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[1A] ⚡ M.D. STEP 3🩺USMLE > 7 ⼀ENDOCRINE/OPHTHO > Flashcards

7 ⼀ENDOCRINE/OPHTHO Flashcards

1
Q

46

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 Retention → Fluid 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 Retention → Fluid 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
Q

How does DKA and HHONKS affect total body K+ levels?

A

⬇︎total body K+ (REGARDLESS OF WHAT SERUM VALUE SAYS)

DKA & HHONK causes severe osmotic diuresis –> ⬇︎total body K+ stores even though serum K+ level may be elevated = [maintain > 5.3K+ ✳]

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26
Q

In DKA and HHONKS management, when do you hold the insulin?

A

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

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27
Q

In DKA and HHONKS management, when do you consider using Sodium Bicarbonate?

A

pH<6.9

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28
Q

You suspect a pt has Cushing Syndrome

How do you work this up?-3

A

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]

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29
Q

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

A

3rd: If ⊕Cushing Syndrome → perform ACTH workup(image) to determine if Cushing Syndrome [ACTH-dependent] or [ACTH-INdependent]

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30
Q

Name the characteristics of Cushing Syndrome - 7

A

“Fat Heavy People May HOG the Cushing”

  1. Fat reDistribution (central obesity, Moon face)
  2. Hyperpigmentation (from excess ACTH activating [Melanocyte MC1 R])
  3. Purple striae with skin atrophy and bruisability
  4. Muscle atrophy
  5. HTN
  6. Osteoporosis
  7. Glucose intolerance

________________

Cushing SYNDROME is caused by ⇪ [CortisolGlucocorticoid](which may be ACTH-INdependent or ACTH-dependent)

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31
Q

autoimmune adrenalitis is known as _____ disease

etx?

A

[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

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32
Q

What are the main causes of [Addison’s Primary Adrenal Insufficiency]? - 4

A
  1. TB
  2. Autoimmune adrenalitis
  3. CA
  4. Adrenal Hemorrhage
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33
Q

Main sx for [Addison’s Primary Adrenal Insufficiency] - 8

A

“Addison was a SNAP FHAG”

  1. [Sodium ⬇︎ DEC]
  2. [NAHA (Normal AG Hyperchloremic metabolic acidosis)]
  3. AnorexiaWT LOSS
  4. [Potassium ⇪ INC]
  5. Fatigue
  6. [Hyperpigmentation(ACTH and MSH)]
  7. [Androgen deficiency(⬇︎axillary/pubic hair)]
  8. GI Sx
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34
Q

What is Cosyntropin?

_________________

Describe how it used to workup ⬜

A

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]

[Addison's Primary Adrenal Insufficiency]
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35
Q

What test should you order to diagnose [Addison’s Primary Adrenal Insufficiency]? (3)

A
  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)
[Addison's Primary Adrenal Insufficiency]
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36
Q

Which 5 drugs cause Drug-Induced Lupus?
_________________

How is Drug-Induced Lupus diagnosed?​ (2)

A

HEMPI to DIL

Hydralazine

[Etanercept (TNFα R Blocker)]

Minocycline

Procainamide

[Infliximab (TNFα R Blocker)]
_________________

+ANA and +antiHistone

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37
Q

Why are frequent ophthalmologic exams necessary for prolonged CTS users?

A

CTS changes lens epithelial gene transcription ➜ CATARACTS

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38
Q

In addition to ⇪ glucose urinary excretion , how do SGLT2 inhibitors delay the progression of DM nephropathy?

A

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

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39
Q

pt p/w eye pain with foreign body sensation

what’s your workup? (4)

A
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40
Q

Both preseptal cellulitis and orbital cellulitis present with (⬜3)
_________________

How are they differentiated? (3)​

A

[eyelid swelling-redness] ​/ fever ​/ conjunctivitis
_________________

orbital = orbit eye pain with movement + proptosis + ophthalmoplegia​

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41
Q

How do you treat Orbital cellulitis? (2)

A

IVAbx ➜ [Surgical debridement (if fluid collection/abscess present)]

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42
Q

How do you workup Hyperthyroidism? -5

A
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43
Q

Exogenous thyrotoxicosis MOD

A

[OTC Thyroid supplement vs surreptitious prescription thyroid med] ➜ supressess [ANT Pit TSH] ➜ ⬇︎thyroid gland synthesis ( ⬇︎RAIU and ⬇︎thyroglobulin)

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44
Q

Common s/s of HYPERthyroidism -9

A

TT Feels ARCHED

  1. Tremor
  2. Tachycardia
  3. [Fatigue(+/- Apathy in Elderly)]
  4. Appetite ⬆︎ but Wt ⬇︎
  5. Reflexes ⬆︎
  6. Cardio* (Tachycardia, Palpitations,Exertional SOB, ⇪Myocontractility→HTN)*
  7. Heat intolerance –> SWEATING
  8. [Exophthalmos with lid lag = GRAVES DISEASE]
  9. Diarrhea +/- dyspepsia

Older pts may only have Fatigue, Cardio, or Apathetic!

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45
Q

For patients taking CTS, which patients need their dose regimens tapered down at the end?

A

[CTS > 3 Weeks] = TAPER DOWN

(taper allows for return of adequate endogenous cortisolglucocorticoid)

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46
Q

How do you workup Hypercalcemia? -4

A

MEASURE PTH!

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47
Q

Hypercalcemia can either be PTH-dependent or PTH-INdependent

What are the causes of [PTH-dependentHypercalcemia]? (4)

A
  • Primary HyperParathyroidism
  • Tertiary HyperParathyroidism(Intractable Hypercalcemia 2/2 Autonomous Parathyroid)
  • [Familial hypOcalciuric Hypercalcemia]
  • Lithium
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48
Q

Hypercalcemia can either be PTH-dependent or PTH-INdependent

What are the causes of [PTH-INdependentHypercalcemia]? (8)

A
  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
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49
Q

normal range for

PTH

A

10-60

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50
Q

After working up Hypercalcemia, you determine cause is Malignancy

List the 3 Causes of [Hypercalcemia of Malignancy] , which Cancers cause them and their MOD

A
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51
Q

Which Rx cause Hypercalcemia (5)

NormalCa+ = 8.4-10.2

A

“LCD-TV with too much Calcium!”

Lithium

Ca+carbonate excess

DVitamin

Thiazides

VitaminA

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52
Q

nml TSH: [0.4-4.0]

which thyroid condition is a/w Thyroid Lymphoma?
​

A

hCAT

[hashimoto Chronic Autoimmune(antiTPO) Thyroiditis]

_________________

hCAT can progresses to Thyroid Lymphoma | [hCAT+ Pemberton = Thyroid Lymphoma]

chronic [antiTPO Lymphocyte] infiltrate thyroid targeting TPO

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53
Q

What is Pemberton’s sign?

_________________

What does it indicate? -2

A

facial plethora or neck vein distension when arms are raised ​
_________________

  • obstructive ENLARGED THYROID
  • [Thyroid lymphoma (if ⊕ in the setting hCAT)]
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54
Q

Medullary thyroid cancer

cp -2

A
  1. [thyroid nodule iTSo MEN]
  2. [Calcitonin ⇪ (from thyroid gland C cell neoplasia)]
    * MEN = Multiple Endocrine Neoplasia // iTSo = in The Setting of*
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55
Q

Describe MEN1 (3)

A

PituitaryMacroAdenoma

Parathyroid hyperplasia

[Pancreatic-GI GLIV tumors ⼀Gastrinoma/gLucagonoma/Insulinoma/VIPoma]

Multiple Endocrine Neoplasia
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56
Q

Describe MEN2A (3)

A
  • Parathyroid Hyperplasia
  • Medullary Thyroid CA
  • Pheochromocytoma
Multiple Endocrine Neoplasia
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57
Q

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?

A

Parathyroid hyperplasia

_________________

1st: {[Plasma free metanephrines] –(confirm by)– >

2nd:

  • [24h urinary fractionated metanephrines]
  • catecholamines
  • abd imaging]}

_________________

Undiagnosed Pheochromocytoma can cause fatal HDUS peri-thyroidectomy

Multiple Endocrine Neoplasia
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58
Q

MEN2A and MEN2B share the same initial workup

List the diagnostic workup for {new dx[MEN2A ] or new dx[MEN2B]} - (5)

A
  1. Calcitonin
  2. CEA
  3. [Neck US (r/o regional metastasis)]
  4. [Chromo10RET protooncogene] germline testing
  5. [Coexisting tumor r/o ([Parathyroid hyperplasia], [Medullary Thyroid Hyperplasia], Pheochromocytoma,)]
Multiple Endocrine Neoplasia
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59
Q

Describe MEN2B (4)

A
Multiple Endocrine Neoplasia
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60
Q

Pt p/w the 3 P’s of MEN1 ( _______ )

What’s the next step in Management of MEN1?

A

PituitaryMacroadenoma/Parathyroid hyperplasia/[Pancreatic-GI GLIV tumors]

_________________

[PARATHYROIDECTOMY with autotransplantation to muscle pocket]

Multiple Endocrine Neoplasia
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61
Q

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?

A

[Prolactinoma]/[Parathyroid hyperplasia]/[Pancreatic&GI GLIV tumors]

_________________

[Pancreatic Gastrinoma (Zollinger Ellison)]

  • normal Ca+ (⇪ Ca+ ➜ falsely elevated gastrin)
  • NO acid-reducing tx (PPI ➜ falsely elevated gastrin)
Multiple Endocrine Neoplasia
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62
Q

How are the thyroid and Calcium related?

A

[T3/T4thyroid hormone] causes bone resorption ➜ ⇪ serum Ca+/Hypercalcemia

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63
Q

Candida Endophthalmitis

clinical features (4)
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_

Treatment?​ (3)

A
  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

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64
Q

What causes [Pancreatogenic DM]?
_________________

Which antiDM should be used to treat this? Which 3 should not? why?

A

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

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65
Q

Glipizide

MOA

A

insulin secretagogues

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66
Q

GLP1 R agonist

MOA

Name 3 examples
_________________

Glucagon-Like Peptide-1 R agonist

A

Food → intestine [GLP1] secretion naturally ➜ GLP1iLAGG → GLP1 is then cleaved-inactivated by DPP4
_________________
⇪ insulin secretion and insulin sensitivity
⬇︎Liver glucose secretion
⬇︎Appetite → wt loss
⬇︎Gastric emptying(⇪pancreatitis risk)
⬇︎Glucagon secretion
_________________

so… [GLP1🟢] → ⇪GLP1iLAGG

________________

liragluTIDE / exenaTIDE / dulagluTIDE

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67
Q

DPP4 inhibitors

MOA

Give 2 examples

A

Targets GI peptides ➜ slows gastric emptying
________________

linaGLIPtin
sitaGLIPtin
saxaGLIPtin

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68
Q

Why are [Pioglitazone thiazolidinedione] contraindicated in CHF?

A

[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

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69
Q

What is Amaurosis fugax?

A

sudden reversible transient monocular blindness 2/2 carotid artery atherosclerotic disease

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70
Q

Amaurosis fugax

tx?

A

carotid endarterectomy

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71
Q

Amaurosis fugax

dx?

A

carotid doppler US

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72
Q

What is subclinical thyrotoxicosis?
_________________

how is it managed?

A

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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73
Q

a Patient with chronic hypOparathyroidism presents with low serum Ca+ but HIGH urinary Ca+ from their Ca+ supplement

How do you mitigate this?

A

HCTZ
_________________

HCTZ [⇪ serum Ca+] while [⬇︎ urinary Ca+]

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74
Q

How is the thyroid system associated with Surgery?

A

[hypOthyroidism] ➜ [poor periOperative outcomes]

⼀BUT 911 surgeries are Ok if hypOthyroidism not severe (i.e. no myxedema coma)

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75
Q

Why must Levothyroxine at first be titrated very slowly in CAD pts ?

A

[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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76
Q

NPH is a ⬜ insulin that is sometimes used as ⬜. Why should it NOT be used in patients who’ve had hypOglycemic episodes?

A

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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77
Q

When is it indicated to switch a T1DM pt from [manual SQ Basal/bolus insulin injection] to [automated SQ continuous infusion insulin pump]?

A

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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78
Q

Patient presenting with new diagnosis T1DM. Tx requires exogenous insulin.

Describe the [manual SQ Basal/bolus insulin injection] regimen the patient will start with

A

T1DM require a

[(long basal) and (rapid bolusx3)] every day

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79
Q

Work up for Thyroid Nodule?

A

[Cancer RF = (> 1cm), fam hx, radiation hx, cervical LAD, compressive sx, thyroid hormone ∆]

[Suspicious US = hypOechoic, microcalcifications, internal vascularity]

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80
Q

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)

A

> > 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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81
Q

Why are hypoglycemic episodes in long standing DM1 pts even more serious than newly diagnosed DM1 pts?

_________________

how is this mitigated?

A

✔︎ 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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82
Q

nml TSH: [0.4-4.0]

Name the 2 [DeTC (Differentiated epithelial Thyroid CA)] subtypes

A
  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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83
Q

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)

A

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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84
Q

nml TSH: [0.4-4.0]

management for [DeTC (papillary vs follicular)] varies and is dependent on ⬜ and importantly ⬜

_________________

(DeTC=Differentiated epithelial Thyroid Cancer)

A

[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]

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85
Q

Name the 3 benefits to [STRICT blood glucose control] in DM pts

A

DECREASES…

  1. [microvascular complications ⼀nephropathy, retinopathy]
  2. [peripheral neuropathy onset]
  3. [peripheral neuropathy progression]
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86
Q

Gastroparesis = ⬜ and is ultimately diagnosed with what test?

A

delayed gastric emptying (2/2 DM, drugs, postviral) ; [nuclear gastric emptying study]

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87
Q

Clinical manifestations of gastroparesis? (5)

A
  • [succussion splash]
  • [early satiety]
  • [Abd fullness postprandial]
  • [dysautonomia (dizziness, diaphoresis)]
  • [labile glucose control]

BE SURE TO R/O MECHANICAL OBSTRUCTION

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88
Q

Name 2 promotility drugs used to treat gastroparesis

A
  1. metoclopramide
  2. erythromycin
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89
Q

When is [screening for diabetic retinopathy and nephropathy] indicated ? (2)

A

[5y after T1DM dx]

and

[AT TIME OF DX for T2DM]

  • give Statin if [age ≥40 with DM]*
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90
Q

What is the preferred antiHTN for DM pts?

A

ACEk2 inhibitor

_________________

this improves diabetic nephropathy AND INC GFR

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91
Q

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

[Cardiac⬜ PLUS Thyroid[AntithyroidMed1st line or _____or _____]

A

positive; diffuse

  1. propranolol
  2. Thyroid Tx ([AntithyroidMed] vs [Radioactive iodine ablation] vs [Thyroidectomy])

tx = [Propranolol] –> [PTU —(1 hr later)]–> [Potassium Iodine and PrednisoneCTS]

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92
Q

Tx for hyperacute [symptomatic Hyperthyroidism] is Cardiac + Thyroid

[Cardiac⬜ PLUS 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)

A
  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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93
Q

Patients with Graves disease have [⬜positive | negative] Thyroid Stimulating Immunoglobulins and ⬜ uptake on radioiodine scintigraphy

_________________

[RadioActive Iodine ablation] is contraindicated c❌d in pregnancy and lactation

When is it indicated for Graves tx? (5)

A

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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94
Q

Patients with Graves disease have [⬜positive | negative] Thyroid Stimulating Immunoglobulins and ⬜ uptake on radioiodine scintigraphy

_________________

When is [ThyroidectomySurgery] indicated for Graves disease ? (5)

A

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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95
Q

What do you use to track thyroid function in pt who just started AntiThyroid Rx(drugs vs Radioactive Iodine vs SURGERY)? (3)

A
  • [TSHnml0.4 - 4 (TSH q 4mo if Chronic Amiodarone Rx)]
  • [FREE T4 nml0.9 - 1.7]
  • [total T3]

[Free T4 = 0.9 - 1.7]

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96
Q

Identify and Explain the finding

What diagnosis does this indicate?

A

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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97
Q

Pt presents with positive Seidel sign

a. Diagnosis?

_________________

b. Management of this diagnosis?

A

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

Positive Seidel test = Full Thickness Corneal LACERATION
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98
Q

How do you manage Corneal Abrasion? -3

A
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99
Q
  • 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?

A

ONLY IF [⊕ WHIPPLE’S TRIAD*] = clinical hypOglycemia = workup indicated

  1. low BG
  2. [SADHAThypOglycemia sx]
  3. [SADHATsx] 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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100
Q
  • 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

A

[⊕ WHIPPLE’S TRIAD] = clinical hypOglycemia = workup indicated

  1. low BG
  2. [SADHAThypOglycemia sx]
  3. [SADHAThypOgluc sx] resolve with glucose admin
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101
Q
  • 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)

A

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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102
Q

What is the [mixed meal challenge] used for?

A

evaluates Pts who only have hypOglycemia sx after eating

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103
Q

What lab is ordered alongside C-Peptide to evaluate endogenous insulin production?

A

Proinsulin

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104
Q

The most common cause of DEC vision in elderly patients are ⬜ with ⬜ .

Why is the evaluation so critical for these conditions? (2)

A

▶([cortical cataracts] ; [AMD])

▶Elderly Cataracts patients must be thoroughly evaluated for severity of [ccaAMD] since they:

1.may require both [Cataract lens extraction Surgery] AND [ccaAMD] tx (PO eye vitamin)]

or

  1. may not benefit from [Cataract lens extraction Surgery] at all (since opacified lens prevent [ccaAMD] progression)

[ccaAMD]: (Cortical Cataract) associated -Age related Macular Degeneration

scotoma
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105
Q

The most common cause of DEC vision in elderly patients are ⬜ with ⬜ .

Describe each condition

A

([cortical cataracts] ; [ccaAMD])

_________________

[cortical cataracts]: nonpainful slow progressive lens opacification ➜ blurry vision but fields intact

with

[ccaAMD]:(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]

[ccaAMD]: (Cortical Cataract) associated -Age related Macular Degeneration

dry AMD [Age related Macular Degeneration] with [Drusen cellular debris]
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106
Q

Similar to CROA amaurosis fugax ⬜ also usually presents with sudden uL nonpainful vision loss

A

Retinal Detachment

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107
Q

Pt with sudden eye pain, has Visualization of leukocytes in the anterior segment of her eye

Dx?

_________________

What other 5 sx would you expect?

A

[IritisAnterior Uveitis]
_________________

  1. photophobia
  2. pain
  3. redness
  4. vision loss
  5. [irregular constricted pupil]
    * 6. [Leukocytes in ANT segment]*
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108
Q

Infectious Keratitis sx (3)

A
  1. corneal opacity
  2. severe photophobia
  3. difficulty keeping affected eye open
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109
Q

s/p coronary angiography, patient soon after develops palpitations, fatigue, heat intolerance, sweating

Diagnosis? Explain

_________________

Which diagnostics support this dx? (3)

A

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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110
Q

s/p newly starting amiodarone, patient soon after develops palpitations, fatigue, heat intolerance, sweating

Diagnosis? Explain

_________________

Tx for this? (2)

A

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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111
Q

[Lugol ⬜ solution] is a solution containing ⬜ that does what mechanistically?

Indications? (2)

A

(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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112
Q

Prednisone is used to treat which 3 thyroid diseases?

A
  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.

THYROID SCHEMATIC
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113
Q

[normal Retina] = (⬜-4) on fundoscopy

describe how a [Papilledema Retina] looks on fundoscopy (4)

🔎[Papilledema Retina] = [Retina io\Papilledema]

A

[normal Retina] = normalDSLs= [Disc margin defined/Small veins linear /Large veins defined]/ [splinter hemorrhage⊝]

_________________

“my Retina loves DSLs”

[Papilledema Retina(Retina in the setting of Papilledema)] = Papilledema⚠️DSLs
= [Disc margin OBSCURED / Small veins SERPENTINE / Large veins OBSCURED] / [splinter hemorrhage⊕]

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114
Q

normal range for

TSH

A

0.4 ⼀ 4.0

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115
Q

normal range for

[free thyroxine T4]

_________________

[Total Thyroxine T4]

A

free thyroxine T4[0.9 ⼀ 1.7]

_________________

5-12

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116
Q

“Thyroiditis” suggest ⬜2. And there’s 3 types: PDSGT, hCAT, [NSLP-hCAT]

[NSLPhCAT] : [Nonpainful(silent) Subacute Lymphocytic Postpartum]hCAT

Clinical Features (4)

_________________

Diagnostics (2)

A

[Lymphocyte infiltration ➜ [Transient HYPERthyroidism]
_________________

  1. variant of hCAT(dx = [⊕TPO antibody], [low RAIU])
  2. HYPERthyroid transiently → hypOthyroid (or sometimes Euthyroid) → spontaneous recovery
  3. GoiterNonpainful, small
  4. includes postpartum thyroiditis (midaged Women postpartum)

🔎TPO = ThyroPerOxidase

thyroiditis

[NSLPhCAT] dx =same as hCAT dx:
a. ⊕TPO antibody
b. low RAI uptake

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117
Q

“Thyroiditis” suggest ⬜2. And there’s 3 types: PDSGT, hCAT, [NSLP-hCAT]

hCAT: [hashimoto Chronic Autoimmune Thyroiditis]

Diagnostics (2)

A

[Lymphocyte infiltration ➜ [Transient HYPERthyroidism]
_________________
* * *
- ⊕[Thyroid PerOxidase Ab]
- [lowRAI uptake]

thyroiditis
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118
Q

“Thyroiditis” suggest ⬜2. And there’s 3 types: PDSGT, hCAT, [NSLP-hCAT]

hCAT: [hashimoto Chronic Autoimmune Thyroiditis]

Clinical Features (5)

A

{[Lymphocyte infiltration ➜ [Transient HYPERthyroidism]}
_________________

  1. [initial Transient HYPERthyroid[damage from AntiTPOLymphocytes(= 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)
thyroiditis
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119
Q

“Thyroiditis” suggest ⬜2. And there’s 3 types: PDSGT, hCAT, [NSLP-hCAT]

PDSGT: [PAINFUL DeQuervain Subacute Granulomatous Thyroiditis]

Clinical Features (5)

A

[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 → **</sup>)
  5. HYPERthyroid(TT Feels ARCHED) symptoms

{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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120
Q

“Thyroiditis” suggest ⬜2. And there’s 3 types: PDSGT, hCAT, [NSLP-hCAT]

PDSGT: [PAINFUL DeQuervain Subacute Granulomatous Thyroiditis]

Dx labs (3)

A

[Lymphocyte infiltration ➜ [Transient HYPERthyroidism]
_________________
- - ⇪ ESR
- ⇪ CRP
- [low RadioActive Iodine Uptake]thyroid scintigraphy

{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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121
Q

“Thyroiditis” suggest ⬜2. And there’s 3 types: PDSGT, hCAT, [NSLP-hCAT]

PDSGT: [PAINFUL DeQuervain Subacute Granulomatous Thyroiditis]

Explain Why does PDSGT have low RAIU??

A

[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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122
Q

“Thyroiditis” suggest ⬜2. And there’s 3 types: PDSGT, hCAT, [NSLP-hCAT]

PDSGT: [PAINFUL DeQuervain Subacute Granulomatous Thyroiditis]

Tx (3)

A

[Lymphocyte infiltration ➜ [Transient HYPERthyroidism]
_________________
1. [NSAIDs ➜ Prednisone(refractory)]
2. [Propranolol (or Atenolol)]
3. [self limited (viral infxn → [PDSGT HYPERthyroid]3w → hypOthyroid → Euthyroid)]
* * *

thyroiditis

{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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123
Q

On Thyroid Scintigraphy, when do you see Patchy uptake?

Clinical features of this condition (3)

A

toxic multinodular goiter

  1. {HYPERthyroidthyrotoxicosis (TT FeelsARCHED)}
  2. nodular enlargement
  3. OLDER patients
ℹ️ THYROID
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124
Q

On Thyroid Scintigraphy, when do you see Diffuse uptake?

why do you see diffuse uptake in this condition?

A

[Graves1º HYPERthyroidthyrotoxicosis]

_________________

[thyrotropin R autoantibodies] stimulate thyroid diffusely to [INC iodine uptake] and [INC thyroid hormone synthesis]

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125
Q

clinical features of Ocular melanoma (4)

A

★ [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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126
Q

In hospital setting, American Diabetes Association suggest maintaining inpatient glucose at ⬜

A

140-180

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127
Q

▶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

A

DM1 (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

[BasalLA or IA]= controls glucose between mealsALL DM1 (and most DM2)

[Nutritional bolusSA] = controls postprandial glucose excursionsreq’d only for patients eating obvi

[Correctional bolus Sliding ScaleSA] = corrects random hyperglycemic excursions

_________________

L/I/SA: Long/Intermediate/Short-ACTING

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128
Q

When should you consider insulin infusion pump for IDDM pts (5)

A
  1. critical illness
  2. DKA
  3. HHONKS
  4. perioperation
  5. [(SQ insulin) failure]
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129
Q

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)

A

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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130
Q

Dx?

A

[NMER]Glucagonoma

(necrolytic migratory erythematous rash)

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</sub>

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131
Q

Sulfonylurea MOA

________________

List examples-5

A

closes {[pancreatic β islet cell] ATP-sensitiveK+ 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

4.1GChlorpropamide
5.1GTolbutamide

G = Generation

[MeglitiNides (“RepagliNide, “NategliNide”)] = same MOA as Sulfonylurea

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132
Q

Meglitinide

MOA
________________

List examples-2

A

insulin secretagogue= (same as Sulfonylurea MOA) stimulates endogenous insulin secretion
__________________

  1. Nateglin_ide_
  2. Repaglin_ide_
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133
Q

[Alpha glucosidase inhibitor] MOA

________________

List examples-2

A

inhibits α-glucosidease ➜ inhibits intestinal carb digestion → ⬇︎postprandial HYPERglycemia

________________

  1. Acarbose
  2. Miglitol
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134
Q

[DPP-4 inhibitors] MOD

________________

List examples-2

A

inhibits [DPP-4 GLP1 peptidase] –> ⬆︎GLP1–> ⬆︎Glucose-induced insulin release

_________________

  1. SitaGliptin
  2. SaxaGliptin
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135
Q

What are the GLP1 homologs?-2 ;

What do they do?

A
  1. ExenaTIDE
  2. LiragluTIDE

These require Injections

⬆︎Glucose-induced insulin release

“GLP1a says… “iLAGG behind food”
[⇪insulin secretion & sensitivity⇪[Glucose-induced Insulin Secretion]
[⬇︎Liver Glucose secretion]
[⬇︎ Appetite(secreted after food intake)]
[⬇︎Gastric emptying(⚠️Pancreatitis risk)]
[⬇︎ Glucagon secretion]

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136
Q

Classic Presentation for DM -5

A

FUDge

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137
Q

Clomiphene Citrate

MOA

_________________

Indication

A

[hypothalamic estrogen🟥]SERM;

PCOS Infertility

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138
Q

Leuprolide

MOA

_________________

Indication

A

[GnRH🟢] ; endometriosis

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139
Q

How does respiratory rate affect Calcium levels?

A

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

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140
Q

[Normal serumCa+: 8.4-10.2]

Pt presents with hypOcalcemia

How do you work this up? -5

A
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141
Q

[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

A
  1. vitD deficiency
  2. Chronic Kidney Disease
  3. Pancreatitis
  4. Sepsis
  5. Tumor lysis syndrome
  6. pseudohypOparathyroidism
142
Q

[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

A
  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
Q

cp for Glucagonoma - 3

A

DAN had a Glucagonoma!

  1. DM
  2. Anorexia weight loss
  3. Necrotic Migratory Erythema (perioral, extremities, perineum)
144
Q

dx for Glucagonoma

DAN had a Glucagonoma!

A

Glucagon >500

Look for Necrotic Migratory Erythema!

145
Q

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)

A

★ [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
Q

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

A
  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
Q

Explain how patients should take Levothyroxine? (2)

A

Take Levothyroxine [on empty stomach30-60m ac]

–and —

Take Levothyroxine [4h before other drugs]

148
Q

Pts with hypOthyroidism will require a [Levothyroxine replacement regimen]

Describe the 3-part [Levothyroxine replacement regimen] for pts with hypOthyroidism

A

IBM

I: { Initial[75-125mcg/day](or 25-50 for elderly | CVD) }

⬇

B:{ [Boost/INC Dose q6w until TSH nml0.4-4 }

⬇

M: {Maintain & Monitor TSH q6-12months]

  • note: elevated TSH despite constant escalating levothyroxine doses = levothyroxine malabsorption (c/s Celiac)*
149
Q

How is an ovarian tumor related to thyroid regulation?

A

[Struma Ovarii ovarian teratoma] = rare ovary tumor that ectopically secretes thyroid hormone → [rare ectopicHYPERthyroidism with low TSH]

HYPERthyroidism workup
150
Q

nml TSH: [0.4-4.0]

clinical features of [NSLPhCAT]
(5)

A

[Nonpainful Subacute Lymphocytic Postpartum Thyroiditis]hCAT = [(transienthyperT) → ( transienthypOT ) → normalT]
_________________
1. within ≤1 year postpartum {[TPO Ab inflammation] → [release of preformed T4 + preformed Thyroglobulin] → [nonpainful goiter + transienthyperT] }
2. {[transienthyperT] → [transienthypOT with ⬇︎RAIUdue to positive feedback’s_⬇︎TSH] ) → normalT] (PDSGT also)}
3. [variant of hCAT] (PDSGT also)
4. [⊕TPO Ab] ⼀(PDSGT also)
5. [⇪T4, ⇪Thyroglobulin, ⬇︎TSH, ⬇︎RAIU]

151
Q

What is Thyroglobulin? (2)

A

used to build thyroid hormone in thyroid follicle, and then co-secreted with endogenous thyroid hormone secretion

= 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
Q

Diabetic retinopathy requires years to develop and occurs 2/2 ⬜3. For patients with sx, what’s most likely to improve their sx?

A
  1. macula edema
  2. proliferative diabetic retinopathy [→ vitreous bleeding → retinal detachment = blindness]
  3. lens edema

improve glycemic control

153
Q

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)

A

Amiodarone’s

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
Q

[T or F]

TSH should be obtained once a year for patients on chronic amiodarone therapy

A

FALSE

chronic Amiodarone pts require TSH every 4 months

155
Q

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.

A

on empty stomach; 30-60m

PREVENT; 4h ;

otherwise Ca+/Fe may possibly cause worsening hypOT in pts taking Levothyroxine

156
Q

Why does T2DM rarely present with ketoacidosis at disease onset? (2)

A

T2DM does not involve absolute insulin deficiency (like T1DM) and glucose metabolism is sufficient to prevent ketosis

157
Q

What is [monogenic DM (MODY)]? (3)

A

MDM [(Monogenic DM (Maturity 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
Q

What are the 4 ways to Diagnose DM

A

“Having Treats Feels Risky”

note: Asymptomatic patients with Abnml screening require a repeat of the same test on a different day for confirmation

159
Q

Central Retinal artery occlusion

symptoms (4)

A

Vision Loss that’s…

  1. monocular
  2. [Severe BUT nonpainful
  3. …with temporal sparing]
  4. [hx of amaurosis fugax]
160
Q

Central Retinal artery occlusion

management (4)

A
  1. optho consult
  2. intraarterial thrombolytics
  3. ocular massage
  4. IOP reduction (ANT chamber paracentesis)
pale fundus with cherry red macula= CRAO
161
Q

Central Retinal artery occlusion

clinical findings -2

A
  • [Pale fundus(2/2 diffuse ischemia)]
  • [cherry red macula]
162
Q

Central Retinal Vein occlusion

symptom

A

blurred-to-severe nonpainful vision loss

163
Q

Central Retinal Vein occlusion

clinical finding

A

Blood & Thunder (Fundus w retinal hemorrhages & optic disc edema)

164
Q

Central Retinal Vein occlusion

management -2

A

[Observation]

[+/- intravitreal injection of VEGF inhibitors]

165
Q

[Torn Retinal Detachment]

symptoms (3)

A
  1. Floaters
  2. [Flashing lights(Photopsia)]
  3. {[Field of periphery nonpainful vision loss 1st]→ [central nonpainful vision loss 2nd]}= “Descending Visual Curtain” progressive vision loss
166
Q

[Torn Retinal detachment]

clinical findings (2)

A
  1. marked elevation of retina
  2. Vitreous hemorrhage
retinal detachment
167
Q

Retinal detachment

management

A

Surgical correction (retinopexy, vitrectomy)

168
Q

Vitreous hemorrhage

symptom (4)

A
  1. [Hazy vision +/- red hue]
  2. nonpainful vision loss
  3. Floaters
  4. Shadows
169
Q

Vitreous hemorrhage

clinical findings (3)

A
  1. [red reflexabsent or DEC ]
  2. floating debris/RBC in Vitreous
  3. obscured fundus view
170
Q

Vitreous hemorrhage

management (3)

A
  1. Bed rest with 30-45° Head-Of-Bed elevation
  2. photocoagulation
  3. vitrectomy (some cases)
171
Q

What are the 4 causes of [acute nonpainful vision loss]?

A

CCTV is a nonpainful way to look😏 ✅

  1. Central Retinal occlusion⼀arterypale fundus + cherry red spot/amaurosis fugax hx
  2. Central Retinal occlusion⼀VeinBlood & Thunder fundoscopy
  3. Torn (Detached) RETINA[flashing lights Photopsia]
  4. Vitreous hemorrhagehazy vision/red hue/absent red reflex/floating debris
172
Q

What are the most common causes of this condition? (4)

A

CAROTID ARTERY ATHEROSCLEROSIS > cardiogenic embolism, clotting DO, [giant cell arteritis (vasculitis)]

  • Central Retinal artery occlusion*
173
Q

clinical presentation of Optic Neuritis (3)

A
  • [subacute (hours to days)] monocular PAINFUL vision loss ⼀ pain worse with eye movement.
  • Fundoscopic optic disc edema
  • (+/- afferent pupillary defect)
Optic neuritis = optic disc edema
174
Q

[Functional Pituitary Adenomas] consist of what 3 adenomas?

________________

Describe etx of [NONFunctional Pituitary Adenoma]

________________

Tx?

A

Functional Pituitary Adenoma=

Lactotrope > Somatotrope > Corticotrope

[NONfunctional 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
Q

Why do pts with hypOthyroid require INC dose of levothyroxine if they start taking estrogen-containing OCP?

________________

how is this managed?

A

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
Q

⬜ is the leading cause of death in pts with Acromegaly. What other comorbidity are they at risk for?

________________

which comorbidity is reversible with treatment?

A

[Cardiovascular disease (REVERSIBLE)] ; Colon CA

________________

Cardiovascular Disease is reversible with tx

177
Q

[Anabolic Androgen Steroids] ➜ symptomatic ⬜ from DEC ⬜

________________

how long after d/c does it take to naturally recover?

A

hypOgonadism ; endogenous testosterone

________________

recovers weeks/months after d/c but will be permanently suppressed if chronic abuse

178
Q

[Anabolic Androgen Steroids]

clinical features -8

A

MEATHEAd

  1. [Muscle mass ⇪]
  2. ERYTHROCYTOSIS
  3. Aggression
  4. [(Testosterone/LH/FSH DEC )→ (Testicular size DEC) + (spermatogenesis DEC)]
  5. [HLD( ⇪ LDL|⬇︎HDL)]
  6. [Erection & Libido[(normal during use) / (DECREASED DURING WITHDRAWAL)]
  7. Acne
  8. doubleD-Gynecomastia
179
Q

Describe insulin regimen for IDDM or Type 1

________________

A

Basal + [3 prn meal]

  • basal = [NPH BID] or [GluLargine QD]*
  • ________________*
  • ​ 3 prn meal = [3 reg insulin c meals]*
180
Q

what adjustments should be made for exercise induced hypoglycemia in a IDDM/Type 1 DM? -3

A
  • [⬇︎basal insulin (NPH BID vs GluLargine QD)]
  • eat before exercise
  • avoid insulin injection into “exercise” limbs
181
Q

tx Conjunctivitis -10

A

CAPE ⼀ CAD ⼀MAD

  1. B-[ContactLens → Fluoroquinolonedrops]
  2. B-[Azithromycindrops]
  3. B-[Polymyxin-trimethoprimdrops]
  4. B-[Erythromycin<u>ointment</u>]
  1. V-[CompressWarm/Cold]
  2. V-[Antihistaminedrops]
  3. V-[Decongestantdrops]
  1. A-[Mast cell stabilizer]freq episodes
  2. A-[Antihistaminedrops]intermittent/freq episodes
  3. A-[Decongestantdrops]freq episodes
182
Q

⬜ is a rare complication of bacterial conjunctivitis and is managed with ⬜
_________________
How does this complication typically present? -3

A

Keratitis (inflammation of cornea) ; URGENT OPHTHALMOLOGY CONSULT FOR TX
_________________
[foreign body sensation] / photophobia / vision impairment

183
Q

What is a [Hordeolum Stye]

A

bacterial infection of [eyelid sebaceous gland]

184
Q

Why do pts with suspected Keratitis must receive URGENT OPHTHALMOLOGY CONSULT?
_________________
How is Keratitis diagnosed?

A

Keratitis can cause corneal scarring which ➜ blindness if untreated by optho
_________________
slit-lamp

185
Q

How is Viral Conjunctivitis spread? -2

A

EYE DISCHARGE directly

Contaminated Surfaces

186
Q

[T or F]

Crusted over eyes in the morning indicates patient is contagious with viral conjunctivitis

A

FALSE

(only EYE DISCHARGE and contaminated surfaces transmit viral conjunctivitis)

187
Q

What are the two definitive treatments for thyroid disease

A
  1. Radioactive Iodine
  2. Thyroidectomy
188
Q

Potassium Iodide Indication - 2

A
  1. PreOp tx for Thyroidectomy in Graves
  2. Thyroid Storm
189
Q

How does looking at Thyroglobulin levels help determine etiology of thyroid disease?

A

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
Q

tx for Thyroid Storm - 3

A

HHH needs PPP

tx = [Propranolol] –> [PTU —(1 hr later)]–> [Potassium Iodine and PrednisoneCTS]

191
Q

cp for Thyroid Storm - 3

A

HHH needs PPP

Hot, Head and Heart

  1. Hot = Fever
  2. Head = CNS dysfunction with tremor
  3. Heart = Tachycardia, palpitations, HTN, HF

________________

tx = [Propranolol] –> [PTU —(1 hr later)]–> [Potassium Iodine and PrednisoneCTS]

192
Q

What is this a complication of?

A

Acute Sinusitis

________________

dx: Orbital Cellulitis

193
Q

tx for [Toxic Adenoma Thyroid Nodule] -3

A

[PreTx (Methimazole)]

➜

[DefinitiveTX (RADIOACTIVE IODINE ABLATION OR SURGERY)]

194
Q

characteristic features of [Toxic Adenoma Thyroid Nodule] -2

A

SYMPTOMATIC HyperThyroid

+

[Radioiodine uptake in nodule] with suppressed uptake in remainder of gland]

195
Q

What’s the single most important risk factor for Osteoporosis?

A

AGE
_________________
less RF: fam hx / smoking / EtOH

196
Q

Chronic Granulomatous Disease is a (⬜(Mode of Inheritance?)) that usually p/w ⬜ shortly after birth from ⬜
_________________

MOD for Chronic Granulomatous Disease

A

[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
Q

Macular degeneration affects [⬜ central | peripheral] vision,

while Glaucoma affects [⬜ central | peripheral] vision

A

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
Q

clinical presentation for [Open Globe Laceration] -2
___________________

what causes this injury?

_________________

management? -4

A

teardrop pupil and [DEC visual acuity]
_________________

[small sharp objects penetrating globe at high velocity]

_________________

[IV abx / eye shielding / eye CT / Optho consult]

199
Q

Elevated Calcitonin in pts with [Medullary Thyroid CA s/p total thyroidectomy] indicates ⬜?
_________________

next steps? -3

A

METASTASIS

_________________
[metastatic medullary thyroid CA dx] ➜ [CT neck/chest (look for metastasis)] ➜ Surgical Resection

200
Q

What type of goiters develop from iodine deficiency?
_________________
How do you treat [retrosternal goiter w/compressive sx]?

A

multiNodular
_________________
Surgery

201
Q

nml TSH: [0.4-4.0]

[Subclinical Hyperthyroidism Thyrotoxicosis] is defined as ⬜2
_________________

When is treatment indicated for [Subclinical Hyperthyroidism Thyrotoxicosis] -4

A

[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
Q

What is the Tuning Fork test ?

A

easy, inexpensive screen that assess for loss of 2TVP (usually of the BL feet) in DM

2TVP = 2-point/Touch/Vibration/Proprioreception

203
Q

How do you treat diabetic neuropathy? (4)

A

[AGGRESSIVE GLYCEMIC CONTROL]

+

[Neuronal transmission adjusters (Duloxetine|Gabapentin-Pregablin|TCA)]

204
Q

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

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

________________

b. pts chronically immunosuppressed (RA on prednisonefor > 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
Q

What is [Inferior petrosal sinus sampling] used for?

A

In patients with elevated ACTH, differentiates source of ACTH ( [Corticotrope Functional Pitutiary Adenoma] vs [Ectopic (SOLC)] )

206
Q

What level of prolactin indicates a Prolactinoma

A

>200

Prolactin inhibits LH release

207
Q

Clinical Presentation of of Anterior Uveitis(4)
_________________

A

(C**a**LEB)

Constricted pupil / ANTERIOR UVEITIS / Limbus erythema / Eye pain / Blurred vision

208
Q

Uveitis is associated with which conditions? (4)

A

systemic inflammatory DO
1. sarcoidosis
2. RA
3. JIA
4. HLA-B27

(C**a**LEB)sx

209
Q

In an eyelid laceration, visible fat within the wound indicates a ______ injury

________________

This raises concern for injury to which structures? -2

A

orbital septal injury

________________

postseptal structures (Extraocular Muscles + eyelid retractors)

210
Q

Between NPH and [long acting insulinDetemir/GLargine/DeGLudec] which is more likely to cause hypOglycemia?

A

NPH

NPH Peak effect MORE likely to → hypOglycemia

211
Q

Microalbuminuria is an indicator of __(3)___.

What lab value is used and what are the values for normal, micro and macro?

A
  1. DM
  2. HTN
  3. PSGN

Urine [Albumin-Creatinine Ratio];

30-300

normal = < 30

micro = 30-300

MACRO = 300+

212
Q

MOD for [High Output Heart Failure]

A
213
Q

Causes of [High Output Heart Failure] -7

________________

What’s the most common?

A
214
Q

[High Output Heart Failure] clinical presentation -3

A
  1. Edema (pulmonary & peripheral)
  2. warm extremities
  3. [systolic flow murmur with laterally displaced PMI]
215
Q

what is [sub-clinical hypOthyroidism] ? -2

A

(INC TSH)

but

(normal [T4 Thyroxine])

216
Q

most common cause of [sub-clinical hypOthyroidism] ?

A

hCAT

_________________

[hashimoto Chronic Autoimmune Thyroiditis]

217
Q

how do you know when [subclinical hypOthyroidism] is advancing to hypOthyroidism

A

[INC anti-TPO (antiThyroid PerOxidase)]

218
Q

[subClinical hypOthyroidism] puts females at risk for ⬜ complication?

A

PREGNANCY

(spontaneous abortion/preeclampsia, abruptio placenta)

219
Q

cp of hypOpituitarism - 5

A

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
Q

In hCAT , which antibodies are responsible for the attack on the thyroid gland?

_________________

hashimoto Chronic Autoimmune Thyroiditis

A

AntiThyroidPerOxidase

AntiTPO is also a/w miscarriage!!

221
Q

sx of hypOglycemia (6)

A

low blood glucose gives you SADHAT

  1. Seizure
  2. AMS
  3. Diaphoresis
  4. HA
  5. Anxiety
  6. Tremor
222
Q

labs for [factitious use of insulin]? -3

A

serum :

I Conceal Glucose

  1. 🔝 insulin
  2. ⬇️ cPeptide
  3. ⬇️ glucose
223
Q

Zollinger Ellison

etx

_________________

cp-2

A

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
Q

for IDDM, how much daily insulin should be prescribed?

A
225
Q

What things cause HYPERKalemia? -6

A
226
Q

What are the opthalmological complications of DM-3; what causes them?

A
  1. Retinopathy (from ⬆︎VEGF –> abnormal angiogenesis)
  2. Glaucoma (⬆︎ Sorbitol eye pressure)
  3. Cataracts (Glycation of Ocular lens
227
Q

What happens to [total thyroid hormone] serum level when drugs displace thyroid hormone?

________________

Which drugs do this?-3

A

[free hormone displacement] ➜ [Thyroid production ⬇︎] –> ⬇︎TOTAL thyroid levels but normal free hormone levels

  1. ASA
  2. Furosemide
  3. Heparin
228
Q

Precocious puberty occurs in [girls less than ⬜ years old] and [boys less than ⬜ years old]

________________

How do you work this up?(see image)

A

[G<8], [B<9]

229
Q

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

A

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
Q

Danazol MOA

________________

Indication

A

testosterone derivative with progestin effects

________________

endometriosis

231
Q

Teenage boy comes in with gynecomastia

How do you work this up?

A

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
Q

How long does it take [RAI ablation] therapy to treat Hyperthyroidism?

_________________

How does radioiodine therapy actually worsen Graves ophthalmopathy?

  • RAI: RadioActiveIodine*
A

1-4 mo

_________________

RAI eventually –> hypothyroidism –>⬆︎ thyroid stimulating autoantibodies –> stimulate [orbital fibroblast] → expands [orbital tissue]

233
Q

Riedel thyroiditis MOD

A

progressive fibrosis of thyroid gland and surrounding tissue (that looks like CA)

234
Q

cp for HyperParathyroidism - 4

A

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)

235
Q

Acromegaly cp - 13

A

etx: GH stimulates IGF1 secretion most of day –> acromegaly sx

heart = concentric LVH
236
Q

Acromegaly Dx (6)

A

etx: GH stimulates IGF1 secretion most of day –> acromegaly

237
Q

Acromegaly etx

A

GH stimulates IGF1 secretion most of day –> Acromegaly

⊝GH secretion is ⬇︎ by glucose and somatostatin
⊕GH secretion is ⇪ by EXERCISE and SLEEP

238
Q

How does immobilization affect Ca+ levels

A

INCREASES

Immobilization –> ⬆︎osteoclast activity –> ⬆︎serum Ca+

239
Q

Acute Rhabdomyolysis causes Ca+ to (⬜ [increase/decrease]) because of what?

A

DECREASE

________________

release of Ca+ and Phosphorous from damaged muscles –> CaPhosphate precipitation –> drops free serum Ca+

________________

HYPERcalcemia and HYPERphosphatemia can occur later during the remobilization phase during recovery

240
Q

iCa+ = 0.76 - 1.49

How does [serum albumin] levels affect [ionized Ca+] levels?

A

IT DOESNT!

[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 [FREEalbumin(which is ⊝)] ⇪ → likely knocks off Ca⊕ from [anions] → ⬇︎[TOTAL Ca+].
[TOTAL Ca+].
_________________
_________________

241
Q

Tx for PCOS - 5

A

[Wt loss–> SOCK]

SOCK:Spironolactone,OCP (1st line after wt loss),Clomiphene for infertility,Ketoconazole

________________

etx: DM/Obesity–>Hyperinsulinemia which –> ⬆︎⬆︎⬆︎LH secretion –> ⬆︎ovarian theca Androgen secretion –> Sx

242
Q

Which CA is known for producing calcitonin?

A

[Medullary Thyroid Carcinoma]

also produces ACTH and VIP

associated with MEN2A and 2B

243
Q

Why should pts with [Medullary Thyroid Carcinoma] have a fractionated metanephrine assay ordered?

A

Screen them for Pheochromocytoma

MTC and Pheochromocytoma are associated with MEN2A and 2B

244
Q

How do you treat [Papillary Thyroid Carcinoma] - 3

A

Surgical Resection –> +/- radioiodine ablation and suppressive doses of thyroid hormone (in pts with risk of recurrence)

245
Q

How is Mg associated with Ca+ levels

A

low Mg+ (especially in alcoholics) –> ⬇︎PTH hormone release and PTH resistance —> ⬇︎serum Ca+ AND low serum K+

serum Phosphorous levels are NOT affected by this phenomena!

246
Q

What are the distinguishing features of Pancreatic VIPoma - 5

A
  1. Tea colored watery secretory diarrhea
  2. hypOkalemia
  3. hypOchlorhydria (from ⬇︎gastric acid)
  4. HYPERcalcemia from ⬆︎bone resorption
  5. Facial flushing

tx = octreotide for diarrhea

247
Q

Pts with untreated Hyperthyroidism are at risk of developing what conditions? - 2

A
  1. Bone loss from ⬆︎osteoclast activity
  2. cardiac tachyarrhythmias

Hyperthyroidism = Graves > toxic adenoma > multinodular goiter

248
Q

What is the most common side effect of AntiThyroid drugs? (i.e. Methimazole, PTU)

A

agranulocytosis

  • Pt on AntiThyroid drugs who develop sore throat with fever should have WBC checked!*
  • Radioactive Iodine tx can –> worsening ophthalmopathy*
249
Q

In HYPERthyroidism, what is the mechanism for why pts have HTN?

A

⬆︎Myocontractility and HR

250
Q

Why are pts who receive > 1 unit of pRBC or whole/blood transfusion at risk for hypOcalcemia?

A

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
Q

What is the most beneficial therapy to ⬇︎ the progression of DM nephropathy?

A

BP control < 130/80

do not push HbA1C < 7%

252
Q

A Pt with Hyperthyroid pt develops Sore throat and Fever after being started on Methimazole

What should you assess for?

A

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*
253
Q

A woman starts to rapidly develop facial and body hair

What test do you order first to determine etiology? - 2

A

DHEA and Testosterone

Hyperandrogenism suggest androgen secreting CA of ovary or adrenal glands so these test will help to determine that

254
Q

Describe Euthyroid Sick Syndrome (2)

A
  • ISOLATED low T3
  • can occur anytime the body is “sick”

[Euthyroid Sick (low T3) Syndrome]

255
Q

Which microscopic finding is associated with Papillary Thyroid CA?

A

Psammoma bodies (large lamellated calcifications with ground glass cytoplasm)

256
Q

Why can’t [Follicular Thyroid CA] be evaluated with fine needle biopsy?

A

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
Q

Tx for {[Prolactinoma 1-3cm] or Symptomatic} - 3

Prolactinoma dx = Prolactin > 200

A
  1. Cabergoline dopamine R agonist OR
  2. Bromocriptine dopamine R agonist
  3. Transsphenoidal resection if refractory
258
Q

Tx for Prolactinoma >3cm

Prolactinoma dx = Prolactin > 200

A

Transsphenoidal resection surgery

{[Prolactinoma 1-3cm] or Sx⊕}= Cabergoline|Bromocriptine|Sgry prn

259
Q

Graves Ophthalmopathy etx

________________

risk factors?-2

A

Activated T cells and Thyrotropin Autoantibodies both stimulate retroorbital fibroblast –> orbital tissue expansion

________________

Smoking, Female

260
Q

cp for DM [LARGE nerve fiber] damage

________________

cp for DM [small nerve fiber] damage

A

[LARGE eNormous nerves] –> NEGATIVE SX = [NO 2TVP] [NO ankle reflexes]

________________

[small petit nerves] –> positive sx = pain, paresthesias

261
Q

cp for [Klinefelter XXY] ?-6

A
  1. small phallus
  2. [hypOgonads (small testes)]
  3. hypOspadia
  4. gynecomastia
  5. Cryptochidism
  6. Eunuchoid body
262
Q

Why do pregnant patients or patients started on OCPs require increased doses of levothyroxine if they’re taking it

A

Estrogen –> ⬇︎clearance of Thyroid Binding Globulin –> additional TBG binds up all the free T4 –> ⬇︎free T4

263
Q

[Toxic Adenoma 1ºHyperthyroid-thyrotoxicosis] MOD

A

autonomous production of thyroid hormones from hyperplastic thyroid follicular cells

if multiple uptake present, consider multinodular goiter

264
Q

How does looking at Thyroglobulin levels help determine etiology of thyroid disease?

A

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
Q

What is Conn’s syndrome

A

Primary Hyperaldosteronism

266
Q

List the ophthalmoscopy findings for [simple Diabetic Retinopathy] - 3

_________________

What procedure prevents this?

A
  1. microhemorrhages
  2. retinal edema
  3. exudates

Argon laser photocoagulation

267
Q

What are the precipitants of Pheochromocytoma?-3

________________

which medication should be given prior to these precipitants?

A

Don’t GAS a Pheochromocytoma

  1. General Beta Blockers (allows unopposed [α] stimulation)
  2. Anesthesia
  3. Surgery

Phenoxybenzamine (irreversible general alpha blocker)

268
Q

PTHrelatedProtein is associated with Cancer (Humoral Hypercalcemia of Malignancy)

________________

What is the major mechanism difference between PTHrP and PTH?

A

PTH ⬆︎ conversion of [25VitaminD] to [1-25VitaminD]

PTHrP comes from [SQC, breast, renal, bladder, ovarian]

269
Q

What are the triggers of Thyrotoxicosis - 5

A
  1. iodine contrast
  2. infection
  3. childbirth
  4. surgery
  5. trauma
270
Q

What is the best way to monitor a pt being treated for DKA - 2

A
  1. Serum Anion Gap
  2. Beta Hydroxybutyrate levels
271
Q

Primary Hyperparathyroidism and Familial hypocalciuric Hypercalcemia both present with serum Ca+ that is _____ (low/high)

How do you differentiate the two?

A

HIGH

FHH = [urine calcium : creatinine ratio < 0.01]

Primary Hyperparathyroidism = uccr>0.02

272
Q

Sialadenosis etx

A

NONinflammatory swelling of the salivary glands caused by liver disease or malnutrition (DM, bulimia)

273
Q

Demeclocycline MOA

________________

Indication?

A

inhibits ADH-mediated renal cortical collecting duct aquaporin insertion

________________

SIADH

274
Q

Tolvaptan MOA

________________

Indication?-2

A

TolVaptan = [V2 vasopressin ADH R blocker] ;

  1. [severe HF Hypervolemia]
  2. [refractory SIADH]
275
Q

In pts with Diabetes Insipidus, how do you differentiate between Central and Nephrogenic causes?

A

Water Deprivation Test

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]

276
Q

cp for Primary Hyperparathyroidism

A

Asymptomatic Hypercalcemia

Hypercalcemia sx: Painful Bones, Renal Stones, Abd Groans and Psychic Moans

277
Q

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?

A

[GLP1 agonist (exenatide, liraglutide)]

278
Q

A DM pt is not well managed on single therapy Metformin

When is it appropriate to consider adding insulin?

A

HBA1c > 8.5%

279
Q

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

A

Insulin

[Thiazolidinediones (pioglitazone)]

Sulfonylurea

“Insulin Tops Scales”

280
Q

etx for Prader Willi Syndrome

_________________

cp?-4

A

“short, Phat & retarded”
PATERNAL deletion of chromo15q11 thru 13 ;

  1. HyperPhagia –> Phat (Obesity), Gastric rupture, DM2
  2. hypOtonia
  3. short stature
  4. Mentally retarded
281
Q

etx for Angelman Syndrome

_________________

cp?-4

A

“short, sMiling & retarded”

maternal deletion of chromo15q11 thru 13 ;

  1. Frequent sMiling/Laughter (Moms make you smile)
  2. Hand Flapping
  3. short stature
  4. mentally retarded
282
Q

explain how DM destroys nerves

A

deposition of [glycosylation products], [oxidative stress] and [microvascular injury] all –> small nerve AND Large nerve-length dependent axonopathy

283
Q

What is the most common cause of primary hypogonadism in males?

A

Klinefelter XXY

284
Q

[McCune Albright] syndrome etx?

A

all [McCune Albright] does is P P P

etx = autonomous activity of endocrine tissue from defect in cAMP kinase

285
Q

causes of hypOparathyroidism -5

A
  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)
hypOparathyroidism
286
Q

hypOparathyroidism sx-7

A

TQT + BOD + Chvostek

hypOparathyroidism

Trousseau(cutting off Tricep/forearm circulation causes Carpal Spasm)

QT prolongation

[Tetany (Seizures/spasm)]

Brain(Parkinsonism/ ⇪ ICP)

Ocular cataracts

Dentition abnormalities

Chvostek(tapping along [Cheek-facial CN7) causes {Mouth/Nose/Eye-Contraction})

287
Q

PseudohypOparathyroidism

clinical features -4

A
  • Organ resistance to PTH
  • AutoDOM
  • short 4th and 5th digits
  • short stature
288
Q

The [Parathyroid gland] secretes ⬜ when the [⬜ receptor] detects ⬜

A

PTH; CaSR;

[(free ionized Ca+) ⬇︎]

289
Q

Name all the functions of [PTHParathyroid gland] - 6

A
  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)2VitD]
  6. Intermittent PTH[⇪bone formation by activating osteoBlast]
290
Q

[Slit Lamp Exam] indication

A

Evalutes for abnormalities of ANT eye (conjunctiva, cornea, ANT chamber, iris)

291
Q

diagnosis?

________________

What’s the most common cause?

A

Vitreous Hemorrhage

________________

DM

Fundoscopy = Dark Red Glow with Loss of Fundus details

292
Q

Causes of Corneal Abrasion - 3

________________

How do you diagnose Corneal Abrasion?

A
  1. Trauma
  2. Foreign Body under eyelid
  3. Contact lens –> Corneal epithelial defect

________________

Fluorescein exam revealing corneal staining defect

Corneal Staining Defect
293
Q

Glaucoma etx -3

A

⇪ 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]*
294
Q

Name the 5 Rx for chronic Glaucoma Tx (5)

________________

how specifically does B-blockers work?

A

Glaucoma Problem 1: [⇪⇪ AH inflow/production] (tx = β🟥|α2🟢| CAI)
_________________

Problem 2[⬇︎⬇︎AH uveoscleraloutflow](tx = [Prostaglandin🟢 LatanoprostTOPICAL]

_________________

Problem: 3[⬇︎⬇︎AH trabecularoutflow](tx =[Muscarinic🟢Pilocarpine </sup>]

β🟥 –> ⬇︎Aqueous humor secretion from Ciliary Epithelium

295
Q

What target organ does the M3 Receptor work in (6)

A

“[M1s need Brain], [M2s need Heart], [M3s BEGs for Private Lounges”

“An M3 BEGS for Private Lounges”

Bladder(contraction) / Eyes / GI / Skin / [Peripheral Vasculature] / Lungs

296
Q

What are the causes of [Acute Closed Angle Glaucoma]? -3

A

Anticholinergics / Sympathomimetics / Dim light

_________________

“Closed angle needs OPMAT .. STAT!”

297
Q

What is the major complaint pts with Glaucoma have?

A

Gradual Tunnel Vision

298
Q

HIGH tone hearing loss = [⬜ sensorineural | conductive] hearing loss

A

Sensorineural

299
Q

Which is more efficient at transmitting sound between Bone and Air?

________________

Why?

A

AIR!

________________

Air interacts with ossicles FIRST, which Amplifies the sound conduction to cochlea

300
Q

Ophthalmoscopy findings include cupping of the optic disc

Diagnosis?

A

Glaucoma

________________

Glaucoma affects peripheral vision –> tunnel vision! OAG is more common in Blacks

👓cupping is caused by thinning of outer rim of optic disc head

301
Q

etx of Cataracts

________________

What are the most common presenting sx of Cataracts? -2

A

[⇪ lens opacity] –>

  1. [gradual BL NIGHT VISION ⬇︎]
  2. halos around lights

________________

Fundoscopy eventually shows lost of red reflex and retinal details

302
Q

What is the treatment for Emergent Acute [Closed angle Glaucoma] - 5

A

“Closed angle needs OPMAT .. STAT!”

[OPHTHO CONSULT STAT!(for Emergent Iris resection!)]

Pilocarpine[Cholinergic M3 R agonist]

Mannitol

AcetazolamideCAI

TimololBB

303
Q

diagnosis?

A

Retinoblastoma leukocoria

304
Q

Dx for [Acute Closed angle Glaucoma] -2

A

Gonioscopy vs Ocular Tonometry

Gonioscopy

_________________

“Closed angle needs OPMAT .. STAT!”

305
Q

diagnosis?

A

Zoster Ophthalmicus

________________

finding = Dendriform Corneal Ulcer

306
Q

MOD for Trachoma

_________________

cp for Trachoma-2

A

Repeated Eye infections with Chlamydia Trachomatis A,B,C –> Inversion of Eyelashes

_________________

(INVERTED & PALE EYELASH HAIR FOLLICLES with Conjunctival injection) –> [Blindness from lash ulceration]

307
Q

Subconjunctival Hemorrhage is self limited to how long?

A

2 days

308
Q

How does this abnormality clinically present? - 2

A
  1. [suddennonpainful uL vision ∆ (hazy|red hue|COMPLETE LOSS)]
  2. Floaters also seen with [Torn Retinal Detachment]

dx = Vitreous Hemorrhage

Vitreous Hemorrhage: Dark Red Glow with Loss of Fundus details
309
Q

When can you mandate parents against their will to accept treatment for a [non emergent ailment] for their child?

A

when the [non-emergent ailment] is a fatal medical condition (i.e. Cancer), M.D. can obtain a court order to give tx

________________

PARENTS ARE NOT ALLOWED TO REFUSE LIFE SAVING TREATMENT FOR THEIR CHILD (EVEN IF BASIS IS RELIGIOUS)

310
Q

Describe ophthalmoscopy findings for Diabetic Retinopathy-3

A
  1. microaneurysms = simple type
  2. retinal edema = simple type
  3. newly formed vessels if malignant type
311
Q

low tone hearing loss = [⬜ sensorineural | conductive] hearing loss

A

conductive

312
Q
Diagnosis?
A

Glaucoma

📖

313
Q

cp for Acute Closed angle Glaucoma - 3

A
  1. PAINFUL Red eye uL
  2. Fixed Dilated pupil
  3. Cloudy Cornea

_________________

“Closed angle needs OPMAT .. STAT!”

314
Q

Prognosis for [Acute Closed angle Glaucoma]

A

Permanent Vision Loss within 2-5 hrs of onset!

_________________

“Closed angle needs OPMAT .. STAT!”

315
Q

Identify finding

A

[(Zoster Ophthalmicus)Dendriform Corneal Ulcer]

________________

dx = Zoster Ophthalmicus

316
Q
A
estrogen/testosterone Pituitary complex
317
Q
A
estrogen/testosterone Pituitary complex
318
Q

[Closed angle Glaucoma] accounts for ⬜% of cases, presents [⬜ gradually | abruptly] , and is a medical Emergency!

What is the etx for [Closed angle Glaucoma]? -4

_________________

AKA: [Acute Glaucoma or angle-closure Glaucoma]

A

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

🔎aLi = angle between Lens and Iris
_________________
🔎[aTic : angle at iris ⼀{TMAD} ⼀cornea] | [TMAD: Trabecular Meshwork AqueousHumor Drain]

319
Q

[Open angle Glaucoma] accounts for ⬜% of cases, and presents [⬜ gradually | abruptly]

What is the etx for [Open angle Glaucoma]? -3

A

65% ; gradually

* * *

⭐[ **aLi**: 🟢]. [ **aTic**: 🟢]. [**TMAD**: ❌].⭐
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
1. idiopathic vs [TMAD❌<sub>(Trabecular Meshwork Aqueous<sub>Humor</sub> Drain ❌bstruction)</sub>]
2. → [*gradually slow* ⇪ IOP] → [*gradual slow* loss of <sup>(peripheral 1st)</sup>sight over years]
3. aTic not affected = remains open

\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_

| 🟢=Open / ❌=closed

## Footnote

*🔎**aLi** = **a**ngle <sub>between</sub> **L**ens and **I**ris*
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
🔎[**aTic** : **a**ngle <sub>at </sub>**i**ris ⼀{**_T_**_MAD}_ ⼀**c**ornea] | [TMAD: Trabecular Meshwork Aqueous<sub>Humor</sub> Drain]

320
Q

definition

Astigmatism

A

abnormally curved cornea that causes different refractive power at different axes

321
Q

definition

PresByopia

A

age-related ⬇︎lens elasticity → [⬇︎accommodation (near-vision)]

👣often needs reading glasses

322
Q

risk factors (8)

cataracts

A
  1. age
  2. smoking
  3. EtOH
  4. CTS
  5. [DM (sorbitol)]
  6. trauma
  7. excessive sunlight
  8. infection
  9. galactosemia / galactokinase deficiency
323
Q

Latanoprost

MOA
_________________
Indication

A

[PGF2αProstaglandin analog ] = ⇪ outflow of aq humor
_________________
Glaucoma

📝side effect = darkens /causes iris “browning”

324
Q

Physiological action of GH in children (5)

A

Linear Growth of

  • long bones(primary determinant of adolescent growth spurt)
  • cartilage
  • muscle
  • organ systems

+ [Blood Glucose promoter]

325
Q

Physiological Action of GH in Adults (3)

A
  1. Catabolic for Fat
  2. Anabolic for Muscle & Bone
  3. Blood Glucose Promoter (INC Blood Glucose)
326
Q

Effects of GH are mostly mediated by _____, which is released from the ____ in response to ___

A

Effects of GH are mostly mediated by IGF1, which is released from the liver in response to GH

[GHRH → GH —> IGF1]

327
Q

In addition to Musculoskeletal changes, what other changes occur in Adults with GH deficiency (3)

A
  • Hyperlipidemia
  • Cardiac Muscle Atrophy
  • [Fatigue / Depression / Malaise]
328
Q

Adult onset GH deficiency is typically due to what?

A

Pituitary problem

329
Q

Drugs for GH deficiency (4)

A

[sermoRELinGHRH]
_________________
SOMATREM

SOMATROPin
_________________
mecasermin

330
Q

Name a Synthetic GHRH

A

sermoRELin

331
Q

Name 2 [Recombinant HumanGH]

A
  1. Somatropin
  2. Somatrem
332
Q

What is Mecasermin?

A

Recombinant IGF1

333
Q

Somatropin Indication (5)

A

SPAWN

  1. Pediatric growth failure (associated w/GH/chronic Renal Failure/Prader Willi/Turner)
  2. No idea: Idiopathic short stature (>2.25 SD below mean height)
  3. Adult GH deficiency
  4. Wasting in AIDS pts
  5. Short Bowel Syndrome in pts receiving nutritional support (it INC SA for digestion)
334
Q

Structure of Somatropin

A

identical to native hGH

(Somatropin = Synthetic GH structurally identical to native hGH)

335
Q

Mecasermin Indication

A

Pediatric IGF1 deficiency from [Laron GH receptor Dwarfism] vs. [Ab against GH]

336
Q

Octreotide [Drug Class and MOA]

A

Somatostatin Analogue (45x more potent and long lasting) –> blocks GH secretion

337
Q

Octreotide Indications (4)

A
  • Pitutiary microadenoma
  • Carcinoid Crisis (flushing/diarrhea/Cyanosis)
  • Secretory Diarrhea 2° to VIP tumors
  • Acute GI Bleeding
338
Q

Name the Gonadotropins (4) and what their MOA is

A

Replaces FSH and LH

  • Menotrophins (FSH and LH)
  • hCG
  • Urofollitropin (FSH from menopausal women urine)
  • Follitropin
339
Q

Gonadotropins Indication (3)

A
  1. Ovulation in [women with hypOgonadotropic hypOgonadism] vs. IVF
  2. PCOS/Obesity
  3. Infertility in [Men with hypogonadotropic hypOgonadism]
340
Q

How does GnRH🟢 or [ short half lifeGnRH analog] affect gonadal axis?

A

Stimulates Gonadotroph cells to make/secrete LH & FSH

341
Q

[ LONG half lifeGnRH analog] MOA

A

Desensitizes GnRH receptors and inhibits FSH and LH release

342
Q

Biphasic Effect of [GnRH analogs]

A

GnRH➿
1st: short1/2 life = FLARE effect = Transient (7-10 days) FLARE (INC) in gonadal hormone levels from agonist effect
2nd: LONG1/2 life-lasting suppresion of Gonadotropins and gonadal hormones from inhibition

{GnRH➿ = GnRH analogs}

343
Q

Goserelin Indication (8)

A

[specific = aef ]
1. androgen dependent Prostate CA] adjunct
2. endometriosis
3. fibroids_Uterine
________+_________
[ALL = BOPIA]
4. Breast CA
5. Ovarian CA
6. PCOS
7. Infertility
8. Amenorrhea

{GnRH➿ = GnRH analogs}

{[Goserelin GnRH➿] indication} = {[specific[a|e|f ]] + [GENERALBOPIA]}

344
Q

Leuprolide Indication (10)

A

aefcr
1. [androgen dependent Prostate CA] adjunct
2. endometriosis
3. fibroids_uterine
4. central precocious puberty
5. [reproductive IVF(keeps LH surge low → multi-oocyte maturation) ]
________+_________
[ALL = BOPIA]
4. Breast CA
5. Ovarian CA
6. PCOS
7. Infertility
8. Amenorrhea

{GnRH➿ = GnRH analogs}

{[Leuprolide GnRH🟢] indication} = {[specific[a|e|f |c|r ]] + [GENERALBOPIA]}

345
Q

List the 3 [GnRH R Blockers]

A

“Don’t Block me from getting my Rolex”

  1. Ganirelix
  2. Cetrorelix
  3. Abarelix

These are Dose-Dependent

346
Q

How is administration between [GnRH synthetic analogs] and [GnRH R Blockers] different (2)

A
  1. [GnRH R Blockers] produce immediate Blocking effect = Duration of Admin is shorter during IVF
  2. [GnRH R Blockers] don’t produce Flare Effect
347
Q

Drugs given during [Follicular Proliferative Phase] during IVF (3)

A
  • 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
348
Q

Physiologic Actions of Prolactin (4)

A
  1. Mammogenesis
  2. Milk production
  3. Milk secretion
  4. [Inhibits GnRH secretion → Suppresses Ovulation]
349
Q

Hyperprolactinemia Tx and why (3)

A
  1. Bromocriptine
  2. Cabergoline
  3. Pergolide

These are [D2 Dopamine R Agonist]

350
Q

Bromocriptine Indication (5)

A
  1. Pituitary Prolactinoma
  2. PMS
  3. Acromegaly (Use High Doses and only if tumor secretes both Prolactin & GH)
  4. Parkinson’s Dz
  5. Type2DM

[1A] ⚡ M.D. STEP 3🩺USMLE (14 decks)

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