Endocrinology Flashcards

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1
Q

Hypoglycemia
Glucose is the sole energy source for the brain
Symptoms of hypoglycemia depend on the glucose level and the rate of glucose drop
Hypoglycemia can mimic stroke, TIA, epilepsy, MS, psychosis, Stokes-Adams
Counterregulatory hormones (glucagon and epinephrine) cause the release of glycogen from the liver
Sympathomimetic symptoms: sweating, tremor, pallor (vasoconstriction), anxiety, nausea
Sympathomimetic symptoms can be masked by beta blockers
Neuroglycopenia symptoms: dizziness, psychosis, confusion, coma
Differential diagnosis
Insulinoma
Medications / drugs / alcohol
Extrapancreatic neoplasm
Hepatic disease (depletion of glycogen stores)
Deficiency of counterregulatory hormones
Critically ill, stressed infants, hypothermia
Dumping syndrome
Artifactual
Continued glycolysis by WBCs in lab tube
Leukemia, polycythemia
Distinguishing excess endogenous insulin from excess exogenous insulin
Pancreas cleaves proinsulin to insulin plus immunoreactive C-peptide
Excess endogenous insulin has measurable C-peptide (not so with excess exogenous insulin)

Standard treatment options
D50
D25 (peds)
D10 (neonates) 
Glucagon 1 mg IM/IV (converts liver glycogen to glucose)
D10 drip if recurrent or overdose
Hydrocortisone (adrenal insufficiency)
Octreotide – inhibits insulin secretion and helps prevent rebound hypoglycemia in the setting of glucose infusion treatment of refractory sulfonylurea-induced hypoglycemia
A
Oral Agents In DiabTwo classes: hypoglycemics & antihyperglycemics
Hypoglycemic agents:
	Sulfonylurea agents
Chlorpropamide, tolbutamide, acetohexamide tolazamide, glipizide, glyburide, glimepiride
Stimulate pancreatic insulin secretion
Cause profound hypoglycemia in overdose
Long duration of action
Chlorpropamide also can cause SIADH
	Repaglinide (Prandin)
Can also cause hypoglycemia
Antihyperglycemic agents
Less likely to cause hypoglycemia in overdose
	Metformin
May cause lactic acidosis (uncommon)
	Alpha-glucosidase inhibitors
Inhibit intestinal hydrolysis of polysacharides
Oral sucrose will not be absorbed
	Thiazolodenediones (Avandia/Actos)
Can worsen CHF; Acute MI (Avandia)
	SGLT2 inhibitors
Increases renal secretion of glucose
Hypotension (osmotic diuresis)

Always admit if sulfonylurea overdose
Most symptomatic in 4 hours (can be delayed)
Octreotide inhibits insulin secretion
Give thiamine with glucose in hypoglycemic malnourished patients
Glucagon may not be effective in chronic alcoholics, those with liver disease or infants with low, liver glycogen stores

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2
Q

Diabetic Ketoacidosis Pathophysiology

Relative lack of insulin + stressors causes hyperglycemia

Hyperglycemia-induced osmotic diuresis causes polyuria, dehydration, hypovolemia, electrolyte loss (K, Mg, Phos)

Switch over to fat breakdown for energy source causes ketonemia (acidosis)

Metabolic acidosis causes compensatory hyperventilation (Kussmaul respirations)

A

Precipitants of DKA

The “I’s” have it!
Infection (UTI, pneumonia, pancreatitis)
Infarction (e.g. AMI)
Insulin noncompliance
IUP (pregnancy)
Ischemia (CVA)
Illegal (substance abuse)
Iatrogenic (drug interactions)
Idiopathic (new onset DM)
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3
Q

Fluids / Bicarbonate in DKA

Initial fluid resuscitation for hypovolemia
Replace electrolytes (phosphate, potassium)
Insulin drip (after checking potassium)
Sodium bicarbonate is rarely indicated
The hazards of bicarbonate use include
Paradoxical CSF acidosis
Decreased oxygen-hemoglobin dissociation (shifts curve to left)
Overload of sodium
Hypokalemia, hypophosphatemia
Cerebral edema in children

A

Sodium / Phosphate in DKA

Pseudohyponatremia
(*Hyperosmolar as opposed to hypoosmolar state)
Sodium is artifactually 1.6 mEq/L for every 100 mg/dL  glucose over 100

Hypophosphatemia is possible:
Respiratory depression, muscle weakness
CHF, decreased mental status
(failure to generate adequate ATP)

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4
Q

Potassium in DKA

Serum K+ level may be elevated, normal or low
Initial hypokalemia indicates massive total body depletion (usual deficit is 3-7 mEq/L)
Replacement recommendations
K < 3.3: Hold insulin, give 40 mEq per hour until ≥ 3.3
K ≥ 3.3 but < 5.0: give 20-30 mEq in each liter IVF to keep K 4-5 mEq/L
K ≥ 5.0: No replacement but check Q2 hr
Serum potassium will decline with insulin and correction of acidosis (drives K+ into cells)
Cardiac arrest in DKA is often 2° to precipitous hypokalemia (insulin therapy, acidosis correction or fluid therapy with increased urinary losses)

A

Complications of DKA Treatment

Hypoglycemia due to excess insulin
Add glucose administration when glucose = 250 mg/dl
Hypokalemia is associated with insulin administration, bicarbonate, hydration
Bicarbonate therapy causes CSF acidosis
Cerebral edema 
 Patients at risk: Young, new onset DM
 Etiology controversial
 Avoid bicarbonate in children
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5
Q

Alcoholic Ketoacidosis

Binge drinking with heavy alcohol consumption and decreased food intake for several days (starvation ketosis)
Imbalance of insulin levels and counter- regulatory hormones
Ethanol metabolism inhibits gluconeogenesis
Abdominal pain, nausea, vomiting, dehydration, disorientation

Alcohol levels are usually low or negative and glucose is often mildly elevated with low bicarbonate and high anion gap
Urinary ketones may be weakly positive
Treatment: Glucose + saline (D5NS), thiamine and potassium repletion

The major and earliest ketone produced from fat
breakdown is beta-hydroxybutyrate, but the
lab-measured ketone is acetoacetate.
Therefore, lab tests for
ketones may be falsely negative.

A

Hyperosmolar Hyperglycemic Non-ketotic State HHNS (1)

Similar to DKA but has important distinctions
No ketoacidosis
Glucose is usually higher, often >1000
Serum osmolality is often greater than 350
Most often occurs with NIDDM
Higher mortality than DKA
DKA has shorter onset

Precipitating factors   include
Infection, especially pneumonia
Myocardial infarction
CVA
GI bleed
Pyelonephritis
Pancreatitis
Uremia
Subdural hematoma
Peripheral vascular occlusion

Common comorbid conditions
Renal insufficiency
Vascular disease
Poor access to water

HHNS is often the initial presentation of NIDDM

Common associated medications
Diuretics
Propranolol
Calcium channel blockers
Corticosteroids
Phenytoin
Cimetidine
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6
Q

Hyperosmolar Hyperglycemic Non-ketotic State HHNS

Physical findings
Dehydration
Altered sensorium
Focal neurologic findings (often mistaken for a stroke)
Coma is rare

Treatment
Normal saline
Average fluid deficit 8-12 liters
½ of deficit in first 12 hours, rest over next 24 hours
Initial 1-2 liter bolus as clinically indicated
Insulin infusion

Cerebral edema possibly 2° to rapid fluid replacement or the severity of the condition

A

Thyroid Hormones

TRH from hypothalamus stimulates TSH release from anterior pituitary
TSH stimulates thyroid gland
Thyroid hormones (T3, [20%]T4 [80%]) are synthesized and released
Thyroid hormone production depends on iodine intake. Excess iodine blocks hormone release
T3 is biologically 4x more active than T4
T3 and T4 provide feedback inhibition of TSH release
T3 and T4 act on cells
Increase rate of cell metabolism
Increase rate of protein synthesis

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7
Q

Hyperthyroidism

Causes
Graves’ disease (most common):
An autoimmune disorder (thyroid-stimulating immunoglobulins mimic the action of TSH)
Toxic thyroid adenoma, toxic multi-nodular goiter
Thyroiditis
Pituitary adenoma
Excess iodine in diet

A

Hyperthyroidism

Signs and symptoms
Nervousness, tremor, insomnia
Heat intolerance, sweating
Weakness, weight loss,                                    hair loss
Tachycardia, palpitations
Hyperdefecation
Irregular menses
Goiter / thyroid bruit
Exopthalmos (Grave’s only), lid lag (the lids move more slowly than the eyes)
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8
Q

Hyperthyroidism (3) Pre-tibial Myxedema

Rare manifestation of Graves’ disease
Bilateral, elevated, firm dermal nodules and plaques
Skin yellow or waxy
Accumulation of mucopolysaccharides

A

Hyperthyroidism

Risk factors: female, family history, other autoimmune disease
Lab: Increased T3 and T4, decreased TSH
Treatment
Beta blockers
PTU or methimazole
Radioactive iodine
Surgery
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9
Q

Thyroid Storm

A life-threatening complication of hyperthyroidism.  May not be directly related to magnitude of excess thyroid hormone
Precipitating events include
Withdrawal of antithyroid medications
Administration of IV contrast
Thyroid hormone overdose 
Pneumonia
CVA
Pulmonary embolus
Toxemia of pregnancy
Diabetes
A

Thyroid Storm

Thyroid storm is a clinical diagnosis
The hallmark is CNS dysfunction

Other diagnostic criteria include
Temperature > 38˚C
Tachycardia out of proportion to the fever
Exaggerated peripheral manifestations of thyrotoxicosis, including tremor and weakness
No laboratory tests distinguish thyroid storm from simple hyperthyroidism – it is a clinical diagnosis

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10
Q
Thyrotoxicosis / thyroid storm is associated with
Elevated free T4 level
Decreased TSH level
Hyperglycemia
Hypercalcemia
Elevated LFTs
Low cholesterol
A

Thyroid Storm Treatment

Five step ORDERED approach

  1. General supportive care: IV fluids, correct electrolyte imbalance, corticosteroids (decrease peripheral conversion of T4 to T3), no ASA (displaces thyroid hormone from thyroglobulin)
  2. Block peripheral thyroid hormone effects: Propranolol 1 mg to 10 mg titrated to symptoms
  3. Block thyroid hormone synthesis: PTU (also inhibits peripheral conversion of T4 to T3) or Methimazole
  4. Block thyroid hormone release: iodine given one hour after PTU
  5. Identification and treatment of precipitating events
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11
Q

Rare disorder seen in elderly patients
Lethargy, slowed mentation, apathetic facies
Goiter is usually present
Droopy eyelids are common
No exophthalmos, stare or lid lag
Symptoms of apathetic hyperthyroidism may be masked because of underlying organ dysfunction
Resting unexplained tachycardia
Resistant atrial fibrillation and CHF are common

A

Apathetic Thyrotoxicosis

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12
Q

Hypothyroidism

Causes
Treatment of Graves’ disease
Iodine deficiency in diet
Autoimmune destruction of thyroid gland (e.g. Hashimoto’s)
Lithium therapy for bipolar disorder
Amiodarone
Pituitary and hypothalamic disorders (rare)

A

Hypothyroidism

Signs and symptoms
Weakness, lethargy
Cold intolerance
Hypothermia
Weight gain
Constipation
Dry, thick skin
Generalized nonpitting edema (myxedema)
Prolonged, heavy periods
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13
Q

Hypothyroidism

Clinical signs of severe hypothyroidism include
Dermatologic: coarse, waxy skin, loss of lateral third of eyebrows, scant pubic hair, puffy face and extremities (myxedema)
CNS: slowed mentation, altered mental status, psychosis (“myxedema madness”), coma
Cardiac: CHF, bradycardia, hypotension, cardiomegaly, pericardial effusion, low voltage

A

Hypothyroidism

Lab
Low T4, elevated TSH (unless problem with hypothalamus or pituitary)
Elevated lipids 
Hyponatremia (dilutional)
Anemia
Myxedema coma
Hypoxemia
Hypothermia
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14
Q

Myxedema Coma
The end of the spectrum of hypothyroidism
Life-threatening, rare, elderly females, winter
Precipitating factors include
Stressors: MI, infections, trauma, cold exposure
Drugs are metabolized slower and therefore have increased effects (narcotics, tranquilizers, beta blockers, amiodarone)
Non-compliance with thyroid replacement

A

Myxedema Coma

Signs
Hypothermia
Altered mental status
“Hung up” reflexes (prolonged relaxation phase of DTRs)
Non-pitting periorbital edema (puffy eyelids)
Generalized non-pitting edema

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15
Q

Myxedema Coma

Treatment
Supportive care: Rewarming, fluid support, search for underlying cause
Specific treatment
IV thyroid hormone (T4, T3 or both)
Avoid excessive IV T3 (increased mortality)
Corticosteroids (because of possible
unrecognized adrenal or pituitary insufficiency)

A

b

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16
Q

Adrenal Gland

Clinical manifestations primarily due to
Cortisol (affects metabolism of most tissues, glucose regulation, increases blood glucose)
Aldosterone (renal Na+ reabsorption & K+ excretion)

A

b

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17
Q

Adrenal Insufficiency (1) Primary Adrenal Failure

Idiopathic (autoimmune):
Addison’s Disease
Infiltrative, infectious
Sarcoid, amyloid
TB, fungal, septicemia
Hemorrhage, infarction
Neoplastic
Drugs (etomidate)
Bilateral adrenal failure is associated with meningococcemia (Waterhouse-Friderichsen)
Presents with abdominal pain, vomiting, fever, hypotension
Diagnosis by serum cortisol level or corticotropin stimulation test

Hyperpigmentation is seen in
Addison’s disease

A

Adrenal Insufficiency

Secondary adrenal failure
Due to hypopituitarism
Tertiary adrenal failure
Usually iatrogenic from prolonged steroid use (most common cause overall)
Causes adrenal atrophy
Usually due to oral steroids (rarely inhaled or topical)
Laboratory abnormalities include
Hyponatremia (most common abnormality) +/- hyperkalemia, eosinophilia (all most common in chronic insufficiency), hypoglycemia
Acute presentation
Refractory hypotension
Non-specific symptoms: Fever/N/V/weakness/AMS
Consider in malignancy

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18
Q

Adrenal Crisis (Insufficiency)

Treatment 
Fluids – NS or D5NS
Glucocorticoids – hydrocortisone 100 mg or dexamethasone 4 mg IV
Pressors
Mortality from adrenal crisis due to
Shock
Dysrhythmias (hyperkalemia)
Underlying disease
A

Diabetes Insipidus

Symptoms similar to DM – excess urination and increased thirst and fluid intake
Lack of ADH activity
Central: Failure to secrete ADH (head trauma, neoplasm, pituitary surgery)
Nephrogenic: Kidney not responding to ADH (lithium toxicity, hypokalemia, hypercalcemia, nephrotoxic drugs)
Presents with polydipsia, polyuria
Lab: Dilute urine in the face of concentrated serum (hypernatremic and hyperosmolar)
Central DI will concentrate urine with ADH; nephrogenic DI will not respond
Treatment
Central = Desmopressin (synthetic vasopressin = DDAVP)
Nephrogenic = Hydrochlorothiazide

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19
Q

Hyperadrenalism (Cushing’s Syndrome)

Excess cortisol
Prolonged steroid use (most common)
Adrenal neoplasm, pituitary microadenoma
ACTH-secreting carcinoma (small cell,
   pancreatic, bronchial carcinoid)

Signs and Symptoms
Truncal obesity, hypertension, hirsutism, edema, glucosuria, Na+
Moon facies, buffalo hump, purple striae
Treatment: Stop steroids, treat cause

A

Pheochromocytoma

Rare cause of treatable hypertension
Often diagnosed at autopsy
Can be malignant
Tumor of adrenal medulla cells (secretes norepinephrine)
Diagnosis: catecholamines and metabolites (VMA) in 24 hour urine
5 Ps (paroxysmal spells) in a 20-45 y/o patient
Pressure (sudden increased hypertension)
Pain (headache, chest pain, abdominal pain)
Perspiration
Palpitations
Pallor

20
Q

Syndrome of Inappropriate Secretion of Antidiuretic Hormone

Normally, ADH is secreted in states of dehydration
ADH increases renal H20 reabsorption
ADH is inhibited in over-hydration (dilutes urine)
SIADH: Inappropriate ADH secretion (inhibits urine production resulting in fluid retention and dilutional hyponatremia)
Inappropriately concentrated urine in the setting of low serum osmolality (low sodium) and normovolemia = SIADH
Causes include CNS (tumor, infection, CVA, injury), Lung (infection including TB, fungal), Drugs (chlorpropamide, vasopressin, diuretics, vincristine, thioridazine, cyclophosphamide)

A

Carcinoid Syndrome

Carcinoid tumor: GI tumors in small intestine, appendix, stomach, colon (can be in lung too)
Common with liver metastases
Tumor secretes serotonin, prostaglandins and other bioactive substances
Attacks of skin flushing, watery stools, hypotension, vasodilation, edema, ascites and bronchoconstriction
Attacks can last from minutes to days
Treat with somatostatin analogs (octreotide)

21
Q

Usually due to too much water relative to sodium
Symptoms depend on level and rate of drop
Early: Nausea, headache
Late: Lethargy, seizures
Symptoms often start around 120 mEq/L

A

Hyponatremia

22
Q

Hyperglycemia
Free water osmotically drawn out of cells and into serum, leading to lower serum Na+ (Remember Na+ drops 1.6 mEq/L for every 100 mg/dL increase in glucose over 100)

Hyperlipidemia, hyperproteinemia
Displaces sodium from the lab specimen

A

Pseudohyponatremia

23
Q

Hyponatremia Treatment

Depends upon etiology, chronicity and severity
Hyponatremia that develops slowly should be corrected slowly
Hypovolemic hyponatremia
Replace fluid deficits with NS
100-150 mL/hr
Euvolemic hyponatremia
Correct underlying cause
Water restriction (+/- furosemide if Na+ < 120)
Hypervolemic hyponatremia
Goal is to increase Na+ and H2O loss
Salt and water restriction
Diuretics to increase Na+ loss
Caveat: May worsen hyponatremia because water leaves in excess of Na+
Faster correction: IV NS & loop diuretics (furosemide)

A

Hyponatremia Treatment

Life-threatening symptoms
Severe hyponatremia (Na+ < 120 PLUS CNS abnormalities)
Goal is to raise level to >120 mEq/L
Rise in Na+ should be no greater than 0.5-1.0 mEq/L per hour (1-2 mEq/L per hour if seizures)
Hypertonic saline (3%) 25-100 mL/hr
Furosemide (Lasix) 20-40 mg IV
Too-rapid correction
CHF
Central pontine myelinolysis (CPM)
24
Q

Results from too rapid correction of hyponatremia

Occurs 24-48 hours after rapid correction
Symptoms include confusion progressing to cranial nerve deficits to quadriparesis to locked-in syndrome; dysphagia, dysarthria, paresis
Concomitant use of furosemide (Lasix) has been shown to decrease incidence of CPM

A

Central Pontine Myelinolysis

25
Q

Too little water relative to Na+
Most commonly due to free water loss or decreased intake
Common in infants and debilitated elderly (limited access to water or impaired thirst)
Also seen with elevated aldosterone levels or diabetes insipidus
Irritability, doughy skin turgor, coma

A

Hypernatremia

26
Q

Most common electrolyte abnormality in patients with weakness
EKG changes: Decreased T waves, increased U waves, ventricular dysrhythmias
Causes
Decreased intake (e.g. NPO)
Increased output
Renal losses
Diuretics, osmotic diuresis
Increased aldosterone
Magnesium deficiency
Renal tubular acidosis
GI losses: Vomiting, diarrhea, NG suction
Shift of K+ into cells
Alkalosis (protons move out of cells to restore pH; K+ moves in to maintain electrical neutrality)
Insulin-mediated transport
Catecholamine-mediated transport
Potassium is primarily an intracellular ion (30:1)
Mild hypokalemia may represent severe total body deficits (especially in the setting of acidosis)
Serum levels determine adverse effects

A

Hypokalemia

27
Q

Treat after urine output established
Oral replacement safest
Correct acid-base abnormality
IV replacement: No more than 40 mEq/L and no faster than 40 mEq/hour
Hypokalemia often is associated with hypomagnesemia
In severe hypomagnesemia, potassium supplements will continue to be excreted in the urine
Resistant hypokalemia: Replace Mg++ & K+

A

Hypokalemia Treatment

28
Q
Lab error: Hemolysis (most common), thrombocytosis, leukocytosis, ischemic blood
Increased intake (rare)
Decreased output (renal failure 
    or low aldosterone)
Aldosterone causes sodium and
   water retention resulting in elevated 
   BP and loss of K in the urine
Aldosterone is blocked by
	spironolactone (a K-sparing diuretic)
Redistribution (lack of insulin, 
    acidosis, digoxin toxicity, tissue 
    damage, succinylcholine)
A

Hyperkalemia Causes

29
Q

Usually asymptomatic
May have muscle weakness
Cardiac
EKG changes: Peaked T waves, increased
PR, flattened P waves, increased QRS width
Dysrhythmias: Conduction blocks (BBB), bradycardia, sine wave pattern, asystole

A

Hyperkalemia Signs and Symptoms

30
Q

Calcium gluconate 10% (10-20 mL) antagonizes the effects of high K+,, especially cardiac
Quick onset, shortest acting
D50 + insulin, bicarbonate, beta agonists
Shift K+ extracellular to intracellular
Diuretics (if patient makes urine)
Exchange resins polystyrene (Kayexalate) to remove K+ (consider risks)
Dialysis if renal failure or treatment fails

A

Hyperkalemia Treatment

Don’t use calcium in hyperkalemia with
digitalis toxicity  cardiac arrest

31
Q
Causes
Parathyroid: hyperparathyroidism (most common)
Addison's disease
Multiple myeloma
Paget’s  disease (during immobilization)
Sarcoidosis
Cancer
Hyperthyroidism
Milk-alkali syndrome
Immobilization
D vitamin
Thiazide diuretic
A

Hypercalcemia

32
Q

Stones, bones, moans (psych) and groans (abdominal)
Neuro: AMS, hyporeflexia, weakness
Increased nerve and muscle resting membrane potentials
EKG: Shortened QT, BBB, heart block
Renal: Polyuria, polydipsia, nephrogenic DI, calculi
GI: Abdominal pain, nausea, constipation
PUD, pancreatitis
Skeletal: Bone pain / fractures
Metastatic calcifications

A

Hypercalcemia

33
Q

IV normal saline
Correct hypovolemia; maintain urine output 100-150 mL/hr
Loop diuretics if CHF or renal failure (not routine)
Calcitonin
Decrease bone resorption and increase Ca++ secretion
Response in 4-6 hours; useful for up to 48 hours
Bisphosphonates (zoledronic acid, pamidronate)
Inhibit osteoclast function and decrease bone resorption
Maximum effect takes 2-4 days
Less often used options
Steroids (if sarcoidosis or lymphoma)
Dialysis (treatment of last resort)

A

Hypercalcemia Treatment

34
Q

Hypoparathyroidism (surgical)
Renal failure
Vitamin D deficiency
Pancreatitis
Hypomagnesemia (Mg++ necessary for PTH activity)
Drugs: Phenytoin, cimetidine, phosphates (extensive list)
DiGeorge Syndrome

A

Hypocalcemia Causes

35
Q

Decreases nerve and muscle resting membrane potential
Signs & Symptoms
Paresthesias, hyperreflexia, seizures
Chvostek’s sign: Twitch of corner of mouth on tapping facial nerve in front of ear
Trousseau’s sign: Carpal spasm when BP cuff is inflated above systolic BP
EKG: Prolonged QT / inverted T waves
Treatment
Goal is to raise Ca++ to low normal levels
Calcium gluconate
Magnesium

A

Hypocalcemia Signs & Treatment

36
Q

Causes: Renal failure, iatrogenic
Symptoms: Weakness, hyporeflexia, respiratory depression, heart blocks
Treatment: IV calcium (the same as with high potassium), dialysis

A

Hypermagnesemia

37
Q

Causes: Malnutrition, alcoholism, diuretics
Symptoms: Similar to hypocalcemia and hypokalemia; serum levels can be normal in spite of significant deficit
Treatment: IV magnesium

A

Hypomagnesemia

38
Q
Causes: ↓PTH, renal failure, increased vitamin D, many problems associated with ↑Ca++ (from secondary ↓PTH)
K+, Mg++ and phosphate (major intracellular components) travel together, ↓ of one = ↓ of the others
Symptoms are usually from associated 
    hypocalcemia and hypomagnesemia
Treatment
Oral phosphate binding gels
Consider dialysis if renal faliure
Treat hypocalcemia if necessary
A

Hyperphosphatemia

39
Q
Phosphate is involved in the function of all hematologic cell lines (i.e., RBC, WBC, platelets)
Causes 
↑ PTH, malignancies with ↑ CA+2
Hyperventilation (respiratory alkalosis) 
Hyperalimentation (common) 
Decreased oral intake (alcoholics) 
DKA (12-24hrs s/p tx) 
Symptoms and signs
Muscle weakness, respiratory depression, altered mental status, CHF, hemolytic anemia, rhabdomyolysis
Treatment
Oral phosphate for minor cases
IV phosphate if symptomatic
A

Hypophosphatemia

40
Q
Occurs if there are additional positive or fewer negative charges 
Hypoalbuminemia (less unmeasured anions)
Multiple myeloma (excess positively charged IgG paraproteins), hypercalcemia, hypermagnesemia, lithium toxicity
Bromide intoxication (mistaken for chloride)
A

Anion Gap

41
Q
Increased anion gap metabolic acidosis: 
                 		"MUDPILES"
Methanol
Uremia
DKA, AKA, starvation ketosis
Paraldehyde or phenformin
Iron or INH
Lactic acidosis
Ethylene glycol
Salicylates
A

Anion Gap

42
Q

The most common cause of metabolic acidosis
Lactate is produced by anaerobic glycolysis
Causes: Hypoperfusion or hypoxia
Medical conditions: Seizures, renal insufficiency, hepatic failure, infection, neoplasm (especially, leukemia, lymphoma and myeloma)
Drugs and toxins: Ethanol, toxic alcohols (also produce organic acidosis), metformin (rare, associated with renal failure), antiretrovirals

A

Lactic Acidosis

43
Q
Normal anion gap metabolic acidosis 
Loss of bicarbonate and Na+ 
Therefore the equation is balanced on both sides with no increase in the anion gap
Non-gap metabolic acidosis: "HARD UP"
Hypoaldosteronism
Acetazolamide
Renal tubular acidosis
Diarrhea
Ureterosigmoidostomy
Pancreatic fistula
A

Non-gap Acidosis

44
Q

H+ loss or HCO-3 excess
Differential diagnosis
Loss of gastric acid (vomiting, NG suction)
Excess diuresis
Mineralocorticoids
Increased citrate or lactate due to transfusions of Ringer’s lactate
Antacids (e.g. milk-alkali syndrome, results from high calcium intake + absorbable alkali-like antacids = hypercalcemia and metabolic alkalosis)
Dehydration

A

Metabolic Alkalosis

45
Q
Increase of renal Na+ resorption with K+ and H+ secretion causes bicarbonate generation
Chloride-sensitive
Chloride loss: Vomiting, diuretics
Volume depletion
Chloride-insensitive
Euvolemia or hypervolemia
Excess mineralocorticoids
Examples: renal artery stenosis, renin-secreting tumor
A

Metabolic Alkalosis

46
Q

Determined by the concentration of low molecular weight solutes
Primarily determinants: Sodium, chloride, glucose and BUN; normal 280-295
A difference between the measured and calculated osmolality of >10 is an osmolal gap
An osmolal gap indicates the presence of other, unmeasured, low molecular weight solutes (ethanol, ethylene glycol, methanol, isopropyl alcohol, mannitol or glycerol)

A

Osmolality

47
Q

Formula to calculate serum osmolality

A

2Na +Glu/18 + BUN/2.8 + EtOH/4.6