Endocrine & Metabolic Flashcards

1
Q

Rx of thyrotoxic storm/meds

A

“<span><b>Thionamides:</b><br></br>PTU 500-1000 mg load then 250 mg Q4 hours<br></br></span><span>Methimazole 60-80 mg qday, divided into doses q4-6 hrs (20 mg Q6)<br></br></span><span><br></br><b>Lugol’s Solution</b> 8 drops PO q 6 <b>OR</b></span><span>Sodium Iodide 0.5 mg IV Q 12 hours(</span><strong>Don’t give until 60 minutes after thionamides)<br></br></strong><h3>Treat Volume Loss<br></br></h3><h3>Treat Sympathetic Surge<br></br><span><span>Propanolol 1 mg IV</span><span>(test dose) then Propranolol 1-2 mg q 15 minutes until</span><span></span><span>HR of 100 bpm</span></span>then start<span></span><span>Propanolol drip</span><span></span><span>at whatever dose it took to get IV load control (Max 3-­5 mg/hr)<br></br></span><br></br>Block Peripheral Conversion and Shield from Adrenal Insufficiency<span><br></br></span></h3><h3><div><span>Dexamethasone 4 mg IV Q 6 hours</span></div><div><span>or</span></div><div><span>Hydrocortisone 300 mg IV and then 100 mg q 8 hours</span></div></h3>”

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2
Q

Spesific Rx of Myxodema coma

A

<ul><li>hydrocortisone 100mg Q 6hourly if adrenal or pituitary insufficiency suspected</li><li>replacement of thyroid hormones (T4 or T3 is controversial):<br></br>(1) T4 – loading dose = 500mcg IV -> 50-100mcg OD IV or orally<br></br>(2) T3 – loading dose = 10mcg IV -> 10mcg Q4 hrly for 24 hours then every 6 hours</li></ul>

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3
Q

Clinical features of Adrenal crisis

A

“<ul><li><a>Hypotension</a>(refractory to fluids/pressors)</li><li><a>Hyponatremia</a>/<a>Hyperkalemia</a>(hyperkalemia is not expected in secondary adrenal insufficiency)</li><li><a>Hypoglycemia</a></li><li>Low bicarbonate, non-anion gap<a>metabolic acidosis</a>(due to decreased acid secretion in kidneys from aldosterone deficiency)<a>[1]</a></li><li><a>Dehydration</a></li><li><a>Abdominal tenderness</a></li><li><a>Confusion/delirium/lethargy</a></li></ul>”

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4
Q

Causes of DKA

A

<b>6 Is:</b><br></br>Infection<br></br>Infarction<br></br>Intoxication<br></br>Incision (surgery/trauma)<br></br>Impregnation<br></br>Insuline failure (non compliance/pump failure)

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5
Q

Labs of DKA

A

Gluc > 12.5<br></br>Anion gap > 10<br></br>Ph < 7.3<br></br>HCO3 < 15<br></br>Ketonemia/ketonuria

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6
Q

What is the total daily insuline requirements?

A

0.2 to 0.4 u/kg/day

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7
Q

Who gets euglycemic DKA?

A

<ul> <li>Just received insulin</li> <li>Young T1DMs vomiting</li> <li>Patient’s with impaired gluconeogenesis (liver failure, EtOH use disorder, starvation)</li> <li><strong>SGLT-2 inhibitors</strong> - Invokana (canaglifozin), Farxiga (dapaglifozin), Jardiance (empaglifozin)</li> </ul>

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8
Q

Indications for admission in DM

A

Life threatening metabolic decompensation (DKA, HHS)<br></br>Severe chronic complications<br></br>Inadequate social situation<br></br>High BS (>22) ass with severe volume depletion<br></br>ALOC, abdn behavior, seizure<br></br>Hypoglycemia due to long acting OHA<br></br>Fever of unknown origin

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9
Q

Hypoglycemia in an infant

A

Cannot use D50==>vein sclerosis<br></br>Rules of 50s:<br></br>- 2ml/kg of D25W<br></br>- 5 ml/kg of D10W

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10
Q

Causes on NON ionic gap metabolic acidosis

A

<b>HARD UP</b><br></br><br></br>Hyperalimentation (TPN)<br></br>Acetazolamide<br></br>Renal tubular acidosis<br></br>Diarrhea<br></br>Uretrosigmoid fistula<br></br>Pancreatic fistula<br></br>

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11
Q

The classic mnemonic often used to remember the causes of anion gap metabolic acidosis

A

“<span>“MUDPILES CAT”</span><ul><li>M – Methanol</li><li>U – Uremia</li><li>D – Diabetic ketoacidosis</li><li>P – Propylene Glycol</li><li>I – Isoniazid</li><li>L – Lactic Acidosis</li><li>E – Ethylene Glycol</li><li>S – Salicylates</li><li>CO, Cyanide</li><li>Aminoglycosides</li><li>Toluene</li></ul>”

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12
Q

Causes of hypoT4

A

“<b>Primary (thyroid):</b><br></br>- Iodine def<br></br>- Hashimoto’s<br></br>- Idiopathic<br></br><b>Secondary (Pitutary):</b><br></br>- Tumors<br></br>- Hge<br></br>- Lack of TRH<br></br><b>Drugs:</b><br></br>- Amiodarone<br></br>- Lithium”

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13
Q

CF of myxedema coma

A

ALOC<br></br>HypoNa<br></br>Hypoglycemia<br></br>Hypotension<br></br>Hypothermia

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14
Q

CVS complications of hyperT4

A

Persistant tachycardia<br></br>SVTs<br></br>Ischemia (ST)<br></br>Afib<br></br>PVCs<br></br>CHF

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15
Q

Dose of propranolol in thyroid storm

A

1000 mcg iv

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16
Q

Cardinal symptoms of adrenal crisis

A

N/V<br></br>Anorexia<br></br>Abd pains<br></br>Weakness<br></br>Dehydration<br></br>ALOC<br></br><br></br>In children (Cong adr hypoplasia):<br></br>Lethargy<br></br>Vomiting<br></br>Poor feeding<br></br>FTT/poor wt gaining

17
Q

Unique signs for adrenal crisis

A

Hypotension<br></br>Tachycardia<br></br>Hyperpigmentation<br></br>Hair thinning<br></br>Dry mucus membrane

18
Q

Causes of Wernicke enceph

A

Malnutrition/Malabsorption:<br></br><br></br>ETOH<br></br>Bariatric surgery<br></br>Ca<br></br>HIV<br></br>Hyperemesis<br></br>Eating disorders<br></br>CHF on lasix

19
Q

Classical triad of Wernicke enceph

A

Ataxia<br></br>Ophthalmoplegia<br></br>Confusion<br></br><br></br>Others:<br></br>HypoBP<br></br>Hypothermia<br></br>Lactic acidosis

20
Q

Features favoring HHS over DKA

A

-Onset over days-weeks<br></br>-Urine/serum ketones low or absent<br></br>-Ph generally > 7.30<br></br>-Bicarb >18<br></br>-Anion gap normal<br></br>-Osmolality usually > 320<br></br>-Glucose frequently > 50mmol/L (higher than DKA)<br></br>-More dehydrated clinically

21
Q

Insulin dose in HHS

A

Insulin R 0.1 u/Kg/hr iv infusion

22
Q

“HHS,<span>What 2 parameters should you use to monitor treatment progress?</span>”

A

-Level of consciousness<br></br>-Glucose<br></br>-Potassium<br></br>-VBG<br></br>-Osmolarity<br></br>-Anion gap

23
Q

“HHS,<span>When can you stop your above treatment? Give one clinical and one laboratory end-point.</span>”

A

<b>Clinical:</b><br></br>-Alert/ no altered mental status<br></br>-Tolerating PO intake<br></br><br></br><b>Lab:</b><br></br>-Osmolality <315<br></br>-Anion gap <10-12<br></br>-Bicarb: >20

24
Q

“<span>Name 4 medications indicated for treatment of thyroitoxicosis, including a brief description of their mechanism/why we give them.</span>”

A

Name: Propylthiouracil / Methimazole<br></br>Purpose: Inhibit new thyroid production<br></br>Mechanism of Action: decrease new hormone synthesis (also inhibits conversion of T4->T3, to a degree)<br></br><br></br>Name: Lugol Iodine / Potassium Iodine<br></br>Purpose: Inhibit thyroid release<br></br>Mechanism of Action: blocks release of pre-stored thyroid hormone/ decreases iodine transport in gland<br></br><br></br>Name: Propranolol<br></br>Purpose: Symptom control<br></br>Mechanism of Action: peripheral B-adrenergic receptor blockade<br></br><br></br>Name: Hydrocortisone / Glucocorticoids<br></br>Purpose: Preventing peripheral conversion of T4 to T3<br></br>Mechanism of Action: preventing peripheral conversion of T4 to T3

25
Q

“<span>in thyrotoxicosis Rx. There is a particular timing/order these medications must be given in, please describe this and the reason why.</span>”

A

-First stop new synthesis with PTU, THEN at least one hour later: give iodine for decreased release (otherwise, the iodine will stimulate new synthesis)

26
Q

Features of Myxedema

A

“<b>Vital Signs:</b><br></br><i>Hypotension<br></br>Hypothermia<br></br>Bradycardia<br></br>Decreased RR</i><br></br><br></br><b>CNS:</b><br></br><i>ALOC<br></br>Prolonged relaxation of DTR</i><br></br><br></br><b>H&N:</b><br></br><i>Goitre/Scar of thyroidectomy<br></br>Facial/periorbital sewlling<br></br>Macroglossia<br></br>Queen Anne’s eyebrows<br></br>Brittle hair</i><br></br><br></br><b>Abdomen:</b><br></br><i>Central obesity</i><br></br><br></br><b>Extremities:</b><br></br><i>Dry skin<br></br>Brittle nails<br></br>Waxy non-pitting edema</i>”

27
Q

Adrenal crisis, important causes

A

<b>Infection</b><br></br>Other acute physiologic <b>stressors </b>(MI, DKA)<br></br><b>Withdrawal </b>from chronic steroids<br></br><b>Drugs</b><br></br><i>Including fluconazole, methadone</i><br></br><b>Pituitary dysfunction</b> (including hemorrhage, infiltration, etc)