7 ⼀ENDOCRINE/OPHTHO Flashcards
46
how are pregnant patients screened for hyperthyroidism? (3)
torn
TSH
(low TSH) ➜ [free T4]
(normal [free T4]) ➜ [Total T3]
use trimester-specific norms
management? (2)
eye shield
+
[hospital admit (strict bed rest + 30° bed + serial intraocular pressures+ [prevent rebleeding and intraocular HTN → vision loss])]
HYPHEMA
Stress Hyperglycemia occurs when ⬜. This presents very similarly to ⬜
_________________
how do you differentiate the two? (2)
Stress Hyperglycemia is a/w ⇪ morbiditiy
[STRESS (severe illness > 39C)] ➜ [CortisolGlucocorticoid] secretion➜ ⇪ Insulin resistance ➜ hyperglycemia ;
DKA
_________________
DKA has [hgbA1C ≥6.5%] +[“FUDGe” DM classic s/s]
patient newly diagnosed with Papillary Thyroid Cancer
What’s 1st step after this?
_________________
What are the treatments? (2)
[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]
Which antiDM are a/w weight gain? (3)
Insulin
[Thiazolidinediones (pioglitazone)]
Sulfonylurea
“Insulin Tops Scales”
What is Euthyroid Sick Syndrome? (4)
_________________
mgmt? (3)
⭐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
What is [reverse ®T3]?
_________________
what is it used for?
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])
How do you workup a patient with suspected [central hypOpituitarism] (5)
patients with [classic Congenital Adrenal Hyperplasia] require prompt therapy with ⬜ and chronic tx with ⬜
Why ? (3)
[high dose hydrocortisone] ; glucocorticoid and mineralocorticoid replacement
_________________
avoid adrenal crisis by maintaining BP / growth/ suppress adrenal androgens
classic CAH = 21hydroxylase deficiency CAH
Recite the Adrenal Gland blueprint for
Zona Glomerulosa (13)
*
Recite the Adrenal Gland blueprint for
Zona Fasciculata -7
Recite the Adrenal Gland blueprint for
Zona Reticularis-6
The most common enzyme deficiency for [Congenital Adrenal Hyperplasia] is
⬜
________________
cp?-3
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
The 2nd most common enzyme deficiency for [Congenital Adrenal Hyperplasia] is
⬜
________________
cp?-5
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
The least common enzyme deficiency for [Congenital Adrenal Hyperplasia] is
⬜
________________
cp?-2
17 αhydroxylase
🅶
▶[⇪ ⇪ AldosteroneMineralocorticoid] ← [⇪⇪ 11DOCSMC]
= Salt Retention → Fluid Retention = HTN
🅵
▶[⬇︎CortisolGlucocorticoid]
🆁
▶[⬇︎Testosterone]
= ALL PATIENTS PHENOTYPICALLY FEMALE
[11dc =11deoxycortisol] | [11DOCS =11DeOxyCorticoSterone] | MC=MineraloCorticoid/GC=GlucoCorticoid
The most common enzyme deficiency for Congenital Adrenal Hyperplasia is ⬜
Which lab value is diagnostic for this deficiency?
21 hydroxylase (complete = classic CAH | reduced=nonClassic CAH)
⬆︎17 HydroxyPROGESTERONE
What benefits does maintaining Tight Glucose Control in DM pts give?
⬇︎ microvascular complications (retinopathy/nephropathy)
What are all the functions of [CortisolGlucocorticoid] - 6
⇪BIG ⬇︎FIB
- ⇪ Blood pressure (⬆︎a1 receptors)
- ⇪Insulin resistance –> DM
- ⇪Gluconeogenesis
_________________ - ⬇︎Fibroblast –> striae
- ⬇︎Immune system (WHITE)
- ⬇︎Bone formation by ⬇︎osteoBlast
what is Apathetic Thyrotoxicosis ? (4)
- [atypical elderly HYPERthyroidism] =
- [APATHY (lack of enthusiasm/interest), mimics DEPRESSION, lethargy, confusion, wt loss]
- (misdiagnosed as depression or dementia),
- likely NO thyromegaly
S/S of hypOthyroidism is mostly opposite of Hyperthyroidism sx
What are 9 symptoms specific to only hypOthyroidism?
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
Clinical definition of Diabetic Ketoacidosis (DKA) -2
[metabolic acidosis (HCO3<15 or pH<7.3)]
in the setting of [hyperglycemia > 200]
how do you manage HHONKS-6?
[HHONKS (Hyperglycemia HyperOsmolar NON Ketone State)]
FIPAAR control
-
Fluid control : (NS) < [Blood Sodium 135] < (1/2 NS)
_________________ -
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]
_________________ -
Potassium control: [✳]
_________________ -
Acid control: give HCO3 for [pH< 6.9 or HCO3< 15]
_________________ -
ANION GAP CONTROL: [correct to 10-14]
_________________ -
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–> ✔︎]}
how do you manage DKA-6?
DKA:Diabetic Ketoacidosis
FIPAAR control
-
Fluid control : (NS) < [Blood Sodium 135] < (1/2 NS)
_________________ -
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]
_________________ -
Potassium control: [✳]
_________________ -
Acid control: give HCO3 for [pH< 6.9 or HCO3< 15]
_________________ -
ANION GAP CONTROL: [correct to 10-14]
_________________ -
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–> ✔︎]}
[HHONKS (Hyperglycemia HyperOsmolar NON Ketonic State)**] is a complication of DM
What Blood Glucose precipitates this?
Blood Glucose > 600
How does DKA and HHONKS affect total body K+ levels?
⬇︎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+ ✳]
In DKA and HHONKS management, when do you hold the insulin?
serumK <3.3
Remember that ALL DKA and HHONKS pts are Total Body K+ depleted due to osmotic diuresis regardless of what serum values say
In DKA and HHONKS management, when do you consider using Sodium Bicarbonate?
pH<6.9
You suspect a pt has Cushing Syndrome
How do you work this up?-3
1st: .Determine if pt has ⇪ [CortisolGC]([Overnight low-dose dexamethasone suppression test] | [late night salivary cortisol assay] | [24 hr urine free cortisol])
2nd. If [CortisolGC] ⇪ = ⊕Cushing Syndrome
3rd: If ⊕Cushing Syndrome → perform ACTH workup(image) to determine if Cushing Syndrome [ACTH-dependent] or [ACTH-INdependent]
You suspect a pt has Cushing Syndrome
After completing step 1 and step 2 of Cushing Syndrome workup, your attending ask you to perform the [3rd step ⼀ACTH workup] to determine _______
What is the ACTH workup? -3
3rd: If ⊕Cushing Syndrome → perform ACTH workup(image) to determine if Cushing Syndrome [ACTH-dependent] or [ACTH-INdependent]
Name the characteristics of Cushing Syndrome - 7
“Fat Heavy People May HOG the Cushing”
- Fat reDistribution (central obesity, Moon face)
- Hyperpigmentation (from excess ACTH activating [Melanocyte MC1 R])
- Purple striae with skin atrophy and bruisability
- Muscle atrophy
- HTN
- Osteoporosis
- Glucose intolerance
________________
Cushing SYNDROME is caused by ⇪ [CortisolGlucocorticoid](which may be ACTH-INdependent or ACTH-dependent)
autoimmune adrenalitis is known as _____ disease
etx?
[Addison’s Primary Adrenal Insufficiency] disease
Autoimmune Primary Adrenal Insufficiency (suspect this in pts with other Autoimmune diseases - pernicious anemia, vitiligo, hypothyroid!)
Sx = HYPERKalelmia, hypOnatremia, wt loss, fatigue
What are the main causes of [Addison’s Primary Adrenal Insufficiency]? - 4
- TB
- Autoimmune adrenalitis
- CA
- Adrenal Hemorrhage
Main sx for [Addison’s Primary Adrenal Insufficiency] - 8
“Addison was a SNAP FHAG”
- [Sodium ⬇︎ DEC]
- [NAHA (Normal AG Hyperchloremic metabolic acidosis)]
- AnorexiaWT LOSS
- [Potassium ⇪ INC]
- Fatigue
- [Hyperpigmentation(ACTH and MSH)]
- [Androgen deficiency(⬇︎axillary/pubic hair)]
- GI Sx
What is Cosyntropin?
_________________
Describe how it used to workup ⬜
ACTH analog ⼀used for ACTH stimulation test – when [basal morning plasma cortisol] and [basal morning plasma ACTH] are equivocal
_________________
[Addison’s Primary Adrenal Insufficiency]
What test should you order to diagnose [Addison’s Primary Adrenal Insufficiency]? (3)
- basal morning plasma cortisol ⼀(dx = low cortisol)
- basal morning plasma ACTH ⼀(dx = HIGH ACTH)
- [Cosyntropin ACTH stimulation test] ⼀(use if 1 and 2 are equivocal)
Which 5 drugs cause Drug-Induced Lupus?
_________________
How is Drug-Induced Lupus diagnosed? (2)
HEMPI to DIL
Hydralazine
[Etanercept (TNFα R Blocker)]
Minocycline
Procainamide
[Infliximab (TNFα R Blocker)]
_________________
+ANA and +antiHistone
Why are frequent ophthalmologic exams necessary for prolonged CTS users?
CTS changes lens epithelial gene transcription ➜ CATARACTS
In addition to ⇪ glucose urinary excretion , how do SGLT2 inhibitors delay the progression of DM nephropathy?
inhibiting Na+/Glucose transporter ➜ [⇪ urinary glucose] AND [⇪ urinary Na+] and the [⇪ urinary Na+] travels to macula densa where it causes ⬇︎renin secretion ➜ [⬇︎Angiotensin II] ➜ ⬇︎efferent arteriole constriction ➜ ⬇︎GFR = delays DM nephropathy
pt p/w eye pain with foreign body sensation
what’s your workup? (4)
Both preseptal cellulitis and orbital cellulitis present with (⬜3)
_________________
How are they differentiated? (3)
[eyelid swelling-redness] / fever / conjunctivitis
_________________
orbital = orbit eye pain with movement + proptosis + ophthalmoplegia
How do you treat Orbital cellulitis? (2)
IVAbx ➜ [Surgical debridement (if fluid collection/abscess present)]
How do you workup Hyperthyroidism? -5
Exogenous thyrotoxicosis MOD
[OTC Thyroid supplement vs surreptitious prescription thyroid med] ➜ supressess [ANT Pit TSH] ➜ ⬇︎thyroid gland synthesis ( ⬇︎RAIU and ⬇︎thyroglobulin)
Common s/s of HYPERthyroidism -9
TT Feels ARCHED
- Tremor
- Tachycardia
- [Fatigue(+/- Apathy in Elderly)]
- Appetite ⬆︎ but Wt ⬇︎
- Reflexes ⬆︎
- Cardio* (Tachycardia, Palpitations,Exertional SOB, ⇪Myocontractility→HTN)*
- Heat intolerance –> SWEATING
- [Exophthalmos with lid lag = GRAVES DISEASE]
- Diarrhea +/- dyspepsia
Older pts may only have Fatigue, Cardio, or Apathetic!
For patients taking CTS, which patients need their dose regimens tapered down at the end?
[CTS > 3 Weeks] = TAPER DOWN
(taper allows for return of adequate endogenous cortisolglucocorticoid)
How do you workup Hypercalcemia? -4
MEASURE PTH!
Hypercalcemia can either be PTH-dependent or PTH-INdependent
What are the causes of [PTH-dependentHypercalcemia]? (4)
- Primary HyperParathyroidism
- Tertiary HyperParathyroidism(Intractable Hypercalcemia 2/2 Autonomous Parathyroid)
- [Familial hypOcalciuric Hypercalcemia]
- Lithium
Hypercalcemia can either be PTH-dependent or PTH-INdependent
What are the causes of [PTH-INdependentHypercalcemia]? (8)
- MALIGNANCY
- [VitD toxicity]
- [VitA toxicity]
- Granulomatous disease
- [LCD-TV Rx]
- Milk-alkali syndrome
- Thyrotoxicosis(Thyroid hormone causes bone resorption → ⇪ Ca+)
- Immobilization
normal range for
PTH
10-60
After working up Hypercalcemia, you determine cause is Malignancy
List the 3 Causes of [Hypercalcemia of Malignancy] , which Cancers cause them and their MOD
Which Rx cause Hypercalcemia (5)
NormalCa+ = 8.4-10.2
“LCD-TV with too much Calcium!”
Lithium
Ca+carbonate excess
DVitamin
Thiazides
VitaminA
nml TSH: [0.4-4.0]
which thyroid condition is a/w Thyroid Lymphoma?
hCAT
[hashimoto Chronic Autoimmune(antiTPO) Thyroiditis]
_________________
hCAT can progresses to Thyroid Lymphoma | [hCAT+ Pemberton = Thyroid Lymphoma]
chronic [antiTPO Lymphocyte] infiltrate thyroid targeting TPO
What is Pemberton’s sign?
_________________
What does it indicate? -2
facial plethora or neck vein distension when arms are raised
_________________
- obstructive ENLARGED THYROID
- [Thyroid lymphoma (if ⊕ in the setting hCAT)]
Medullary thyroid cancer
cp -2
- [thyroid nodule iTSo MEN]
- [Calcitonin ⇪ (from thyroid gland C cell neoplasia)]
* MEN = Multiple Endocrine Neoplasia // iTSo = in The Setting of*
Describe MEN1 (3)
PituitaryMacroAdenoma
Parathyroid hyperplasia
[Pancreatic-GI GLIV tumors ⼀Gastrinoma/gLucagonoma/Insulinoma/VIPoma]
Describe MEN2A (3)
- Parathyroid Hyperplasia
- Medullary Thyroid CA
- Pheochromocytoma
Pt with new diagnosis MEN2B
Prior to thyroidectomy, patient must be 1st evaluated for coexisting tumors such as ⬜ and Pheochromocytoma.
Name the dx labs for Pheochromocytoma (4)
_________________
Why is this important?
Parathyroid hyperplasia
_________________
1st: {[Plasma free metanephrines] –(confirm by)– >
2nd:
- [24h urinary fractionated metanephrines]
- catecholamines
- abd imaging]}
_________________
Undiagnosed Pheochromocytoma can cause fatal HDUS peri-thyroidectomy
MEN2A and MEN2B share the same initial workup
List the diagnostic workup for {new dx[MEN2A ] or new dx[MEN2B]} - (5)
- Calcitonin
- CEA
- [Neck US (r/o regional metastasis)]
- [Chromo10RET protooncogene] germline testing
- [Coexisting tumor r/o ([Parathyroid hyperplasia], [Medullary Thyroid Hyperplasia], Pheochromocytoma,)]
Describe MEN2B (4)
Pt p/w the 3 P’s of MEN1 ( _______ )
What’s the next step in Management of MEN1?
PituitaryMacroadenoma/Parathyroid hyperplasia/[Pancreatic-GI GLIV tumors]
_________________
[PARATHYROIDECTOMY with autotransplantation to muscle pocket]
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?
[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)
How are the thyroid and Calcium related?
[T3/T4thyroid hormone] causes bone resorption ➜ ⇪ serum Ca+/Hypercalcemia
Candida Endophthalmitis
clinical features (4) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Treatment? (3)
- [fundoscopic fluffy yellow-white chorioretinal lesions]
- [floaters + eye pain and ⬇︎acuity]
- [hospitalized patients on Parenteral nutrition = RF1]
- [s/p GI surgery or GI perforation = RF2]
_________________
Tx = [Vorizonazole + Intravitreal antifungal + vitrectomy]
_________________
RF = Risk Factor
What causes [Pancreatogenic DM]?
_________________
Which antiDM should be used to treat this? Which 3 should not? why?
Chronic pancreatitis (RF cystic fibrosis) ➜ islet cell damage ➜ ⬇︎insulin secretion then insulin deficiency ➜ glucose intolerance ➜ DM
_________________
✔︎ = INSULIN-replace Insulin pt stopped producing
❌❌= [GI peptide antiDM (DPP4 inhibitors / GLP1🟢)] - since these target GI peptides ➜ slows gastric emptying and ⇪ risk for pancreatitis
or
❌= [insulin secretagogues (Glipizide)]- impaired ability to secrete endogenous insulin from DEC islet beta cell reserve
Glipizide
MOA
insulin secretagogues
GLP1 R agonist
MOA
Name 3 examples
_________________
Glucagon-Like Peptide-1 R agonist
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
DPP4 inhibitors
MOA
Give 2 examples
Targets GI peptides ➜ slows gastric emptying
________________
linaGLIPtin
sitaGLIPtin
saxaGLIPtin
Why are [Pioglitazone thiazolidinedione] contraindicated in CHF?
[Pioglitazone thiazolidinedione] ⇪ insulin sensitivity by stimulating [PPAR-γ] on liver/muscle/fat]
BUT
it also stimulates [PPAR-γ] on renal CD ➜ ⇪ Na+ reabsorption ➜ fluid retention ➜ precipitates CHF
What is Amaurosis fugax?
sudden reversible transient monocular blindness 2/2 carotid artery atherosclerotic disease
Amaurosis fugax
tx?
carotid endarterectomy
Amaurosis fugax
dx?
carotid doppler US
What is subclinical thyrotoxicosis?
_________________
how is it managed?
mildly low TSH but [normal free T4, normal T3 and normal physiology (normal HR, bone density)]
_________________
RECHECK Thyroid function test in 8WKS (most TSH normalize on its own)
a Patient with chronic hypOparathyroidism presents with low serum Ca+ but HIGH urinary Ca+ from their Ca+ supplement
How do you mitigate this?
HCTZ
_________________
HCTZ [⇪ serum Ca+] while [⬇︎ urinary Ca+]
How is the thyroid system associated with Surgery?
[hypOthyroidism] ➜ [poor periOperative outcomes]
⼀BUT 911 surgeries are Ok if hypOthyroidism not severe (i.e. no myxedema coma)
Why must Levothyroxine at first be titrated very slowly in CAD pts ?
[levothyroxine T4] ⇪ myocardial O2 demand which can ➜ Myocardial ischemia ➜ in CAD pts can cause MI or arrhythmia = slow gradual [levothyroxine T4] titration
NPH is a ⬜ insulin that is sometimes used as ⬜. Why should it NOT be used in patients who’ve had hypOglycemic episodes?
intermediate-acting ; [basal insulin when injected BID]
_________________
NPH has a pronounced peak which can ➜ hypOglycemia = bad for patients who already have hypOglycemic episodes
When is it indicated to switch a T1DM pt from [manual SQ Basal/bolus insulin injection] to [automated SQ continuous infusion insulin pump]?
Pump Indicated if T1DM pt (on current manual injection) has…
- hypOglycemic episodes
- [suboptimal glycemic control HbA1C>7]
- highly variable BG readings
Patient presenting with new diagnosis T1DM. Tx requires exogenous insulin.
Describe the [manual SQ Basal/bolus insulin injection] regimen the patient will start with
T1DM require a
[(long basal) and (rapid bolusx3)] every day
Work up for Thyroid Nodule?
[Cancer RF = (> 1cm), fam hx, radiation hx, cervical LAD, compressive sx, thyroid hormone ∆]
[Suspicious US = hypOechoic, microcalcifications, internal vascularity]
After RF and US eval – Any Thyroid Nodule > ⬜ cm needs work up with FNA
List all the [High Risk Thyroid features] that warrant FNA for Thyroid Nodule (9)
> > 1 cm_________________
[Cancer RF = (> 1cm), fam hx, radiation hx, cervical LAD, compressive sx, thyroid hormone ∆]
[Suspicious US = hypOechoic, microcalcifications, internal vascularity]
Why are hypoglycemic episodes in long standing DM1 pts even more serious than newly diagnosed DM1 pts?
_________________
how is this mitigated?
✔︎ long standing DM1 pts overtime develop blunting of their autonomic feedback to [hypOglycemia (tremor, sweating, AMS)] = ⬇︎[hypOglycemia awareness system (HAS)]
✔︎ so this means… if long-standing DM1 present with hypOglycemia ⼀ it’s likely to be a SEVERE HYPOGLYCEMIA EPISODE (since , in a {blunted HAS} pt, only SEVERE HYPOGLYCEMIA can activate a {blunted HAS} to induce sx necessary to make pt aware/get help]
_________________
[Strict avoidance of any hypOglycemia x 2-3 weeks] restores patient’s HAS
nml TSH: [0.4-4.0]
Name the 2 [DeTC (Differentiated epithelial Thyroid CA)] subtypes
- [papillary thyroid cancer]
- [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]
nml TSH: [0.4-4.0]
Why is it important to [prevent elevated TSH] in pts with DeTC?
Considering this, how do you determine the ideal TSH level DeTC patients should be kept? (3)
_________________
(DeTC=Differentiated epithelial Thyroid Cancer)
in [DeTC s/p thyroidectomy] pts, elevated TSH actually stimulates growth of residual thyroid cancer cells = goal TSH depends on Risk of Recurrence
[LR =TSH (0.1-0.5)6-12mothen → (low nml TSH range)]
[IR=TSH (0.1-0.5)]
[HR=TSH (<0.1)]x years
TSH*=DeTC TSH goal
nml TSH: [0.4-4.0]
management for [DeTC (papillary vs follicular)] varies and is dependent on ⬜ and importantly ⬜
_________________
(DeTC=Differentiated epithelial Thyroid Cancer)
[initial stage of CA] ; [Risk of Recurrence]
_________________
DeTC target TSH : [LR =TSH(0.1-0.5)6mo→ (Ln)] | [IR=TSH(0.1-0.5)] | [HR=TSH(<0.1)x yrs]
Name the 3 benefits to [STRICT blood glucose control] in DM pts
DECREASES…
- [microvascular complications ⼀nephropathy, retinopathy]
- [peripheral neuropathy onset]
- [peripheral neuropathy progression]
Gastroparesis = ⬜ and is ultimately diagnosed with what test?
delayed gastric emptying (2/2 DM, drugs, postviral) ; [nuclear gastric emptying study]
Clinical manifestations of gastroparesis? (5)
- [succussion splash]
- [early satiety]
- [Abd fullness postprandial]
- [dysautonomia (dizziness, diaphoresis)]
- [labile glucose control]
BE SURE TO R/O MECHANICAL OBSTRUCTION
Name 2 promotility drugs used to treat gastroparesis
- metoclopramide
- erythromycin
When is [screening for diabetic retinopathy and nephropathy] indicated ? (2)
[5y after T1DM dx]
and
[AT TIME OF DX for T2DM]
- give Statin if [age ≥40 with DM]*
What is the preferred antiHTN for DM pts?
ACEk2 inhibitor
_________________
this improves diabetic nephropathy AND INC GFR
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 _____]
positive; diffuse
- propranolol
- Thyroid Tx ([AntithyroidMed] vs [Radioactive iodine ablation] vs [Thyroidectomy])
tx = [Propranolol] –> [PTU —(1 hr later)]–> [Potassium Iodine and PrednisoneCTS]
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)
- Cardiacpropranolol
- 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]
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)
positive; diffuse
_________________
- alternative to AntiThyroids(if unable to tolerate)
- alternative to [ThyroidectomySurgery ](if surgery not preferred)
- [SEVERE hyperthyroidism +/- ophthalmopathy]
- [Moderate hyperthyroidism +/- ophthalmopathy]
- [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
Patients with Graves disease have [⬜positive | negative] Thyroid Stimulating Immunoglobulins and ⬜ uptake on radioiodine scintigraphy
_________________
When is [ThyroidectomySurgery] indicated for Graves disease ? (5)
positive; diffuse
_________________
a.{Pregnant (and can’t 1st tolerate [ThionamidesAntithyroid])}
[b. GOITER(LARGE | Retrosternal_obstructive)]
c. [Thyroid CA (suspicion|confirmed)]
d. [1º Hyperparathyroidism superimposed]
e. SEVERE OPHTHALMOPATHY
What do you use to track thyroid function in pt who just started AntiThyroid Rx(drugs vs Radioactive Iodine vs SURGERY)? (3)
- [TSHnml0.4 - 4 (TSH q 4mo if Chronic Amiodarone Rx)]
- [FREE T4 nml0.9 - 1.7]
- [total T3]
[Free T4 = 0.9 - 1.7]
Identify and Explain the finding
What diagnosis does this indicate?
Seidel Sign ⼀concentrated fluorescein uptake (indicating corneal epithelial defect) with subsequent clearing in a waterfall pattern (indicating fluorescein is being washed out by inappropriately draining aqueous humor)
_________________
Full Thickness Corneal laceration
Pt presents with positive Seidel sign
a. Diagnosis?
_________________
b. Management of this diagnosis?
a. Full thickness Corneal LACERATION
_________________
b. ⼀URGENT OPTHO CONSULT!!
If laceration extends through the full thickness of cornea ➜ can create [perforated open globe injury] = STAT SURGICAL REPAIR
_________________
Seidel sign= concentrated fluorescein uptake with subsequent clearing (from draining aqueous humor) in waterfall pattern
How do you manage Corneal Abrasion? -3
- Both insulinoma and [surreptitious med use(Exogenous insulin vs Oral hypOglycemic agents)] can present with hypOglycemia sx*
- _________________*
When is it clinically indicated to workup a patient with hypOglycemia?
ONLY IF [⊕ WHIPPLE’S TRIAD*] = clinical hypOglycemia = workup indicated
- low BG
- [SADHAThypOglycemia sx]
- [SADHATsx] resolve with glucose admin
_________________
*Whipple’s Triad is required because many people have low BG without hypOglycemia sx = not clinically significant hypoglycemia
- Both insulinoma and [surreptitious med use(Exogenous insulin vs Oral hypOglycemic agents)] can present with hypOglycemia sx*
- _________________*
clinical hypOglycemia is characterized by the presence of ⬜
How do you workup clinical hypOglycemia? -4
[⊕ WHIPPLE’S TRIAD] = clinical hypOglycemia = workup indicated
- low BG
- [SADHAThypOglycemia sx]
- [SADHAThypOgluc sx] resolve with glucose admin
- Both insulinoma and [surreptitious med use(Exogenous insulin vs Oral hypOglycemic agents)] can present with hypOglycemia sx*
- _________________*
Why is [HIGH or normal serum Insulin] in a patient p/w hypOglycemia sx concerning and require additional workup? (2)
1) Normally, hypOglycemia ➜ negative feedback ➜ suppression of release of [Insulin/CPeptide/ProInsulin] = [low serum Insulin ✅]
2) If Pt has sx hypOglycemia but [High or normal serum Insulin] there must be an abnormal additional source of Insulin (exogenous vs endogenous) = additional workup
What is the [mixed meal challenge] used for?
evaluates Pts who only have hypOglycemia sx after eating
What lab is ordered alongside C-Peptide to evaluate endogenous insulin production?
Proinsulin
The most common cause of DEC vision in elderly patients are ⬜ with ⬜ .
Why is the evaluation so critical for these conditions? (2)
▶([cortical cataracts] ; [AMD])
▶Elderly Cataracts patients must be thoroughly evaluated for severity of [ccaAMD] since they:
1.may require both [Cataract lens extraction Surgery] AND [ccaAMD] tx (PO eye vitamin)]
or
- may not benefit from [Cataract lens extraction Surgery] at all (since opacified lens prevent [ccaAMD] progression)
[ccaAMD]: (Cortical Cataract) associated -Age related Macular Degeneration
The most common cause of DEC vision in elderly patients are ⬜ with ⬜ .
Describe each condition
([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
Similar to CROA amaurosis fugax ⬜ also usually presents with sudden uL nonpainful vision loss
Retinal Detachment
Pt with sudden eye pain, has Visualization of leukocytes in the anterior segment of her eye
Dx?
_________________
What other 5 sx would you expect?
[IritisAnterior Uveitis]
_________________
- photophobia
- pain
- redness
- vision loss
- [irregular constricted pupil]
* 6. [Leukocytes in ANT segment]*
Infectious Keratitis sx (3)
- corneal opacity
- severe photophobia
- difficulty keeping affected eye open
s/p coronary angiography, patient soon after develops palpitations, fatigue, heat intolerance, sweating
Diagnosis? Explain
_________________
Which diagnostics support this dx? (3)
Iodine-induced hyperthyroidism;
[pts with Nodular thyroid dz or Chronic iodine deficiency] have INC risk for thyrotoxicosis following [iodine exposure (radiocontrast for Coronary angio or imaging /amiodarone) .
_________________
[DEC TSH], [⊝thyrotropin R Ab], [US: ⇪ vascularity +/- nodules]
s/p newly starting amiodarone, patient soon after develops palpitations, fatigue, heat intolerance, sweating
Diagnosis? Explain
_________________
Tx for this? (2)
Iodine-induced hyperthyroidism;
[pts with Nodular thyroid dz or Chronic iodine deficiency] have INC risk for thyrotoxicosis following [iodine exposure (radiocontrast for Coronary angio or imaging /amiodarone) .
_________________
- [BBlocker Propranolol]
- [Methimazole (add if Severe hyperthyroidism vs elderly heart disease)]
[Lugol ⬜ solution] is a solution containing ⬜ that does what mechanistically?
Indications? (2)
(LARGE LOAD iodiNe)
_________________
👄 (Wolff-Chaikoff phenomenon) = any [LARGE LOAD iodiNe] →actually paradoxically inhibits TPO (temporarily) → [⬇︎iodiNe organification and coupling] → [⬇︎thyroid hormone synthesis]
👄[Lugol (LARGE LOAD iodiNe) solution] = clinically activates (Wolff-Chaikoff phenomenon) → [⬇︎thyroid hormone synthesis] for:
_________________
1. [prethyroidectomy in Graves disease]
2. [acutethyroid storm tx]
Prednisone is used to treat which 3 thyroid diseases?
- [PDSGT-(Painful Dequervain Subacute Granulomatous Thyroiditis)] *
- [amiodarone destructive Type 2 thyroiditis] *
- thyroid storm ⼀DEC conversion of T4 ➜ [active T3]
_________________
*used in thyroid when destruction of gland ➜ preformed thyroid hormone being released.
[normal Retina] = (⬜-4) on fundoscopy
describe how a [Papilledema Retina] looks on fundoscopy (4)
🔎[Papilledema Retina] = [Retina io\Papilledema]
[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⊕]
normal range for
TSH
0.4 ⼀ 4.0
normal range for
[free thyroxine T4]
_________________
[Total Thyroxine T4]
free thyroxine T4[0.9 ⼀ 1.7]
_________________
5-12
“Thyroiditis” suggest ⬜2. And there’s 3 types: PDSGT, hCAT, [NSLP-hCAT]
[NSLPhCAT] : [Nonpainful(silent) Subacute Lymphocytic Postpartum]hCAT
Clinical Features (4)
_________________
Diagnostics (2)
[Lymphocyte infiltration ➜ [Transient HYPERthyroidism]
_________________
- variant of hCAT(dx = [⊕TPO antibody], [low RAIU])
- HYPERthyroid transiently → hypOthyroid (or sometimes Euthyroid) → spontaneous recovery
- GoiterNonpainful, small
- includes postpartum thyroiditis (midaged Women postpartum)
🔎TPO = ThyroPerOxidase
[NSLPhCAT] dx =same as hCAT dx:
a. ⊕TPO antibody
b. low RAI uptake
“Thyroiditis” suggest ⬜2. And there’s 3 types: PDSGT, hCAT, [NSLP-hCAT]
hCAT: [hashimoto Chronic Autoimmune Thyroiditis]
Diagnostics (2)
[Lymphocyte infiltration ➜ [Transient HYPERthyroidism]
_________________
* * *
- ⊕[Thyroid PerOxidase Ab]
- [lowRAI uptake]
“Thyroiditis” suggest ⬜2. And there’s 3 types: PDSGT, hCAT, [NSLP-hCAT]
hCAT: [hashimoto Chronic Autoimmune Thyroiditis]
Clinical Features (5)
{[Lymphocyte infiltration ➜ [Transient HYPERthyroidism]}
_________________
- [initial Transient HYPERthyroid[damage from AntiTPOLymphocytes(= Lymphocytes that secrete AntiTPO Abs) → infiltrate thyroid follicles → [preformed T4/T3/TG] thyroid reservoir release]
- damage ultimately → hypOthyroid(since damage impairs thyroid function)
- GoiterDIFFUSE
- daughter condition = [NSLPhCAT]
- → CA(hCAT can → Thyroid DLBL)
“Thyroiditis” suggest ⬜2. And there’s 3 types: PDSGT, hCAT, [NSLP-hCAT]
PDSGT: [PAINFUL DeQuervain Subacute Granulomatous Thyroiditis]
Clinical Features (5)
[Lymphocyte infiltration ➜ [Transient HYPERthyroidism]
_________________
- Postviral inflammatory process
- self-limited
- PAINFUL DIFFUSE ENLARGED GOITER
- FEVER [from postviral inflammatory process(*etx: viral antigens provoke [CD8 cytotoxic T-lymphocytes] against Thyroid follicles → follicular injury → **</sup>)
- 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**}
“Thyroiditis” suggest ⬜2. And there’s 3 types: PDSGT, hCAT, [NSLP-hCAT]
PDSGT: [PAINFUL DeQuervain Subacute Granulomatous Thyroiditis]
Dx labs (3)
[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**}
“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??
[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**}
“Thyroiditis” suggest ⬜2. And there’s 3 types: PDSGT, hCAT, [NSLP-hCAT]
PDSGT: [PAINFUL DeQuervain Subacute Granulomatous Thyroiditis]
Tx (3)
[Lymphocyte infiltration ➜ [Transient HYPERthyroidism]
_________________
1. [NSAIDs ➜ Prednisone(refractory)]
2. [Propranolol (or Atenolol)]
3. [self limited (viral infxn → [PDSGT HYPERthyroid]3w → hypOthyroid → Euthyroid)]
* * *
{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**}
On Thyroid Scintigraphy, when do you see Patchy uptake?
Clinical features of this condition (3)
toxic multinodular goiter
- {HYPERthyroidthyrotoxicosis (TT FeelsARCHED)}
- nodular enlargement
- OLDER patients
On Thyroid Scintigraphy, when do you see Diffuse uptake?
why do you see diffuse uptake in this condition?
[Graves1º HYPERthyroidthyrotoxicosis]
_________________
[thyrotropin R autoantibodies] stimulate thyroid diffusely to [INC iodine uptake] and [INC thyroid hormone synthesis]
clinical features of Ocular melanoma (4)
★ [1º malignant melanocytes from uvea(choroidal pigmented nevus)]
★ [identified incidentally frequently] ⼀[gold standard dx = US]
★ {⊝sx or [small (diameter<10mm) (thickness<3mm) pigmented lesion] = [observation (repeat exam in 3 mo, then q6 mo)]}
★ {⊕SX or [LARGE (d ≥10mm)(t ≥3mm)] = XBRT –(if VERY LARGE or extrascleral extension)–> Enucleation
Enucleation: removal of entire globe and intraocular contents
In hospital setting, American Diabetes Association suggest maintaining inpatient glucose at ⬜
140-180
▶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
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
When should you consider insulin infusion pump for IDDM pts (5)
- critical illness
- DKA
- HHONKS
- perioperation
- [(SQ insulin) failure]
nml TSH: [0.4-4.0]
TSH-secreting pituitary adenomas cause ⬜ with elevated ⬜ and ⬜ levels. How can this pituitary adenoma be differentiated from other (FLAT PiG) pituitary adenomas? (3)
central Hyperthyroidism; [TSH] & [T4/T3]
- Although [mass effect (HA, visual ∆ )] = common pituitary adenoma sx…*
- 85% [TSH pituitary adenoma] tumors secrete [biologically inactive alpha subunit] =
- elevated [(Bi)alpha subunit]? = likely from ⊕[TSH pituitary adenoma]
tx = somatostatin analog vs transsphenoidal surgery
Dx?
[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>
Sulfonylurea MOA
________________
List examples-5
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
________________
- 2GGlimepir_ide
- 2GGlybur_ide
- 2GGliPiz_ide
4.1GChlorpropamide
5.1GTolbutamide
G = Generation
[MeglitiNides (“RepagliNide, “NategliNide”)] = same MOA as Sulfonylurea
Meglitinide
MOA
________________
List examples-2
insulin secretagogue= (same as Sulfonylurea MOA) stimulates endogenous insulin secretion
__________________
- Nateglin_ide_
- Repaglin_ide_
[Alpha glucosidase inhibitor] MOA
________________
List examples-2
inhibits α-glucosidease ➜ inhibits intestinal carb digestion → ⬇︎postprandial HYPERglycemia
________________
- Acarbose
- Miglitol
[DPP-4 inhibitors] MOD
________________
List examples-2
inhibits [DPP-4 GLP1 peptidase] –> ⬆︎GLP1–> ⬆︎Glucose-induced insulin release
_________________
- SitaGliptin
- SaxaGliptin
What are the GLP1 homologs?-2 ;
What do they do?
- ExenaTIDE
- 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]
Classic Presentation for DM -5
FUDge
Clomiphene Citrate
MOA
_________________
Indication
[hypothalamic estrogen🟥]SERM;
PCOS Infertility
Leuprolide
MOA
_________________
Indication
[GnRH🟢] ; endometriosis
How does respiratory rate affect Calcium levels?
Tachypnea causes ⬇︎CO2 acid –> H+ ions dissociate from albumin so they can help maintain pH –> ⬆︎free albumin which bind to free ionized Ca+ –> overall ⬇︎ in ionized unbound calcium
[Normal serumCa+: 8.4-10.2]
Pt presents with hypOcalcemia
How do you work this up? -5