. For patients with sx, what's most likely to improve their sx?
1. macula edema 2. proliferative diabetic retinopathy [→ vitreous bleeding → retinal detachment = blindness] 3. lens edema * * * improve glycemic control
153
# Amiodarone....is Thyrotoxic lol and TSH should be obtained every 4 months while on chronic Amiodarone therapy Explain all the mechanisms for how Amiodarone cause thyroid dysfunction? (5)
Amiodarone's ## Footnote hypOT1: nml pt[**LARGE LOAD IODINE]***= Wolff-Chaikoff Effect: [large load iOdine] DEC thyroid hormone synthesis = hypOT)* hypOT2. **[intrinsic inhibition (Thyroid hormone synthesis)***= hypOT***]TX: LEVOTHYROXINE** hypOT3. **[intrinsic inhibition (T4 → T3 conversion)***= hypOT* **]TX: NONE** * * * HyperT1. Nodular/Graves[**LARGE LOAD IODINE**]*= AIT1: large iOdine load INC thyroid hormone synthesis = HyperT)*]**TX: Antithyroids** HyperT2. [[**AIT2**]*=destructive thyroiditis: ( → preformed T hormone release→ INC thyroid hormone = HyperT )*]**TX: Prednisone CTS-GC**]
154
[T or F] TSH should be obtained once a year for patients on chronic amiodarone therapy
FALSE | *chronic Amiodarone pts require TSH **every 4 months***
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Pts taking Levothyroxine must take it [\_\_\_\_ with water] ⬜ minutes before breakfast. [Calcium supplements] and [Iron supplements] ⬜ absorption of levothyroxine; thus *Ca+/Fe* should only be taken ≥ ⬜ hours after taking levothyroxine.
on empty stomach; 30-60m PREVENT; 4h ; *otherwise Ca+/Fe may possibly cause worsening hypOT in pts taking Levothyroxine*
156
Why does T2DM rarely present with ketoacidosis at disease onset? (2)
T2DM does not involve absolute insulin deficiency (like T1DM) and glucose metabolism is sufficient to prevent ketosis
157
What is [monogenic DM (MODY)]? (3)
**MDM** [(**M**onogenic **D**M (**M**aturity Onset DM of Young)]: 1. **AUTO DOM EARLY ONSET DM = 2-3 GEN FAM HX** 2. defective glucose sensing and defective insulin secretion 3. Young/normal wt but early DM
158
What are the 4 ways to Diagnose DM
“**H**aving **T**reats **F**eels **R**isky” ## Footnote *note: Asymptomatic patients with Abnml screening require a repeat of the same test on a different day for confirmation*
159
Central Retinal artery occlusion symptoms (4)
*_Vision Loss_ that's…* 1. monocular 2. [Severe BUT nonpainful 3. …with **temporal sparing**] 4. [hx of amaurosis fugax]
160
Central Retinal artery occlusion management (4)
1. optho consult 2. intraarterial thrombolytics 3. ocular massage 4. IOP reduction (ANT chamber paracentesis)
161
Central Retinal artery occlusion clinical findings -2
- [Pale fundus*(2/2 diffuse ischemia)*] - [cherry red macula]
162
Central Retinal Vein occlusion symptom
blurred-to-severe nonpainful vision loss
163
Central Retinal Vein occlusion clinical finding
**Blood & Thunder** (Fundus w retinal hemorrhages & optic disc edema)
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Central Retinal Vein occlusion management -2
[Observation] [+/- intravitreal injection of VEGF inhibitors]
165
[**T**orn Retinal Detachment] symptoms (3)
1. **F**loaters 2. [**F**lashing lights(Photopsia)] 3. {[**F**ield of periphery nonpainful vision *loss 1st*]→ [central nonpainful vision *loss 2nd*]}*= “Descending Visual Curtain” progressive vision loss*
166
[Torn Retinal detachment] clinical findings (2)
1. marked elevation of retina 2. Vitreous hemorrhage
167
Retinal detachment management
Surgical correction (retinopexy, vitrectomy)
168
Vitreous hemorrhage symptom (4)
1. [Hazy vision +/- red hue] 2. nonpainful vision loss 3. Floaters 4. Shadows
169
Vitreous hemorrhage clinical findings (3)
1. [red reflexabsent or DEC ] 2. floating debris/RBC in Vitreous 3. obscured fundus view
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Vitreous hemorrhage management (3)
1. Bed rest with 30-45° Head-Of-Bed elevation 2. photocoagulation 3. vitrectomy (some cases)
171
What are the 4 causes of [acute **nonpainful** vision loss]?
***CCTV** is a nonpainful way to _look_😏 ✅* 1. **C**entral Retinal occlusion⼀arterypale fundus + cherry red spot/amaurosis fugax hx 2. **C**entral Retinal occlusion⼀VeinBlood & Thunder fundoscopy 3. **T**orn (Detached) RETINA[flashing lights Photopsia] 4. **V**itreous hemorrhagehazy vision/red hue/absent red reflex/floating debris
172
What are the most common causes of this condition? (4)
**CAROTID ARTERY ATHEROSCLEROSIS** \> cardiogenic embolism, clotting DO, [giant cell arteritis (vasculitis)] ## Footnote * * * * Central Retinal artery occlusion*
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clinical presentation of Optic Neuritis (3)
- [subacute (hours to days)] monocular **PAINFUL** vision loss ⼀ pain worse with eye movement. - Fundoscopic optic disc edema - (+/- afferent pupillary defect)
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*[Functional Pituitary Adenomas] consist of what 3 adenomas?* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Describe etx of [**NON**Functional Pituitary Adenoma] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Tx?
Functional Pituitary Adenoma= **Lactotrope** **\> Somatotrope \>** Corticotrope * * * [**NON**functional pituitary adenomas] arise from [LH/FSH Gonatrope cells of the PITUITARY GLAND ➜ *unique* [isolated ⇪ (nonfunctional)αlpha subunit] ➜ [⊕feedback on hypothalamusGonatrope] → [decreased low LH/FSH gonadotropin levels] ➜ hypOgonadism + mass effect if tumor large enough * * * Tx = Trans-Sphenoidal Surgery
175
Why do pts with hypOthyroid require INC dose of levothyroxine if they start taking estrogen-containing OCP? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ how is this managed?
**Estrogen** stimulates liver to make ⇪ [thyroxine binding globulin] ➜ ⇪ binding sites to saturate➜ DEC free T3/T4 Normal thyroid ⇪ [free T3/T4] to saturate the additional TBG binding sites BUT hypOthyroid patients are unable to INC thyroid hormone synthesis \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ get TSH weeks after starting Estrogen-OCP and titrate to normal thyroid function
176
⬜ is the leading cause of death in pts with Acromegaly. What other comorbidity are they at risk for? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ which comorbidity is reversible with treatment?
[Cardiovascular disease (REVERSIBLE)] ; Colon CA \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Cardiovascular Disease is reversible with tx
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[Anabolic Androgen Steroids] ➜ symptomatic ⬜ from DEC ⬜ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ how long after d/c does it take to naturally recover?
hypOgonadism ; endogenous testosterone \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ recovers weeks/months after d/c but will be permanently suppressed if chronic abuse
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[Anabolic Androgen Steroids] clinical features -8
**MEATHEAd** 1. [**M**uscle mass ⇪] 2. ****_E_**RYTHROCYTOSIS** 3. **A**ggression 4. [(**T**estosterone/LH/FSH DEC )→ (Testicular size DEC) + (spermatogenesis DEC)] 5. [**H**LD( ⇪ LDL|⬇︎HDL)] 6. [**E**rection & Libido[(normal during use) / (DECREASED DURING WITHDRAWAL)] 7. **A**cne 8. ***d**oubleD-*Gynecomastia
179
Describe insulin regimen for IDDM or Type 1 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Basal + [3 prn meal] ## Footnote * basal = [NPH BID] or [GluLargine QD]* * \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_* * ​ 3 prn meal = [3 reg insulin c meals]*
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what adjustments should be made for exercise induced hypoglycemia in a IDDM/Type 1 DM? -3
- [⬇︎*basal* insulin (NPH BID vs GluLargine QD)] - eat before exercise - avoid insulin injection into "exercise" limbs
181
tx Conjunctivitis -10
**CAPE** ⼀ **CAD ⼀MAD** 1. **B**-[***C**ontactLens* → Fluoroquinolonedrops] 2. **B**-[**A**zithromycindrops] 3. **B**-[**P**olymyxin-trimethoprimdrops] 4. **B**-[**E**rythromycinointment] * * * 1. **V**-[**C**ompressWarm/Cold] 2. **V**-[**A**ntihistaminedrops] 3. **V**-[**D**econgestantdrops] * * * 1. **A**-[**M**ast cell stabilizer]*freq episodes* 2. **A**-[**A**ntihistaminedrops]i*ntermittent/freq episodes* 3. **A**-[**D**econgestantdrops]*freq episodes*
182
⬜ is a rare complication of bacterial conjunctivitis and is managed with ⬜ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ How does this complication typically present? -3
Keratitis (inflammation of cornea) ; **URGENT OPHTHALMOLOGY CONSULT FOR TX** \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [**foreign body sensation**] / photophobia / vision impairment
183
What is a [Hordeolum Stye]
bacterial infection of [eyelid sebaceous gland]
184
Why do pts with suspected Keratitis must receive **URGENT OPHTHALMOLOGY CONSULT**? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ How is Keratitis diagnosed?
Keratitis can cause corneal scarring which ➜ blindness if untreated by optho \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ slit-lamp
185
How is Viral Conjunctivitis spread? -2
EYE DISCHARGE directly Contaminated Surfaces
186
[T or F] Crusted over eyes in the morning indicates patient is contagious with viral conjunctivitis
FALSE (only EYE DISCHARGE and contaminated surfaces transmit viral conjunctivitis)
187
What are the two definitive treatments for thyroid disease
1. Radioactive Iodine 2. Thyroidectomy
188
Potassium Iodide Indication - 2
1. PreOp tx for Thyroidectomy in Graves 2. Thyroid Storm
189
How does looking at Thyroglobulin levels help determine etiology of thyroid disease?
Thyroglobulin is the base needed to make thyroid hormone. If thyroid hormone is elevated...and Thyroglobulin is also elevated then Thyroid is naturally producing a lot of thyroid hormone \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ If thyroid hormone is elevated ...but Thyroglobulin is low then that means thyroid hormone must had been exogenousouly given
190
tx for Thyroid Storm - 3
***HHH*** needs ***PPP*** tx = [**P**ropranolol] --\> [**P**TU ---(1 hr later)]--\> [**P**otassium Iodine and PrednisoneCTS]
191
cp for Thyroid Storm - 3
***HHH*** needs ***PPP*** Hot, Head and Heart 1. **H**ot = Fever 2. **H**ead = CNS dysfunction with tremor 3. **H**eart = Tachycardia, palpitations, HTN, HF \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ tx = [**P**ropranolol] --\> [**P**TU ---(1 hr later)]--\> [**P**otassium Iodine and PrednisoneCTS]
192
What is this a complication of?
Acute Sinusitis \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *dx: Orbital Cellulitis*
193
tx for [Toxic Adenoma Thyroid Nodule] -3
[PreTx (Methimazole)] ➜ [DefinitiveTX (RADIOACTIVE IODINE ABLATION OR SURGERY)]
194
characteristic features of [Toxic Adenoma Thyroid Nodule] -2
SYMPTOMATIC HyperThyroid + [Radioiodine uptake in nodule] with suppressed uptake in remainder of gland]
195
What's the single most important risk factor for Osteoporosis?
AGE \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *less RF: fam hx / smoking / EtOH*
196
Chronic Granulomatous Disease is a (⬜*(Mode of Inheritance?)*) that usually p/w ⬜ shortly after birth from ⬜ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ MOD for Chronic Granulomatous Disease
[X-linked **recessive** 1° immunodeficiency] ; recurrent infections ; [catalase positive organisms (**Aspergillus** = MAJOR COD / **Staph A**=liver/skin abscess/adenitis)] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [Loss of NADPH oxidase] impairs intracell killing of [phagocytosed bacteria and fungi] ➜ recurrent infections
197
Macular degeneration affects [⬜ central | peripheral] vision, while Glaucoma affects [⬜ central | peripheral] vision
central * -[straight lines appearing curvy (wet/exudative-neovascular= aggressive and uL] while* * -[dry/atrophic=gradual and BL)]* * “Of course Mac is the Center!"* * * * peripheral [Glaucoma --\> Gradual tunnel vision (from gradual loss of peripheral vision)]
198
clinical presentation for [Open Globe Laceration] -2 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ what causes this injury? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ management? -4
teardrop pupil and [DEC visual acuity] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [small sharp objects penetrating globe at high velocity] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [IV abx / eye shielding / eye CT / Optho consult]
199
Elevated *Calcitonin* in pts with [Medullary Thyroid CA s/p total thyroidectomy] indicates ⬜? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ next steps? -3
**METASTASIS** \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [*metastatic* medullary thyroid CA dx] ➜ [CT neck/chest (look for metastasis)] ➜ Surgical Resection
200
What type of goiters develop from iodine deficiency? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ How do you treat [retrosternal goiter w/compressive sx]?
multiNodular \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Surgery
201
# nml TSH: [0.4-4.0] [Subclinical Hyperthyroidism Thyrotoxicosis] is defined as ⬜2 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ When is treatment indicated for [Subclinical Hyperthyroidism Thyrotoxicosis] -4
[low TSH] with [normal free T4] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ \* **ONLY** Treat(Antithyroid v RAI ablation) **IF** 1. [TSH \< 0.1] 2. or [≥65 yo] 3. or [⊕comorbidities (heart disease, osteoporosis)]
202
What is the Tuning Fork test ?
easy, inexpensive screen that assess for loss of 2TVP (usually of the BL feet) in DM *2TVP = 2-point/Touch/Vibration/Proprioreception*
203
How do you treat diabetic neuropathy? (4)
[AGGRESSIVE GLYCEMIC CONTROL] + [Neuronal transmission adjusters (Duloxetine|Gabapentin-Pregablin|TCA)]
204
a. What role does adrenal gland play in sepsis physiology? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ b. What are [stress dose steroids] ? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ c. What is the actual [stress dose steroids] *dose* for treating sepsis ?
a. normally, [stress (sepsis, surgery)] ➜ adrenal gland ⇪ [*endogenous* CortisolGlucocorticoid CTS] ➜ [⇪ adrenergic receptor sensitivity to catacholamines] ➜ [⇪ peripheral vasconstriction and ⇪ cardiac contractility] = **MAINTAINS BLOOD PRESSURE DURING STRESS** \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ## Footnote b. pts chronically immunosuppressed (RA on prednisone*for > 3 weeks*) have hypofunction of adrenal glands (due to iatrogenic Cushing syndrome) = [relative cortisol deficiency during [stress/sepsis/surgery]➜ require [exogenous corticosteroid] = [stress dose steroids] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ c. [Hydrocortisone IV 200 mg/day]*to prevent/treat septic shock*
205
What is [Inferior petrosal sinus sampling] used for?
In patients with elevated ACTH, differentiates source of ACTH ( [Corticotrope Functional Pitutiary Adenoma] vs [Ectopic (SOLC)] )
206
What level of prolactin indicates a Prolactinoma
\>200 ## Footnote Prolactin inhibits LH release
207
Clinical Presentation of of Anterior Uveitis(4) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
(***C**a**LEB***) **C**onstricted pupil / *ANTERIOR UVEITIS* / **L**imbus erythema / **E**ye pain / **B**lurred vision
208
Uveitis is associated with which conditions? (4)
*systemic inflammatory DO* 1. sarcoidosis 2. RA 3. JIA 4. HLA-B27 ## Footnote (***C**a**LEB***)sx
209
In an eyelid laceration, visible fat within the wound indicates a ______ injury \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ This raises concern for injury to which structures? -2
orbital septal injury \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ **post**septal structures (Extraocular Muscles + eyelid retractors)
210
Between NPH and [long acting insulinDetemir/GLargine/DeGLudec] which is more likely to cause hypOglycemia?
NPH | *NPH Peak effect MORE likely to → hypOglycemia*
211
Microalbuminuria is an indicator of __(3)\_\_\_. What lab value is used and what are the values for normal, micro and macro?
1. DM 2. HTN 3. PSGN Urine [**A**lbumin-**C**reatinine **R**atio]; 30-300 normal = \< 30 micro = 30-300 MACRO = 300+
212
MOD for [High Output Heart Failure]
213
Causes of [High Output Heart Failure] -7 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ What's the most common?
214
[High Output Heart Failure] clinical presentation -3
1. Edema (pulmonary & peripheral) 2. warm extremities 3. [systolic flow murmur with laterally displaced PMI]
215
what is [sub-clinical hypOthyroidism] ? -2
(INC TSH) but (normal [T4 Thyroxine])
216
most common cause of [sub-clinical hypOthyroidism] ?
hCAT ## Footnote \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *[hashimoto Chronic Autoimmune Thyroiditis]*
217
how do you know when [*subclinical* hypOthyroidism] is advancing to hypOthyroidism
[INC anti-TPO (antiThyroid PerOxidase)]
218
[subClinical hypOthyroidism] puts females at risk for ⬜ complication?
PREGNANCY ## Footnote *(spontaneous abortion/preeclampsia, abruptio placenta)*
219
cp of hypOpituitarism - 5
FLAT PiG 1. FSH/LH ⬇︎ --\> **Amenorrhea, testicular atrophy** 2. ACTH ⬇︎ --\> **⬇︎Cortisol BUT NOT ALDOSTERONE --\>** hypotension from ⬇︎arterial resistance 3. TSH⬇︎ --\> **Fatigue/hypOthyroidism** 4. Prolactin⬇︎ --\> **LACTATION FAILURE (1ST SIGN OF SHEEHAN!)** 5. GH⬇︎ --\> **Anorexia**
220
In *hCAT* , which antibodies are responsible for the attack on the thyroid gland? ## Footnote \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *hashimoto Chronic Autoimmune Thyroiditis*
Anti**T**hyroid**P**er**O**xidase ## Footnote *AntiTPO is also a/w miscarriage!!*
221
sx of hypOglycemia (6)
*low blood glucose gives you* **SADHAT** ## Footnote 1. **S**eizure 2. **A**MS 3. **D**iaphoresis 4. **H**A 5. **A**nxiety 6. **T**remor
222
labs for [factitious use of insulin]? -3
serum : ***I C**onceal **G**lucose* 1. 🔝 insulin 2. ⬇️ cPeptide 3. ⬇️ glucose
223
# Zollinger Ellison etx \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ cp-2
gastrin producing tumor in pancreas or duodenum --\> [⬆︎⬆︎gastric acid \> 1000] --\> 1. multiple duodenal/jejunal ulcers **REFRACTORY** to PPI 2. steatorrhea from pancreatic enzyme inactivation *Be sure to screen Zollinger Ellison pts for MEN1 using PTH, Ca+ and Prolactin studies*
224
for IDDM, how much daily insulin should be prescribed?
225
What things cause HYPERKalemia? -6
226
What are the opthalmological complications of DM-3; what causes them?
1. Retinopathy (from ⬆︎VEGF --\> abnormal angiogenesis) 2. Glaucoma (⬆︎ Sorbitol eye pressure) 3. Cataracts (Glycation of Ocular lens
227
What happens to [total thyroid hormone] serum level when drugs displace thyroid hormone? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Which drugs do this?-3
[free hormone displacement] ➜ [Thyroid production ⬇︎] --\> ⬇︎TOTAL thyroid levels but normal free hormone levels 1. ASA 2. Furosemide 3. Heparin
228
Precocious puberty occurs in [girls less than ⬜ years old] and [boys less than ⬜ years old] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ How do you work this up?*(see image)*
[G\<8], [B\<9]
229
# Precocious Puberty = [g\<8] [b\<9] *A pt has just been diagnosed with [Gonadotropin Dependent (Central) Precocious Puberty]* What are the major causes of this?-2
**IDIOPATHIC** \> Pituitary tumor *ALL PTS WITH THIS SHOULD UNDERGO CONTRAST BRAIN MRI REGARDLESS OF +/- HA/VISION SX. Precocious Puberty may be the first sign before the tumor*
230
Danazol MOA \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Indication
testosterone derivative with progestin effects \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ endometriosis
231
*Teenage boy comes in with gynecomastia* How do you work this up?
**YOU DONT!** - Pubertal gynecomastia is seen in up to 66% of teenage boys mid-late puberty. It can be uL, BL and/or painful Tx = self-limited to ≤2 years
232
How long does it take [RAI ablation] therapy to treat Hyperthyroidism? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ How does radioiodine therapy actually worsen Graves ophthalmopathy? * * * * RAI: RadioActiveIodine*
1-4 mo \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ RAI eventually --\> hypothyroidism --\>⬆︎ thyroid stimulating autoantibodies --\> stimulate [orbital fibroblast] → expands [orbital tissue]
233
Riedel thyroiditis MOD
progressive **fibrosis** of thyroid gland and surrounding tissue (that looks like CA)
234
cp for HyperParathyroidism - 4
Painful **Bones***([brown tumor], [VR osteitis fibrosa cystica], fx, pseudogout)* **Renal Stones** *(Nephrolithiasis, Polyuria)* **Abdominal Groans***(constipation, pancreatitis, peptic ulcer, cholelithiasis)* **Psychic Moans***(Depression, Seizure)*
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Acromegaly cp - 13
*etx: GH stimulates IGF1 secretion most of day --\> acromegaly sx*
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Acromegaly Dx (6)
*etx: GH stimulates IGF1 secretion most of day --\> acromegaly*
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Acromegaly etx
GH stimulates IGF1 secretion most of day --\> Acromegaly ## Footnote ⊝*GH secretion is ⬇︎ by glucose and somatostatin* ⊕*GH secretion is ⇪ by EXERCISE and SLEEP*
238
How does immobilization affect Ca+ levels
**INCREASES** Immobilization --\> ⬆︎osteoclast activity --\> ⬆︎serum Ca+
239
Acute Rhabdomyolysis causes Ca+ to (⬜ [increase/decrease]) because of what?
DECREASE \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ release of Ca+ and Phosphorous from damaged muscles --\> CaPhosphate precipitation --\> drops free serum Ca+ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *HYPERcalcemia and HYPERphosphatemia can occur later during the **re**mobilization phase during recovery*
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# iCa+ = 0.76 - 1.49 How does [*serum* albumin] levels affect [*ionized* Ca+] levels?
IT DOESNT! ## Footnote [*serum *albumin] does NOT affect iCal+ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ when *BOUND*albumin*which is neutral* ⬇︎(*i.e. liver dz)* → ⬇︎[ Ca normally bound to *[albumin]*] → ⬇︎[**TOTAL** Ca+]. \_\_ \_\_ \_\_ {{ ⬇︎boundAlb 1.0 = ⬇︎TOTALCa+ 0.8}} \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ when [*FREE*albumin*(which is ⊝)*] ⇪ → likely *knocks off* Ca from *[anions]* → ⬇︎[**TOTAL** Ca+]. [**TOTAL** Ca+]. \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
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Tx for PCOS - 5
[Wt loss--\> **SOCK**] ## Footnote **S****OCK**:**S**pironolactone,**O**CP (1st line after wt loss),**C**lomiphene for infertility,**K**etoconazole \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *etx: DM/Obesity--\>Hyperinsulinemia which --\> ⬆︎⬆︎⬆︎LH secretion --\> ⬆︎ovarian theca Androgen secretion --\> Sx*
242
Which CA is known for producing calcitonin?
[*Medullary* Thyroid Carcinoma] ## Footnote also produces ACTH and VIP *associated with MEN2A and 2B*
243
Why should pts with [Medullary Thyroid Carcinoma] have a fractionated metanephrine assay ordered?
Screen them for Pheochromocytoma ## Footnote *MTC and Pheochromocytoma are associated with MEN2A and 2B*
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How do you treat [*Papillary* Thyroid Carcinoma] - 3
Surgical Resection --\> +/- radioiodine ablation and suppressive doses of thyroid hormone (in pts with risk of recurrence)
245
How is Mg associated with Ca+ levels
low Mg+ (especially in alcoholics) --\> ⬇︎PTH hormone release and PTH resistance ---\> ⬇︎serum Ca+ **AND low serum K+** ## Footnote serum Phosphorous levels are NOT affected by this phenomena!
246
What are the distinguishing features of Pancreatic VIPoma - 5
1. **Tea colored** watery secretory diarrhea 2. hypOkalemia 3. hypOchlorhydria (from ⬇︎gastric acid) 4. HYPERcalcemia from ⬆︎bone resorption 5. Facial flushing ## Footnote *tx = octreotide for diarrhea*
247
Pts with untreated Hyperthyroidism are at risk of developing what conditions? - 2
1. Bone loss from ⬆︎osteoclast activity 2. cardiac tachyarrhythmias ## Footnote Hyperthyroidism = Graves \> toxic adenoma \> multinodular goiter
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What is the most common side effect of AntiThyroid drugs? (i.e. Methimazole, PTU)
agranulocytosis * * * * Pt on AntiThyroid drugs who develop **sore throat with fever** should have WBC checked!* * Radioactive Iodine tx can --\> worsening ophthalmopathy*
249
In HYPERthyroidism, what is the mechanism for why pts have HTN?
⬆︎Myocontractility and HR
250
Why are pts who receive \> 1 unit of pRBC or whole/blood transfusion at risk for hypOcalcemia?
pRBC and whole blood **CONTAIN CITRATE** and citrate chelates **Ca+** and chelates **Mg** → DEC Ca+ and DEC Mg --\> paresthesias, Chvostek, Trousseau, Hyperreflexia | *Leukoreduction ⬇︎[Febrile Nonhemolytic Rxn] risk from transfusion*
251
What is the most beneficial therapy to ⬇︎ the progression of DM nephropathy?
BP control \< 130/80 ## Footnote *do not push HbA1C \< 7%*
252
A Pt with Hyperthyroid pt develops Sore throat and Fever after being started on Methimazole What should you assess for?
agranulocytosis * * * D/C the drug! * Pt on AntiThyroid drugs who develop **sore throat with fever** should have WBC checked!* * Radioactive Iodine tx can --\> worsening ophthalmopathy*
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A woman starts to rapidly develop facial and body hair What test do you order first to determine etiology? - 2
DHEA and Testosterone ## Footnote Hyperandrogenism suggest androgen secreting CA of ovary or adrenal glands so these test will help to determine that
254
Describe Euthyroid Sick Syndrome (2)
- **ISOLATED low T3** - can occur anytime the body is "sick" | *[Euthyroid Sick (low T3) Syndrome]*
255
Which microscopic finding is associated with Papillary Thyroid CA?
Psammoma bodies (large lamellated calcifications with ground glass cytoplasm)
256
Why can't [*Follicular* Thyroid CA] be evaluated with fine needle biopsy?
FTC involves **invasion of the tumor capsule** and/or blood vessels which can only be examined via surgical excision This is also the reason FTC has the tendency to hematogenously spread
257
Tx for {[Prolactinoma 1-3cm] or Symptomatic} - 3 | ***Prolactinoma dx = Prolactin > 200***
1. Cabergoline dopamine R agonist OR 2. Bromocriptine dopamine R agonist 3. Transsphenoidal resection if refractory
258
Tx for Prolactinoma \>3cm | ***Prolactinoma dx = Prolactin > 200***
Transsphenoidal resection surgery | {[Prolactinoma 1-3cm] or Sx⊕}= Cabergoline|Bromocriptine|*Sgry prn*
259
Graves Ophthalmopathy etx \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ risk factors?-2
Activated T cells and **Thyrotropin Autoantibodies** both stimulate retroorbital fibroblast --\> orbital tissue expansion \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Smoking, Female
260
cp for DM [LARGE nerve fiber] damage -2 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ cp for DM [small nerve fiber] damage-2
[LARGE *e**N**ormous* nerves] --\> **N**EGATIVE SX = [**N**O 2TVP] [**N**O ankle reflexes] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [small ***p**etit* nerves] --\> **p**ositive sx = **p**ain, **p**aresthesias
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cp for [Klinefelter XXY] ?-6
1. small phallus 2. [hypOgonads (small testes)] 3. hypOspadia 4. gynecomastia 5. Cryptochidism 6. Eunuchoid body
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Why do pregnant patients or patients started on OCPs require increased doses of levothyroxine if they're taking it
Estrogen --\> ⬇︎clearance of Thyroid Binding Globulin --\> additional TBG binds up all the free T4 --\> ⬇︎free T4
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[Toxic Adenoma 1ºHyperthyroid-thyrotoxicosis] MOD
autonomous production of thyroid hormones from hyperplastic thyroid follicular cells ## Footnote *if multiple uptake present, consider multinodular goiter*
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How does looking at Thyroglobulin levels help determine etiology of thyroid disease?
Thyroglobulin is the base needed to make thyroid hormone. If thyroid hormone is elevated...and Thyroglobulin is also elevated then Thyroid is naturally producing a lot of thyroid hormone \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ If thyroid hormone is elevated ...but Thyroglobulin is low then that means thyroid hormone must had been exogenousouly given
265
What is Conn's syndrome
Primary Hyperaldosteronism
266
List the ophthalmoscopy findings for [simple Diabetic Retinopathy] - 3 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ What procedure prevents this?
1. microhemorrhages 2. retinal edema 3. exudates Argon laser photocoagulation
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What are the precipitants of Pheochromocytoma?-3 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ which medication should be given prior to these precipitants?
*Don't **GAS** a Pheochromocytoma* 1. **G**eneral Beta Blockers (allows unopposed [α] stimulation) 2. **A**nesthesia 3. **S**urgery Phenoxybenzamine (irreversible general alpha blocker)
268
PTHrelatedProtein is associated with Cancer (Humoral Hypercalcemia of Malignancy) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ What is the major mechanism difference between PTHrP and PTH?
PTH ⬆︎ conversion of [25VitaminD] to [1-25VitaminD] *PTHrP comes from [SQC, breast, renal, bladder, ovarian]*
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What are the triggers of Thyrotoxicosis - 5
1. **[iodiNe contrast]** 2. **infxn** 3. {**pregnancy**[gestational transient thyrotoxicosis | childbirth]} 4. **surgery** 5. **trauma**
270
What is the best way to monitor a pt being treated for DKA - 2
1. Serum Anion Gap 2. Beta Hydroxybutyrate levels
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Primary Hyperparathyroidism and Familial hypocalciuric Hypercalcemia both present with serum Ca+ that is _____ (low/high) How do you differentiate the two?
HIGH FHH = [urine calcium : creatinine ratio \< 0.01] *Primary Hyperparathyroidism = uccr\>0.02*
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Sialadenosis etx
NONinflammatory swelling of the salivary glands caused by liver disease or malnutrition (DM, bulimia)
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Demeclocycline MOA \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Indication?
inhibits ADH-mediated renal cortical collecting duct aquaporin insertion \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ SIADH
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Tolvaptan MOA \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Indication?-2
Tol**V**aptan = [**V**2 vasopressin ADH R blocker] ; 1. [severe HF Hypervolemia] 2. [refractory SIADH]
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In pts with Diabetes Insipidus, how do you differentiate between Central and Nephrogenic causes?
Water Deprivation Test ## Footnote give Demopressin AVP after water deprivation and if urine becomes more concentrated = Central DI. If no change = nephrogenic DI. This is ALSO helpful for r/o Primary Polydipsia \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_x\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *DI* = inability to concentrate urine 2/2 [*(central DI)*⬇︎ADH] vs [*(nephrogenic DI)*renal *ADH R*⼀resistance]
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cp for Primary Hyperparathyroidism
Asymptomatic Hypercalcemia ## Footnote *Hypercalcemia sx: Painful Bones, Renal Stones, Abd Groans and Psychic Moans*
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A DM pt is not well managed on single therapy Metformin Out of the other DM drug classes, which is most effective for inducing weight loss?
[GLP1 agonist (*exenatide, liraglutide*)]
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A DM pt is not well managed on single therapy Metformin When is it appropriate to consider adding insulin?
HBA1c \> 8.5%
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A DM pt is not well managed on single therapy Metformin Out of the other DM drug classes, which have the potential to actually cause weight gain?-3
**I**nsulin [**T**hiazolidinediones (pioglitazone)] **S**ulfonylurea | *"**I**nsulin **T**ops **S**cales"*
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etx for Prader Willi Syndrome \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ cp?-4
*"short, **P**hat & retarded"* **PATERNAL** deletion of chromo15q11 thru 13 ; 1. Hyper**P**hagia --\> **P**hat (Obesity), Gastric rupture, DM2 2. hypOtonia 3. short stature 4. Mentally retarded
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etx for Angelman Syndrome \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ cp?-4
*"short, s**M**iling & retarded"* **maternal** deletion of chromo15q11 thru 13 ; 1. Frequent s**M**iling/Laughter (Moms make you smile) 2. Hand Flapping 3. short stature 4. mentally retarded
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explain how DM destroys nerves
deposition of [glycosylation products], [oxidative stress] and [microvascular injury] all --\> small nerve AND Large nerve-length dependent axonopathy
283
What is the most common cause of primary hypogonadism in males?
Klinefelter XXY
284
[McCune Albright] syndrome etx?
*all [McCune Albright] does is **P P P*** etx = autonomous activity of endocrine tissue from defect in cAMP kinase
285
causes of hypOparathyroidism -5
1. surgery(inadvertent removal) 2. Autoimmune hypOparathyroidism 3. Congenital(failure to develop = DiGeorge vs 22q11 syndrome) 4. [Familial Isolated hypOparathyroidism](Rare mutation in PTH precursor) 5. [AutoDOM hypOparathyroidism](CaSR gain-of-function mutation)
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hypOparathyroidism sx-7
**TQT** + **BOD** + **C**hvostek ## Footnote **T**rousseau(cutting off **T**ricep/forearm circulation causes Carpal Spasm) **Q**T prolongation [**T**etany (Seizures/spasm)] **B**rain(Parkinsonism/ ⇪ ICP) **O**cular cataracts **D**entition abnormalities **C**hvostek(tapping along [**C**heek-facial CN7) causes {Mouth/Nose/Eye-Contraction})
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PseudohypOparathyroidism ## Footnote clinical features -4
- Organ resistance to PTH - AutoDOM - short 4th and 5th digits - short stature
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The [Parathyroid gland] secretes ⬜ when the [⬜ receptor] detects ⬜
PTH; CaSR; [(free ionized Ca+) ⬇︎] * * *
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Name all the functions of [*PTH*Parathyroid gland] - 6
1. [ ⇪ Ca+ bone resorption*(via osteoclast activation)* → ⇪ serum Ca+] 2. [⇪renalPCT Ca+ reabsorption] 3. [⇪GI Ca+ absorption] 4. renally kicks out (P) 5. Converts [inactive 25(OH)VitD] to [**active 1,25(OH)2**VitD] 6. *_Intermittent PTH_*[⇪bone formation by activating osteoBlast]
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[Slit Lamp Exam] indication
Evalutes for abnormalities of ANT eye (conjunctiva, cornea, ANT chamber, iris)
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diagnosis? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ What's the most common cause?
Vitreous Hemorrhage \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ DM *Fundoscopy = Dark Red Glow with Loss of Fundus details*
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Causes of Corneal Abrasion - 3 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ How do you diagnose Corneal Abrasion?
1. Trauma 2. Foreign Body under eyelid 3. Contact lens --\> Corneal epithelial defect \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Fluorescein exam revealing corneal staining defect
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Glaucoma etx -3
**⇪ intraocular pressure from…** \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [⇪⇪ AH inflow/production](tx = BB|[α2 R agonist] | CAI) - - -or - - - [⬇︎⬇︎AH uveoscleraloutflow = OaG](tx = Latanoprosttopical prostaglandin) - - -or - - - \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [⬇︎⬇︎AH trabecularoutflow = CaG](tx =Muscarinic agonist ) * * * * [AH: Aqueous Humor] |[OaG/CaG: Open/Closed angle Glaucoma]*
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Name the 5 Rx for *chronic* Glaucoma Tx (5) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ how specifically does B-blockers work?
Glaucoma Problem 1: [⇪⇪ AH inflow/production] (tx = **β🟥**|**α2🟢**| **CAI**) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ - - - - - - Problem 2[⬇︎⬇︎AH uveoscleraloutflow](tx = **[Prostaglandin🟢 *Latanoprost**TOPICAL*]** - - - - - - \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Problem: 3[⬇︎⬇︎AH trabecularoutflow](tx =**[Muscarinic🟢*Pilocarpine* ]** * * * ## Footnote β🟥 --\> ⬇︎Aqueous humor secretion from Ciliary *Epithelium*
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What target organ does the M3 Receptor work in (6)
"[M1s need Brain], [M2s need Heart], [M3s BEGs for Private Lounges" "An M3 **BEGS** for **P**rivate **L**ounges" **B**ladder(contraction) / **E**yes / **G**I / **S**kin / [**P**eripheral Vasculature] / **L**ungs
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What are the causes of [Acute Closed Angle Glaucoma]? -3
Anticholinergics / Sympathomimetics / Dim light ## Footnote \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *"Closed angle needs* **OPMAT ..** STAT!"
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What is the major complaint pts with Glaucoma have?
**Gradual Tunnel Vision**
298
HIGH tone hearing loss = [**⬜** sensorineural | conductive] hearing loss
Sensorineural
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Which is more efficient at transmitting sound between Bone and Air? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Why?
**AIR!** ## Footnote \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Air interacts with ossicles FIRST, which **A**mplifies the sound conduction to cochlea
300
*Ophthalmoscopy findings include cupping of the optic disc* Diagnosis?
Glaucoma \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *Glaucoma affects peripheral vision --\> tunnel vision! OAG is more common in Blacks* ## Footnote 👓*cupping is caused by thinning of outer rim of optic disc head*
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etx of Cataracts \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ What are the most common presenting sx of Cataracts? -2
[⇪ lens **opacity**] --\> 1. [gradual BL NIGHT VISION ⬇︎] 2. halos around lights \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *Fundoscopy eventually shows lost of red reflex and retinal details*
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What is the treatment for Emergent Acute [Closed angle Glaucoma] - 5
*"Closed angle needs* **OPMAT ..** STAT!" [**O**PHTHO CONSULT STAT!(for Emergent Iris resection!)] **P**ilocarpine*[Cholinergic M3 R agonist]* **M**annitol **A**cetazolamide*CAI* **T**imolol*BB*
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diagnosis?
Retinoblastoma leukocoria
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Dx for [Acute Closed angle Glaucoma] -2
**Gonioscopy** vs Ocular Tonometry ## Footnote \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *"Closed angle needs* **OPMAT ..** STAT!"
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diagnosis?
Zoster Ophthalmicus \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *finding = Dendriform Corneal Ulcer*
306
MOD for Trachoma \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ cp for Trachoma-2
Repeated Eye infections with Chlamydia Trachomatis A,B,C --\> **Inversion of Eyelashes** \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ (**INVERTED** & **PALE EYELASH HAIR FOLLICLES** with Conjunctival injection) --\> [Blindness from lash ulceration]
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Subconjunctival Hemorrhage is self limited to how long?
2 days
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How does this abnormality clinically present? - 2
1. [*sudden*nonpainful uL vision ∆ (hazy|red hue|COMPLETE LOSS)] 2. Floaters *also seen with [Torn Retinal Detachment]* | *dx = Vitreous Hemorrhage*
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When can you mandate parents against their will to accept treatment for a [non emergent ailment] for their child?
PARENTS CAN NOT REFUSE TX for any **F.A.T.** conditions!! | *🔎F.A.T.. = FATAL Although Treatable* ## Footnote PARENTS CAN NOT REFUSE ANY TX THAT IS **LIFE SAVING** 911 | non911 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ If pt [nonrmergent ailment] is a [*treatable* & **FATAL condition** (i.e. Cancer)] -- PARENTS CAN NOT REFUSE THAT LIFE SAVING TX → *M.D. can obtain a court order to give tx* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ PARENTS ARE **NOT** ALLOWED TO REFUSE TX for *treatable* LIFE SAVING TREATMENT FOR THEIR CHILD (EVEN IF BASIS IS RELIGIOUS)
310
Describe ophthalmoscopy findings for Diabetic Retinopathy-3
1. microaneurysms = simple type 2. retinal edema = simple type 3. newly formed vessels if malignant type
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low tone hearing loss = [**⬜** sensorineural | conductive] hearing loss
conductive
312
Glaucoma ## Footnote 📖
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cp for Acute Closed angle Glaucoma - 3
1. **PAINFUL** Red eye uL 2. Fixed Dilated pupil 3. Cloudy Cornea \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *"Closed angle needs* **OPMAT ..** STAT!"
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Prognosis for [Acute Closed angle Glaucoma]
Permanent Vision Loss within 2-5 hrs of onset! ## Footnote \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *"Closed angle needs* **OPMAT ..** STAT!"
315
Identify finding
[*(Zoster Ophthalmicus)*Dendriform Corneal Ulcer] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *dx = Zoster Ophthalmicus*
316
317
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[Closed angle Glaucoma] accounts for ⬜% of cases, presents [**⬜** gradually | abruptly] , and is a medical Emergency! ## Footnote * * * What is the etx for [Closed angle Glaucoma]? -4 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *AKA: [Acute Glaucoma or angle-closure Glaucoma]*
10% ; abruptly * * * ⭐{[ **aLi**: CL❌SES 1st]*(idiopathic vs iris hypoxia)* ➜ [ **aTic**: CL❌SES 2nd] = [**TMAD**❌]}⭐ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 1) centralIris and lens stick together*= **aLi** closes 1st* 2) → *rapid* ⇪ IOP pushes peripheralIris against Cornea 3) → *CLOSING* off **aTic** 2nd → [*RAPID* ⇪ ⇪ ⇪ IOP] 4) [*RAPID* ⇪ ⇪ ⇪ IOP] → [*RAPID* optic n damage] → Blindnesswithin 2-5h of onset⚠️! \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *"Closed angle needs* **OPMAT ..** STAT!" | 🟢=Open / ❌=closed ## Footnote *🔎**aLi** = **a**ngle between **L**ens and **I**ris* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 🔎[**aTic** : **a**ngle at **i**ris ⼀{**_T_**_MAD}_ ⼀**c**ornea] | [TMAD: Trabecular Meshwork AqueousHumor Drain]
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[Open angle Glaucoma] accounts for ⬜% of cases, and presents [**⬜** gradually | abruptly] ## Footnote * * * What is the etx for [Open angle Glaucoma]? -3
65% ; gradually * * * ⭐[ **aLi**: 🟢]. [ **aTic**: 🟢]. [**TMAD**: ❌].⭐ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 1. idiopathic vs [TMAD❌(Trabecular Meshwork AqueousHumor Drain ❌bstruction)] 2. → [*gradually slow* ⇪ IOP] → [*gradual slow* loss of (peripheral 1st)sight over years] 3. aTic not affected = remains open \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ | 🟢=Open / ❌=closed ## Footnote *🔎**aLi** = **a**ngle between **L**ens and **I**ris* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 🔎[**aTic** : **a**ngle at **i**ris ⼀{**_T_**_MAD}_ ⼀**c**ornea] | [TMAD: Trabecular Meshwork AqueousHumor Drain]
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# definition Astigmatism
abnormally curved cornea that causes different refractive power at different axes
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# definition PresByopia
age-related ⬇︎lens elasticity → [⬇︎accommodation (near-vision)] ## Footnote 👣often needs reading glasses
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# risk factors (8) cataracts
1. age 2. smoking 3. EtOH 4. CTS 5. [DM (sorbitol)] 6. trauma 7. excessive sunlight 7. infection 8. galactosemia / galactokinase deficiency
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# **Latano*prost*** MOA \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Indication
[PGF*Prosta*glandin analog ] = ⇪ outflow of aq humor \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Glaucoma ## Footnote 📝*side effect = darkens /causes iris "browning"*
324
Physiological action of GH in children (5)
Linear Growth of * long bones*(primary determinant of adolescent growth spurt)* * cartilage * muscle * organ systems + [Blood Glucose promoter]
325
Physiological Action of GH in Adults (3)
1. Catabolic for Fat 2. Anabolic for Muscle & Bone 3. Blood Glucose Promoter (INC Blood Glucose)
326
Effects of GH are mostly mediated by \_\_\_\_\_, which is released from the ____ in response to \_\_\_
Effects of GH are mostly mediated by **IGF1**, which is released from the **liver** in response to **GH** ## Footnote [GHRH → GH ---> IGF1]
327
In addition to Musculoskeletal changes, what other changes occur in Adults with GH deficiency (3)
* Hyperlipidemia * Cardiac Muscle Atrophy * [Fatigue / Depression / Malaise]
328
Adult onset GH deficiency is typically due to what?
Pituitary problem
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Drugs for GH deficiency (4)
[SERMorelin*GHRH*] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ SOMAtrem SOMAtropin \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ mecaSERMin
330
Name a Synthetic GHRH
sermoRELin
331
Name 2 [Recombinant Human**GH**]
1. Somatropin 2. Somatrem
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What is Mecasermin?
Recombinant IGF1
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Somatropin Indication (5)
**SPAWN** 1. **P**ediatric growth failure (associated w/GH/chronic Renal Failure/Prader Willi/Turner) 2. **N**o idea: Idiopathic short stature (\>2.25 SD below mean height) 3. **A**dult GH deficiency 4. **W**asting in AIDS pts 5. **S**hort Bowel Syndrome in pts receiving nutritional support (it INC SA for digestion)
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Structure of Somatropin
identical to native hGH ## Footnote *(Somatropin = Synthetic GH structurally identical to native hGH)*
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Mecasermin Indication
Pediatric IGF1 deficiency from [Laron GH receptor Dwarfism] vs. [Ab against GH]
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Octreotide [Drug Class and MOA]
Somatostatin Analogue (45x more potent and long lasting) --\> blocks GH secretion
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Octreotide Indications (4)
* Pitutiary microadenoma * Carcinoid Crisis (flushing/diarrhea/Cyanosis) * Secretory Diarrhea 2° to VIP tumors * Acute GI Bleeding
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Name the Gonadotropins (4) and what their MOA is
Replaces FSH and LH - Menotrophins (FSH and LH) - hCG - Urofollitropin (FSH from menopausal women urine) - Follitropin
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Gonadotropins Indication (3)
1. Ovulation*[in women with hypOgonadotropic hypOgonadism] vs. IVF* 2. Infertility*[in Men with hypOgonadotropic hypOgonadism]* 3. PCOS/Obesity | *ex: Menotrophins | Follitropin | UroFollitropin | hcG*
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How does GnRH🟢 or [ ***short** half life*GnRH analog] affect gonadal axis?
Stimulates Gonadotroph cells to make/secrete LH & FSH
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[ ***LONG** half life*GnRH analog] MOA
**Desensitizes** GnRH receptors and **inhibits** FSH and LH release *[LONG half life GnRH analog] = GnRH🟥*
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Biphasic Effect of [GnRH analogs]
GnRH➿ 1st: ***short**1/2 life* = FLARE effect = Transient (7-10 days) FLARE (INC) in gonadal hormone levels from agonist effect 2nd: ***LONG**1/2 life*-lasting suppresion of Gonadotropins and gonadal hormones from inhibition | {GnRH➿ = *GnRH analogs*}
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Goserelin Indication (8)
[*specific* = **aef** ] 1. **a**ndrogen dependent Prostate CA] adjunct 2. **e**ndometriosis 3. **f**ibroids_Uterine \_\_\_\_\_\_\_\_+\_\_\_\_\_\_\_\_\_ [*ALL* = **BOPIA**] 4. **B**reast CA 5. **O**varian CA 6. **P**COS 7. **I**nfertility 8. **A**menorrhea | {GnRH➿ = *GnRH analogs*} ## Footnote {[_Goserelin_ GnRH🟢➿] indication} = {[*specific***[a|e|f ]**] + [*GENERAL***BOPIA**]}
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Leuprolide Indication (10)
**aefcr** 1. [**a**ndrogen dependent Prostate CA] adjunct 2. **e**ndometriosis 3. **f**ibroids_uterine 4. **c**entral precocious puberty 5. [**r**eproductive IVF*(keeps LH surge low → multi-oocyte maturation)* ] \_\_\_\_\_\_\_\_+\_\_\_\_\_\_\_\_\_ [*ALL* = **BOPIA**] 4. **B**reast CA 5. **O**varian CA 6. **P**COS 7. **I**nfertility 8. **A**menorrhea | {GnRH➿ = *GnRH analogs*} ## Footnote {[_Leuprolide_ GnRH🟢] indication} = {[*specific***[a|e|f |c|r ]**] + [*GENERAL***BOPIA**]}
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List the 3 [GnRH🟥]
"Don't Block me from getting my *Rolex*" 1. Ganirelix 2. Cetrorelix 3. Abarelix *These are Dose-Dependent*
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How is administration between [GnRH synthetic analogs] and [GnRH R Blockers] different (2)
1. [GnRH R Blockers] produce immediate Blocking effect = Duration of Admin is shorter during IVF 2. [GnRH R Blockers] **don't produce Flare Effect**
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Drugs given during [Follicular Proliferative Phase] during IVF (3)
* Gonadotropin injection is given 3 days after menses to immediately start developing Follicles. * {[_LONG_1/2GnRH analogs] or [GnRH R Blockers]} are given to prevent premature LH surge
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Physiologic Actions of Prolactin (4)
1. Mammogenesis 2. Milk production 3. Milk secretion 4. [Inhibits GnRH secretion → Suppresses Ovulation]
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Hyperprolactinemia Tx (3) and why
1. Bromocriptine 2. Cabergoline 3. Pergoline These are [D2-dopamine🟢] *(Dopamine blocks [Lactotrope_PROLACTIN] secretion)*
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Bromocriptine Indication (5)
1. Pituitary Prolactinoma 2. PMS 3. Acromegaly (Use High Doses and only if tumor secretes both Prolactin & GH) 4. Parkinson's Dz 5. Type2DM