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Metabolic/Endocrine Flashcards

1
Q

Which oral diabetes med drug class can cause prolonged or rebound hypoglycemia?

A

Sulfonylureas, such as glipizide, are a class of drugs used for glycemic control that work by blocking potassium channels in the pancreas, leading to depolarization and insulin release. Sulfonylureas have a longer half-life than many diabetes medications and thus can cause prolonged hypoglycemia that may persist for > 24 hours when ingested in overdose.

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2
Q

What are the symptoms of Vitamin C deficiency (Scurvey)?

A

↑ bleeding, anemia, loose teeth

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3
Q

What is the goal rate for increasing serum sodium in acute hyponatrimia?

A

Small increase in sodium often sufficient to resolve symptoms (ex. 2 mEq/L/hour for the first 2–3 hours or 4–6 mEq/L over 6 hours); monitor sodium closely

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4
Q

What is the goal rate for increasing serum sodium in chronic hyponatrimia?

A

Chronic: correct by 8–12 mEq/L in 24 hours

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5
Q

What does increasing serum sodium to fast in hyponatremia cause?

A

Osmotic demyelination syndrome formerly central pontine myelinolysis (dysarthria, dysphagia, paralysis, death) if corrected too fast

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6
Q

What lab abnormalities are seen in
Primary Adrenal Insufficiency (Addison Disease)?

A

Labs: hyponatremia and hyperkalemia

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7
Q

What is the firstline treatment for Primary Adrenal Insufficiency (Addison Disease)?

A

Tx: hydrocortisone or other glucocorticoid
Most patients also require mineralocorticoid (fludrocortisone)

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8
Q

First line treatment in Pheochromocytoma?

A

Alpha-blocker (phentolamine, phenoxybenzamine) prior to beta-blockade to prevent unopposed alpha-agonism.

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9
Q

What lab abnormalities are seen in Pheochromocytoma?

A

↑ 24h urinary catecholamines and metanephrines, or ↑ plasma metanephrine levels

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10
Q

What genetic disorder is associated with Pheochromocytoma?

A

MEN2 (medullary thyroid cancer, pheochromocytoma, +/- primary hyperparathyroidism)

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11
Q

What is the most common cause of hypercalcemia?

A

Malignancy (most common inpatient cause)
Primary hyperparathyroidism (most common outpatient cause, and overall)

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12
Q

What lab findings are seen in Hypoparathyroidism?

A

Labs will show low PTH, low calcium, high phosphorus.

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13
Q

What is Chvostek sign?

A

Contraction of facial muscles after tapping facial nerve

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14
Q

What is Trousseau sign?

A

Induction of carpopedal spasm by a sphygmomanometer

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15
Q

What are two medications that can cause hypercalcemia?

A

Lithium and thiazide diuretics.

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16
Q

Which of the following subtypes of thyroid carcinoma is associated with multiple endocrine neoplasia?

A

Medullary: associated with MEN2, calcitonin can be used as a tumor marker

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17
Q

Hashimoto thyroiditis is associated with what type of thyroid cancer?

A

Thyroid diffuse large-cell lymphoma.

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18
Q

Treatment of thyroid storm in order?

A

Tx:
Beta-blocker (propranolol)
Thioamide (propylthiouracil or methimazole)
Iodine solution
Glucocorticoids

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19
Q

Which metabolic derangements would you expect in tumor lysis syndrome?

A

Hyperuricemia
Hyperkalemia
Hyperphosphatemia
Hypocalcemia

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20
Q

What is Anion Gap?

A

Anion gap (AG) is the difference between the sodium, chloride, and bicarbonate concentrations (Na - [Cl + HCO3]). A normal AG is 3–11 mEq/L, whereas an increased anion gap is > 11–20 mEq/L. This represents a metabolic acidosis.

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21
Q

What is the most common cause of hyperthyroidism?

A

Graves Disease

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22
Q

What are common causes of hypophos?

A
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23
Q

What is the strong ion difference?

A

Strong ion difference = ([Na+ + K+ ] − [Cl− ]). When significantly less than 40, an acidosis is present.

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24
Q

What is the delta gap?

A

The delta gap (ΔG) = (AG − 12) − (24 − [HCO3 − ]). Its calculation determines if the anion gap is accounted for by the change in serum bicarbonate concentration. An elevated anion gap and ΔG more than 6 indicates that a metabolic alkalosis in addition to a metabolic acidosis is likely to be present.

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25
Q

What is the anion gap?

A

Anion gap = Na+ − (Cl− + HCO3 − ). Causes of an elevated anion gap include ketoacidosis, lactic acidosis, toxins metabolized to acids, and renal failure.

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26
Q

Symptoms of Korsakoff syndrome?

A

Confabulation
Anterograde Amnesia
Retrograde Amnesia

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27
Q

Symptoms of Wernicke encephalopathy?

A

Classically characterized by encephalopathy, gait ataxia, and ophthalmoplegia. Ocular findings commonly include nystagmus, lateral rectus palsy (mostly bilateral).

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28
Q

Symptoms of niacin or vitamin B3 deficiency (Pellagra).

A

Dermatitis
Diarrhea
Dementia

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29
Q

Multiple Endocrine Neoplasia (MEN)

A

Autosomal dominant
MEN1: parathyroid tumors (resulting in primary hyperparathyroidism), pancreatic tumors, and pituitary adenoma
MEN2A: medullary thyroid carcinoma, pheochromocytoma, and parathyroid hyperplasia
MEN2B: medullary thyroid carcinoma, marfanoid habitus, mucosal neuromas and pheochromocytoma

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30
Q

Vitamin A Deficiency

A

A: night vision loss, xerophthalmia, dry skin (xerosis), growth retardation, Bitot spots on the conjunctivae

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31
Q

Vitamin B1 Deficiency

A

B1 (thiamine): beriberi, Wernicke-Korsakoff syndrome, cardiac failure; alcoholism, malnutrition

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32
Q

Vitamin B2 Deficiency

A

B2 (riboflavin): cheilosis, corneal vascularization (the two Cs of B2)

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33
Q

Vitamin B3 Deficiency

A

B3 (niacin): dermatitis, dementia, diarrhea; corn-based diet (pellagra)

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34
Q

Vitamin B6 Deficiency

A

B6 (pyridoxine): sideroblastic anemia, convulsions, peripheral neuropathy; INH use

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35
Q

Vitamin B12 Deficiency

A

B12 (cobalamin): megaloblastic anemia + neurological symptoms, hypersegmented neutrophils

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36
Q

Vitamin C Deficiency

A

C (ascorbic acid): scurvy (↑ bleeding, anemia, loose teeth)

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37
Q

Vitamin D Deficiency

A

D: rickets (children), osteomalacia, tetany

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38
Q

Vitamin E Deficency

A

E: anemia, peripheral neuropathy, ataxia

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39
Q

Vitamin K Deficency

A

K: ↑ bleeding, ↑ PT/INR, ↑ PTT if severe

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40
Q

Folate Deficency

A

Folate: megaloblastic anemia, sensory neuropathy

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41
Q

Causes of acute respiratory acidosis?

A

Airway obstruction
Pulmonary disease (pneumonia, asthma, pulmonary edema, aspiration pneumonitis)
CNS depression (recreational drugs, intracranial catastrophe, neuromuscular disorders, thoracic trauma)

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42
Q

Causes of chronic respiratory acidosis?

A

Lung disease (COPD, IPF)
Neuromuscular disorders (ALS, muscular dystrophy, obesity hypoventilation)

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43
Q

What are the clinical features of postpartum panhypopituatrism.

A
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44
Q

What disorders cause a normal anion gap metabolic acidosis?

A
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45
Q

Most common cause of DKA and HHS is…

A

Most common cause of DKA and HHS is infection (30-50% of cases). Of those, UTI or PNA is the most common.

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46
Q

5 I’s of DKA

A

5 I’s- Insulin (low/absent), Insemination, Infection, Infarction, Initiation (first time presentation)

47
Q

Review expected bicarb and
pCO2 levels for Metabolic
Acidosis, Metabolic Alkalosis,
Respiratory Acidosis, Respiratory
Alkalosis

A

M.Acid: ↓ HCO3, ↓ pCO2 (hypervent);
M.Alk: ↑ HCO3, ↑ pCO2(hypovent);
R.Acid: ↑ pCO2, ↑ HCO3 (↑ renal reabsorption);
R.Alk: ↓ pCO2, ↓ HCO3 (↓ renal reabsorption).
Normal values: pH 7.4 / HCO3 24/ pCO2 40 / AG 12 ±

48
Q

What is the appropriate
metabolic compenstion for
Respiratory Acidosis and
Alkalosis?

A

(Delayed metabolic compensation) Acid/Alk: ‘1325’: Acute/Chronic;
R.Acid: for every ↑ of pCO2 by 10, HCO3 should ↑ by 1 (Acute) and 3
(Chronic); R.Alk: for every ↓ in pCO2 by 10, HCO3 should ↓ by 2
(Acute) and 5 (Chronic); If NOT true then a mixed disorder is present

49
Q

What is the appropriate
respiratory compensation for
Metabolic Acidosis and Alkalosis

A

(Immediate respiratory compensation) Acid: Rule of 15s; Alk: 007;
M.Acid- 1.5 x HCO3 + 15 (±2) = PCO2 & last two digits of pH (±2);
M.Alk: for every ↑ of HCO3 by 1, pCO2 should ↑ by 0.7; If NOT true then a mixed disorder is present

50
Q

What is the differential for an
anion-gap metabolic acidosis?

A

A CAT MUDPILE: Aspirin, Carbon monoxide, Cyanide, Caffeine,
Acetaminophen, Theophylline, Methanol, Metformin, Uremia, DKA
(AKA), Propylene Glycol, Isoniazid, Ibuprofen, Iron, Lactic Acidosis,
Ethylene glycol

51
Q

What are the most common
causes of non-anion-gap
metabolic acidosis?

A

Diarrhea & spironolactone

52
Q

What are the most common
causes of metabolic alkalosis?

A

Vomiting, diuretics

53
Q

What is the primary difference
between Type I and Type II
diabetes?

A

I: insulin deficiency (auto-immune),
II: insulin resistance

54
Q

What are the criteria for
diagnosis of diabetes?

A

Fasting blood sugar >126 (2 separate occasions),
Random glucose >200 with ssx of DM,
Glucose >200 after OGTT,
HbA1c > 6.5%

55
Q

Suspected DKA and coffeeground
emesis

A

Erosive esophagitis & hemorrhagic gastritis in up to 9% of DKA, rarely need treatment/endoscopy

56
Q

What are the keys to diagnosis
of DKA?

A

SSx: Polyuria, polydipsia, abd pain, vomiting, acetone (fruity) smell, ± unstable vitals/shock, AMS, possible coffee-ground emesis;
Labs: glucose > 250, pH < 7.3 (VBG ok), HCO3 <18, AG >10, +Serum/urine ketones;
Note: workup should include eval for cause of DKA (infection rule out) and EKG due to lyte abnormalities

57
Q

What lab value is critical to know
prior to giving insulin for DKA?

A

Serum potassium: patients have an overall deficiency of K (initial labs may show high K), if initial low K and pt given insulin they will become too hypokalemia and code

58
Q

What is the appropriate
approach to fluid resuscitation in
DKA?

A

Rx: 2L NS IVF bolus (kids: 10-20cc/kg), when glucose < 250, start
glucose-containing fluids (D51⁄2 NS)

59
Q

What is the appropriate
approach to electrolyte repletion
in DKA?

A

Key = POTASSIUM! Know level before insulin. K<3.3: HOLD Insulin & give K, K 3.3-5.2: can start insulin but give K in each liter of IVF; K>5.2:
Start Insulin & NS, no supplemental K needed; BICARB: controversial, only Rx if severe DKA + intubated; MAG: replete with K; SODIUM: falsely low, abnormal Na will typically correct with fluids.

60
Q

What is the appropriate
approach to insulin
administration in DKA?

A

Eval K level first, then give 0.1 U/kg/hr gtt (double if glucose not down by 50 after first hour); initial bolus not necessary; can also follow SQ regimen; **Transition to regular insulin SQ when gap closed and pH >7.3, dose 5U per 50 over 150 (max 20U), stop insulin gtt 1hr after pt given SQ insulin

61
Q

How do you correct sodium for
hyperglycemia (pseudo
hyponatremia)?

A

Add 1.6 to Na for each glucose value of 100 over 100 mg/dL

62
Q

Treatment for DKA followed by
new AMS or seizure

A

Cerebral edema, more common in kids and new onset type I, Rx:
mannitol (1-2g/kg)

63
Q

What is the mechanism of action
and possible adverse effect of
Sulfonylureas (Glipizide, glyburide)

A

Stimulates insulin release from the pancreas, can cause prolonged hypoglycemia in overdose

64
Q

What is the mechanism of action
and possible adverse effect of
Biguanides (Metformin)

A

Suppress hepatic gluconeogenesis (NO hypoglycemia), ± GI upset, lactic acidosis

65
Q

What is the mechanism of action
and possible adverse effect of
Thiazolidenediones (TZDs-
Actos, Avandia)

A

Increase sensitivity to insulin (muscle & fat); ± hepatitis & edema; NO hypoglycemia

66
Q

What distinguishes Hyperosmolar
Coma from DKA?

A

Occurs in Type II DM. SSx: more likely to have CNS ssx (stupor/coma).
Labs: glucose > 600, pH >7.3, HCO3 >18, ± urine ketones, AG <12, severe dehydration (8-12L deficit). Rx: IVF, insulin

67
Q

What lab test can help identify
facticious hypoglycemia
(exogenous administration)?

A

C-peptide, value will be low 2/2 suppression of endogenous insulin

68
Q

What is the rule to calculate
MIVF rate?

A

4cc/kg for first 10kg, 2cc/kg for second 10kg, 1cc for each additional kg to max of 120cc/hr total

69
Q

What are typical causes and
appropriate treatment for
Hypervolemic, Euvolemic and
Hypovolemic Hyponatremia?

A

HyperV: CHF, ESRD, cirrhosis; Rx: water restrict + diuretics;
EuV: SIADH, psychogenic polydipsia; Rx: water restrict;
HypoV: vomiting, diarrhea, third spacing, diuretics; Rx: NS vs 1/2 NS

70
Q

What is the approach to
correction of hyponatremia?

A

Overall goal correction rate 0.5 mEq/hr or 10-20 mEq/day. Note: rapid
correction risks central pontine myelinolysis/demyelination. Rx:
asymptomatic & Na >120 = no emergent treatment; Na <120 & +neuro ssx, give 3% NaCl (100cc over 10m, additional 100cc over 50m)

71
Q

How and when does central
pontine myelinolysis present?

A

How: AMS (lethergy and coma) w/ spastic quadriplegia after treatment for hyponatermia. When: 1-6 days after treatment for hyponatremia. Pts with chronic hyponatremia (e.g. alcoholics) are most at risk for this.

72
Q

What is the approach to
treatment of hypernatremia?

A

Overall goal correction rate 1-2 mEq/hr. Note: rapid correction risks cerebral edema.. Calculate Free Water Deficit (0.6 x wt(kg) x (Na/140 -1)) and replace with NS until euvolemic, then D5W vs D5 1/2 NS. Give 50% over 12h, remainder over the next 24hr

73
Q

What is the most common cause
of hyperkalemia?

A

Lab error, resend lab

74
Q

What EKG changes are seen in
hyperkalemia?

A

Peaked TW, PR long, loss of P wave, wide QRS, sine wave, VT/VF

75
Q

What is the general approach to
treatment of hyperkalemia?

A

Cardioprotection (Calcium Gluconate or Chloride ONLY if ekg changes, K shifters: Insulin/glucose, bicarb if acidotic, albuterol), K excretion: lasix, kayexylate, HD

76
Q

Dx and Tx of hypokalemia?

A

Most common electrolyte disturbance. 2/2 ↑ losses (GI loss or diuretics), intracellular shift.
SSx: cramps, weakness, arrhythmias, cardiac arrhythmias, rhabdo;
Rx: K repletion 100 mEq K for every 0.3 below normal, give 10-20 mEq/hr; **Note: supplement with Magnesium (↑absorption)

77
Q

What is the most specific EKG
change associated with
hypokalemia?

A

Flattened or inverted T wave, U waves = specific, prolonged QT, STD

U Wave

78
Q

Dx and Tx of Hypercalcemia

A

Ca > 10.5. Causes: hyperparathyroid (overall most common cause), malignancy (most common inpatient cause);
SSx: BONES (bone pain), STONES (renal, biliary), GROANS (abd pain, n/v), THRONES (polyuria) and PSYCHIATRIC OVERTONES (depression, anxiety, insomnia);
EKG: short QT;
Rx: immediate if Ca > 14 (12-14 per ssx) with IVF (first step),
Calcitonin (↑ excretion, inhibits osteoclasts), Bisphosphonates (inhibits osteoclasts, requires days to work), Steroids (↓ GI absorption), Lasix (if volume overload)

79
Q

Dx and Tx of Hypocalcemia

A

Ca < 8.5. Causes: 2/2 hypoparathyroid (thyroidectomy = most comon cause), Vit D deficiency, high phos, low or high Mg;
SSx: paresthesias, tetany, Chvostek’s sign, Trousseau’s sign, seizure. EKG: QT prolongation;
Rx: IV calcium (if <7.5 and severe ssx), give Vit D and Mg prn

80
Q

Dx and Tx of Hypermagnesemia

A

SSx: weakness, loss of reflexes, dysrhythmias, respiratory depression;
Rx: calcium gluconate

81
Q

Alcoholic with AMS, ataxia,
nystagmus

A

Wernicke’s Encephalopathy 2/2 Thiamine (B1) deficiency;
Rx: Thiamine 500 mg IV, improvement in hours

82
Q

Alcoholic with short term memory
loss

A

Korsakoff’s Psychosis 2/2 Thiamine deficiency, irreversible

83
Q

Poor nutrition and high output
cardiac failure (dyspnea,
peripheral edema)

A

“Wet” Beriberi 2/2 chronic thiamine deficiency; Rx: Thiamine 100mg IV

84
Q

Diarrhea, Dermatitis, Dementia

A

Pellagra 2/2 Niacin (B3) deficiency

85
Q

Crohn’s patient with macrocytic
anemia and paresthesias

A

Cobalamin (B12) deficiency; high risk include Crohns, vegans,
alcoholics, PPIs, pernicious anemia (antibody to intrinsic factor); causes megaloblastic anemia + neuro deficits, hypersegmented neutrophils

86
Q

Alcoholic with macrocytic anemia

A

Folic Acid deficiency. High risk: alcoholics, elderly, phenytoin; no neuro changes. Hypersegmented neutrophils seen as well.

87
Q

Child with poor diet and bowed
legs

A

Rickets 2/2 Vitamin D deficiency (Calcium absorption); Osteomalacia: adult equivalent, normal height

88
Q

Bad skin, bleeding gums and
poor wound healing

A

Scurvy caused by Vitamin C deficiency (collagen formation)

89
Q

What vitamins are toxic in
overdose?

A

Fat soluable ADEK;
A: bear liver consumption, skin changes,
pseudotomor cerebri,
D: hypercalcemia, hypercalciuria,
E: ↑ bleeding,
K: hemolytic anemia, jaundice in newborns

90
Q

What hormones are secreted
from the pituitary?

A

GOAT FLAP: Growth Hormone, Oxytocin, ADH, TSH, FSH, LH, ACTH, Prolactin;
ALL but Oxy/ADH are from anterior pituitary

91
Q

What are potential causes of
hypopituitarism?

A

Mass lesions, bleeds (pituitary apoplexy), hypothalamic disease,
Sheehan’s syndrome; Dx: check hormone levels

92
Q

Low cortisol but normal
aldosterone

A

ACTH deficiency, causes 2° adrenal insufficiency

93
Q

Inability to lactate post-partum

A

Sheehans syndrome causing prolactin deficiency (and panhypopit)

94
Q

Visual field deficits, headache,
hormonal abnormalities

A

Pituitary adenoma (macro if >1cm), Rx: transsphenoidal surgery

95
Q

What is the treatment for
prolactinoma?

A

Most common pituitary tumor. Rx: Bromocriptine (does not require
surgery)

96
Q

Dx and Tx of Cushing’s
syndrome

A

Cortisol excess. ACTH secreting pituitary adenoma or exogenous
steroids (most common cause):
SSx (‘CUSHING’): Central obesity, Urinary cortisol ↑, Striae, HTN/Hyperglycemia/Hirsutism, Iatrogenic, Neoplasms, Glucose intolerance.
Rx: surgery (tumor)

97
Q

Headache and tunnel vision in
oversized person

A

Growth Hormone secreting pituitary adenoma;
Labs: ↑ GH & ILGF1.
Children: gigantism, adults: acromegaly;
Rx: surgery

98
Q

What hormones are produced by
the adrenal glands?

A

Medulla: epinephrine & norepinephrine;
Cortex: cortisol, androgens, aldosterone

99
Q

Identify the key differences
between primary and secondary
adrenal insufficiency

A

Deficiency of adrenal gland hormone production. 1° (adrenal disease): ↑ CRH & ACTH, Addisons dz (autoimmune) = most common cause, rapid withdrawal of steroids = most common cause in US, SSx: shock, hypoglycemia ,↓ mineralocorticoid = ↓ Na/gluc, ↑ K, HYPERpigmentation (buccal, 2/2 ↑ ACTH); 2° (pituitary dz): ↑ CRH, ↓ ACTH: ↓ Na/gluc, normal K, NO hyperpigmentation; Rx: IVF, glucocorticoids, vasopressors

100
Q

Dx and Tx of adrenal crisis

A

Lif threatening exacerbation of adrenal insufficiency. Hallmark = shock that is refractory to IVF / vasopressors. Cause: acute stressor (infxn, trauma, MI); SSx: shock, ↓ Na/gluc, ↑ K; Rx: glucocorticoids (Hydrocortisone v Dexamethasone)

101
Q

Young child with mass in
abdomen and HTN

A

Neuroblastoma (adrenal medulla tumor)

102
Q

HTN, headache, palpitations,
elevated catecholamines

A

Pheochromocytoma (adrenal medulla tumor)

103
Q

Review the hormone cascade
and general function of thyroid
hormones

A

Thyroid Releasing Hormone (hypothalamus) → Thyroid Stimulating
Hormone (Ant Pituitary) → T4 (inactive from thyroid gland) → converted
to T3 (active form) in peripheral tissues, requires iodine for conversion;
T3 functions in glucose absorption, muscle building, increases
catecholamines, increases basal metabolic rate

104
Q

What are common causes of
hyperthyroidism

A

Graves (most common cause, young person), Toxic nodular goiter (elderly), iodine-induced (amiodarone), Thyroiditis (amiodarone)

105
Q

Review common SSx and Dx of
hyperthyroid

A

SSx: heat intolerance, palpitations, wt loss, tachycardia, anxiety,
hyperreflexia, goiter, exophthalmos, pretibial edema; Labs: ↓ TSH level, ↑ T4/T3

106
Q

Difference between
thyrotoxicosis and thyroid storm

A

Thyrotoxicosis: any condition that results in excessive thyroid hormone concentration. Thyroid storm: life threatening decompensation of thyrotoxicosis (hyperthyroid + acute event)

107
Q

What is the appropriate
treatment for Thyroid storm?

A

1) Beta-blockers (Propanolol): ↓ sympathetic activity + blocks peripheral conversion of T4 → T3. 2) Antihormone Rx: PTU (if Pregnant) or Methimazole (blocks new hormone synthesis). 3) Potassium Iodine (AFTER above, blocks release of preformed hormone). 4) Steroids (blocks peripheral conversion of T4 → T3. 5) Treat precipitant & prevent decompensation (IVF, tylenol, cool prn) // The order is controversial. Some sources say give PTU before beta-blockers, but just know that PTU comes BEFORE iodine. That’s what they typically test.

108
Q

What are common causes of
hypothyroid

A

Hashimoto’s (MCC in US, autoimmune), meds, postpartum, Iodine deficiency (MCC worldwide)

109
Q

Review common symptoms,
diagnosis and treatment of
hypothyroid

A

SSx: fatigue, weight gain, cold intolerance, brittle hair and nails,
constipation, periorbital edema, slow reflexes, edema; Labs: TSH (↑ with 1°, ↓ with 2°), ↓ free T3 / T4; Rx: synthroid.

110
Q

Hypothyroidism + AMS

A

Myxedema coma. Rx: steroids (for concurrent adrenal crisis), IV
Levothyroxine (T4)

111
Q

Dx and Tx of Thyroid Ca

A

5% thyroid nodules are cancerous, common CA overall but low mortality;
Dx: FNA; Rx: thyroidectomy, radioactive iodine-131, thyroid
supplementation

112
Q

Dx and Tx of
Hyperparathyroidism

A

↑ PTH → ↑ Ca, ↓ Phos; SSx of hypercalcemia (see above); Rx: lower Ca with IVF (first line), calcitonin, bisphosphonates, steroids, surgery

113
Q

Dx and Tx of Hypoparathyroidism

A

↓ PTH → ↓ Ca, ↑ Phos; may be 2/2 thyroid surgery; SSx of hypoCa; Rx: replacement of Ca, Vit D

114
Q

Pt w/ hx of anorexia, presents
with signs of heart failure after
starting an outpatient refeeding
program.

A

Refeeding syndrome. Happens when refeeding begins before
correcting electrolyte abnormalities. Leads to profound
hypophosphatemia, hypokalemia, hypomagnesium, and ultimately volume overload and CHF. Tx: stop refeeding, correct electrolyte abnormalities.

ITE (18 decks)

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