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KChan Saves the World > KC Endo > Flashcards

KC Endo Flashcards

1
Q

*What are 4 risk factors for metformin-induced lactic acidosis?

A

Impaired renal function
Heart failure
Coexisting metabolic acidosis
IV contrast media
Concurrent liver disease
Active alcohol abuse
Prior hx of lactic acidosis during metformin therapy
Decreased tissue perfusion / hemodynamic instability

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2
Q

*What are 4 harms of giving sodium bicarbonate?

A

Paradoxical CNS acidosis
Hypokalemia
Volume overload
Hyperosmolality
Overshoot alkalosis

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3
Q

*What are 3 indications of giving sodium bicarbonate?

A

ASA OD
TCA OD
Acidemia primarily driven by bicarb loss or impaired acid secretion (renal failure)

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4
Q

*Why do we need to measure albumin when looking at an anion gap (3 marks)

A

Correction for albumin is important because significant depression of the serum albumin level will reduce the anion gap, potentially masking the presence of an important unmeasured anion

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5
Q

*What are two causes of a low anion gap?

A

Increased unmeasured cation (lithium toxicity)
Decreased unmeasured anion (low albumin)
Spurious ion measurements

or

Lithium toxicity
Hypergammaglobulinemia seen in multiple myeloma.
Bromide toxicity may cause spurious hyperchloremia, and hypertriglyceridemia may cause spurious hyponatremia, which can also cause a low or negative anion gap.
unmeasured anions such as albumin, sulfate, phosphate, and citrate (so hypoalbuminemia)

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6
Q

*pH 7.27, CO2 78, HCO3 35.
i. What is the primary acid base disturbance?
ii. Is it acute or chronic?
iii. List 4 disorders that can cause this disturbance.

A

i. Resp acidosis
ii. Chronic
- Airway obstruction
- Pulmonary disease (pneumonia, asthma, pulmonary edema, aspiration pneumonitis)
- Central nervous system depression (recreational drugs, ICH)
- Neuromuscular disorders (myasthenia gravis, Guillain-Barre syndrome)
- Thoracic trauma (pneumothorax, flair chest)

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7
Q

*pH 7.15, CO2 20, HCO3 5
i. What is the primary disturbance?
ii. List 5 TOXIC causes

A

i. Met acidosis
- Methanol
- Ethylene glycol
- Toluene
- Paraldehyde
- Aspirin
- Carbon monoxide
- Methemoglobinemia
- Cyanide
- Metformin
- Reverse transcriptase inhibitors - Paracetamol
- Iron
- Isoniazid

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8
Q

*58M CAD chronic back pain, DM on asa, metoprolol, oxycontin, metformin found with decreased LOC. pH 7.29 pCO2 73 pO2 65
a. What is the primary cause of his altered mental status?
b. What are 3 causes of his acid base abnormality
c. What is the most important intervention
d. What is one contraindication to NIPPV
e. What would you expect his bicarbonate to be?
f. What would you expect it to be if this was chronic?

A

a. CO2 retention
b. hypoventilation from oxy, or from ICH, or pna impairing gas exchange
c. needs to be ventilated (NIPPV)
d.
- need for emergency intubation
- decreased level of consciousness
- lack of respiratory drive
- increased secretions
- hemodynamic instability
- conditions that would prevent an adequate mask seal (eg facial trauma)
e.
73-40=33
330.1 = 3.3
24+3.3 = 27
f.
73-40 = 33
33 0.35 = 12
24+12 = 36

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9
Q

List 5 causes of respiratory acidosis

A

Won’t breathe - recreational drugs, intracranial catastrophe (ICH, stroke, SAH)
Can’t breathe - neuromuscular disorder (myastheniaTravis, Guillain-Barre), ALS, airway obstruction
Can’t breathe enough - narrowing of the airways/trapping from COPD/asthma, obesity, pulmonary disease (pneumonia, edema), pneumothorax

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10
Q

Describe the two physiologic buffer systems in acid base disturbances

A

Renal buffers generally determine HCO3-
- H+/K+ exchange in the kidneys
- The kidney regulates HCO3- excretion, reabsorption, and formation (takes 4-5 days)
- Retention of H+ (i.e. in alkalemia) cannot occur unless potassium stores are sufficient to allow urinary K+ extraction
Respiratory processes generally determine PaCO2
- Adjusted through minute ventilation

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11
Q

List 5 causes of respiratory alkalosis

A

Hyperventilation
- Anxietyor psychogenic
- Central - CNS tumors or bleeds, increased ICP
- Tox - salicylates, thyroxine, caffeine
- Pulmonary/hypoxia - high altitude, anemia, V/Q mismatch, PE, pneumonia, edema, asthma
- Endocrine - hyperthyroid, hepatic encephalopathy
- Pregnancy - should be alkaloid at baseline; normal pH suggests hypoventilation

Pain, pregnancy

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12
Q

Why does a respiratory alkalosis present with symptoms of hypocalcemia

A

Sx: lip and extremity parasthesias, muscle cramps, lightheadedness, syncope
Higher pH (alkalosis), calcium binds more strongly to albumin, decreases free calcium

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13
Q

List 7 causes of elevated AG metabolic acidosis

A

Keto acids (diabetic, starvation, alcohol)
Lactic acids
- Type A: inadequate oxygen (shock, mesenteric ischemia, muscle hyperactivity/seizure, hypoxia)
- Type B: adequate oxygen (liver failure, malignancy, thiamine deficiency, drug toxicity)
Uremia
Tox: IMPACTS - Iron/isoniazid (due to seizures), metformin, phenformin/paraldehyde, ASA/acetaminophen/alcohols, cyanide/CO, Toluene, salicylates

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14
Q

List 7 causes of non AG metabolic acidosis

A

Overall due to an imbalance of chloride and bicarb
- GI: diarrhea, colostomy or ileostomy, enteric fistulas, Kayexalate, TPN
- Renal: RTA, interstitial renal disease, hyperparathyroidism
- Normal saline infusion: urologic procedures, ureterosigmoidostomy
- Ingestions: acetazolamide, calcium chloride, magnesium sulfate
- Other: hypoaldosteronism, hyperkalemia, toluene

Mnemonic - HARD UP: hyperalimentation (TPN), acetazolamide, renal tubular acidosis, diarrhea, uretosigmoid fistula, pancreatic fistula

remember - gain chloride means H breaks off weak acids, bicarb loss, TPN is accumulation of organic acids (dont count), diamox is bicarb loss

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15
Q

List 5 causes of metabolic alkalosis

A

Due to gain of bicarb of loss of acid
Volume contraction - vomit (lose H)
diuretics (contraction alkalosis)
Endocrine - hyperaldosteronism, hypercortisolemia, hypoalbuminemia,
milk-alkali syndrome,
hypercalcemia, massive transfusion (generates citrate)

more calcium intake means more bicarb gets resorbed
More aldosterone get rid of more H ions
loop diuretics get rid of Cl
MTP - citrate gets turned into bicarb

Contraction alkalosis - when you try to keep volume, the kidneys keep water, salt and bicarb
Hypoalbuminemia - volume contraction

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16
Q

Describe the expected metabolic compensation in acute and chronic respiratory acidosis and alkalosis

A

See photo compensation
(1-2-HCOS-4-5)

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17
Q

Describe the expected respiratory compensation in metabolic acidosis and alkalosis

A

See photo compensation 2
Whether an appropriate respiratory compensation to a metabolic acidosis has occurred can be approximated by comparing the Paco2 to the last two digits of the serum pH. Ex. a patient with a pH of 7.20 should have a PaCO2 of 20mmHg

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18
Q

How do you calculate the anion gap

A

Na-(Cl+HCO3)

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19
Q

What is a normal anion gap

A

~8-12

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20
Q

How do you correct anion gap for albumin

A

Albumin corrected anion gap = anion gap +2.5*(normal albumin-measured albumin)

Albumin is an anion. AG will be lowered in the presence of hypoalbuminemia, thereby masking an elevated AG - a normal AG may actually represent a metabolic acidosis

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21
Q

What is the strong ion difference

A

(Na+K-Cl) <40 suggests an acidosis is present

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22
Q

What is the delta gap? How do you calculate it and what does it represent

A

Delta gap = (AG-12)-(24-HCO3-)
Determines if the anion gap is accounted for by the change in Bicarb
An elevated anion gap and a delta gap >6 indicates a metabolic alkalosis + a metabolic alkalosis. There is another process that is increasing bicarbonate levelsex. DKA with severe vomiting
An elevated anion gap and a delta gap <-6 indicates a metabolic acidosis (elevated AG) + a metabolic acidosis (normal AG). Ex. lactic acidosis with severe diarrhea

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23
Q

What is Winter’s equation? What does it represent

A

PaCO2 = (1.5*serum HCO3-) + (8 )
Used to calculate the expected arterial PCO2 for the serum bicarbonate level. Tells us if there is a mixed picture. If the PCO2 is higher than expected the patient may be fatiguing and need ventilator support

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24
Q

What is base excess

A

Defined as the amount of acid (H+) required to restore a Litre of blood to its normal pH and a PaCO2of 40 mmHg.
Estimates the metabolic component of the acid-base balance
A positive base excess means excess base, i.e. a metabolic alkalosis
A negative base excess means reduced base, i.e. a metabolic acidosis

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25
Q

What electrolyte abnormality is expected in chronic respiratory acidosis

A

Hypochloremia; Cl is excreted by the kidneys to maintain HCO3

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26
Q

What electrolyte abnormality is expected in chronic respiratory alkalosis

A

Hyperchloremia, Cl is kept by the kidneys to excrete HCO3
Hypokalemia, K+ is excreted by the kidneys to keep H+

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27
Q

*3 reasons why cancer patients get hypercalcemia

A
  • Ectopic secretions of parathyroid hormone
  • Multiple myeloma
  • Cancer metastatic to bone
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28
Q

*5 treatments for hypercalcemia

A
  • Oral rehydration
  • IV normal saline infusion
  • Bisphosphonate
  • Calcitonin
  • Glucocorticoids
  • Phosphates
  • Mab
  • Hemodialysis
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29
Q

*2 ECG changes for hypercalcemia

A

Short QT interval
ST segment elevation
In severe cases:
- Sinus bradycardia
- Bundle branch block
- High degree AV block
- J waves

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30
Q

*Most common cause of hyperCa in hospitalized patients?

A

cancer metastatic to bone

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31
Q

*2 causes of hyperCA in each category:
• MALIGNANT DISEASE
• ENDOCRINE
• GRANULOMATOUS DISEASE
• PHARMACOLOGIC AGENTS
• MISCELLANEOUS

A

• MALIGNANT DISEASE
• Ectopic secretions of parathyroid hormone, multiple myeloma, cancer metastatic to bone
• Most common: Breast, lung, hematologic, kidney, prostate
• ENDOCRINE
• Hyperparathyroidism, multiple endocrine cancers, hyperthyroidism, pheochromocytoma, adrenal insufficiency
• GRANULOMATOUS DISEASE
• Sarcoidosis, tuberculosis, histoplasmosis, berylliosis, coccidioidomycosis
• PHARMACOLOGIC AGENTS
• Vitamins A and D, thiazide diuretics, estrogens, milk-alkali syndrome
• MISCELLANEOUS
• Dehydration, prolonged immobilization, iatrogenic, rhabdomyolysis, familial, laboratory error

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32
Q

*Hypomagnesemia: cause of each category
Dietary
Gastrointestinal
Renal
Endocrine or metabolic
Drug induced

A

Dietary: chronic EtOH and malnutrition
Gastrointestinal: chronic diarrhea or inflammatory bowel conditions
Renal: mostly related to diuretics, pure renal wasting is rare
Endocrine or metabolic: hypokalemia, hypocalcemia, hyponatremia,
Drug induced: loop or thiazide diuretics, long term PPI

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33
Q

*2 uses for IV Mg in ED

A

Torsades / long QTC
Eclampsia / pre-eclampsia
Asthma
Hypokalemia/hypomag

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34
Q

*2 side effects of rapid IV magnesium in ED

A

• Hyporeflexia
• Brady
• Hypotension
• Flushing
• Resp arrest/apnea

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35
Q

*EKG findings of hyperkalemia

A
  • Peaked T wave
  • Flattened P wave
  • Prolonged PR
  • Absent P wave
  • Wide QRS
  • Sine wave
  • “Slow” ventricular tachycardia
  • Wide-complex bradycardia
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36
Q

*6 medications you can give to treat hyperK

A
  • Calcium gluconate/chloride
  • Ventolin
  • Insulin/dextrose
  • Kayexalate
  • Bicarbonate
  • Lasix (if making urine)
  • Dialysis (if anuric)
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37
Q

*Recent thyroidectomy with perioral numbness and tingling. Most likely diagnosis

A

Hypocalcemia

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38
Q

*2 EKG findings of hypocalcemia

A

o Arrythmias
o Long QT

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39
Q

*Treatment of hypocalcemia

A

Mild symptoms can be treated with oral calcium supplementation, such as calcium carbonate.
Hypocalcemic tetany: 100-300 mg elemental calcium (~3 g calcium gluconate) IV over 5-10 minutes, followed by continuous IV infusion at 0.5 mg/kg/hr (may be increased to 2 mg/kg/hr)

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40
Q

*Two special tests and descriptions for hypocalcemia

A

o Chvostek sign: When examiner taps the facial nerve, facial or eye muscle twitching occurs
o Trousseau sign: When examiner inflates blood pressure cuff to 20 mmHg above systolic blood pressure for 3 minutes, carpal spasms will occur

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41
Q

*Max correction in 24h for hyponatremia

A

Previous guidelines have endorsed the safety of raising the serum sodium by up to 10 to 12 mEq within the first 24 hours. However, in patients believed to have been hyponatremic for more than 48 hours, severe hyponatremia should be corrected by no more than 0.5 mmol/hr or 8 mEq in the first 24 hours.

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42
Q

*Causes of hyponatremia with high serum osmolality

A

? pseudohyponatremia
Hyperglycemia
Positive osmotic gap ( sorbitol, mannitol, lab error)

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43
Q

*Causes of SIADH

A

Lung Masses
Cancer (especially small cell)
Pneumonia
Tuberculosis
Abscess
Central Nervous System Disorders
Infection (meningitis, brain abscess)
Mass (subdural, postoperative, cerebrovascular accident)
Psychosis (with psychogenic polydipsia)
Drugs
Thiazide diuretics
Narcotics
Oral hypoglycemic agents
Barbiturates
Antineoplastics

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44
Q

*69F with advanced small cell lung cancer presents with confusion. Hemodynamically stable with normal cardiac exam. He is not clinically dehydrated. Sodium of 112 on his routine blood work. What other tests would you like to order for this patient in order to further characterize the nature of his hyponatremia?

A

Urine lytes
Serum osmolality

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45
Q

*What is the specific treatment for seizures from hyponatremia?

A

3% hypertonic saline 100 mL IV over 10 minutes (though she should get it for her confusion anyway)

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46
Q

*Why is it probably not a great idea to give a bolus of normal saline?

A

It would worsen the hyponatremia given that the extra water would be retained through the SIADH but the extra sodium would be excreted

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47
Q

*What is the pathophysiology for her confusion and twitchiness?

A

Cerebral edema from increased fluid shift in the cells, including cerebral cells

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48
Q

*How to correct mild hyponatremia from SIADH

A

Fluid restriction

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49
Q

*What is the delayed neurologic consequence if hyponatremia is corrected too rapidly?

A

osmotic demyelinating syndrome (ODS)

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50
Q

*What common BP medication should patients with hypercalcemia not take?

A

HCTZ (thiazides promote calcium reabsorption at kidneys)

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51
Q

*List hematological causes of high potassium

A

Cell death: Rhabdomyolysis, tumor lysis syndrome, massive hemolysis or transfusion, crush injury, burn

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52
Q

*What’s the difference between calcium chloride and calcium gluconate? What are 2 benefits to caCl in addition to 1 drawback?

A
  • Contains 3 times as much calcium molecules in the same volume
  • (but needs to be infused centrally),
  • less volume needs to be given and therefore faster and easier;
  • CaCl is a salt therefore dissociates right away and doesn’t need enzymatic cleavage by the liver
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53
Q

*What medications cause high potassium

A

Beta-blockers, acute digitalis overdose, succinylcholine, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, nonsteroidal anti-inflammatory drugs (NSAIDs), spironolactone, amiloride, potassium supplementation

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54
Q

*How does Adrenal insufficiency cause hyperkalemia

A

Low aldosterone signals to kidneys to spit out sodium and fluid and to retain potassium

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55
Q

*ECG features of low potassium

A

Flat T wave
U wave
Biphasic T waves (down then up)
QT prolongation
Torsades

56
Q

*What are some clinical features of hypokalemia?

A

Usually asymptomatic
Nonspecific complaints, primarily weakness and muscle pain
Cardiovascular instability
Neurologic dysfunction incl paralysis, hyporeflexia, parasthesias
Glucose intolerance
Gastrointestinal symptoms incl nausea, ileus
Renal failure

57
Q

*Symptoms of hypercalcemia

A

stones (kidney stones and polydipsia), groans (GI pain ex. pancreatitis, nausea, vomiting, constipation, body aches), bones (MSK pain), moans (psychiatric)

58
Q

*3 causes pseudohyperkalemia

A

hemolysis during or after the blood draw
post–blood sampling leak from markedly elevated white blood cells, red blood cells, or platelets

59
Q

List 10 causes of hyperkalemia

A

Increased K: rhabdo, burn, hemolysis, increased intake, tumor lysis syndrome
Shifted K: acidosis (DKA,Addison’s), insulin deficiency, digoxin, renal tubular acidosis
Decreased excretion: kidney failure, Ace and ARBs, spironolactone, Septra, dialysis,hypoaldosteronism (Addison’s)
Hemolysis due to drawing of the sample

60
Q

Other than ECG changes, list 4 clinical signs of hyperkalemia

A

Muscle weakness, fatigue, confusion, tetany, N/V/D

61
Q

List the expected ECG changes with a K of >5.5, >6/5. and >7.0

A

K>5.5depolarization abnormalities; peaked Ts
K>6.5 paralysis of the atria; p wave flattens, PR segment lengthens
K>7.0 conduction abnormalities prolonged QRS, AV block, sine waves, bradycardia

62
Q

List 5 causes of hypokalemia

A

Losses
- Renal: diuretics (thiazide and loop), hyperaldosteronism, polyuria, renal tubular damage, steroid use
- GI losses: diarrhea, vomiting, sweating, laxatives.
Decreased intake: ethanol, malnutrition
Intracellular shift: alkalosis, insulin, adrenergic
Endocrine: Cushing’s disease, Bartter’s syndrome, insulin therapy

63
Q

List 5 methods of potassium replacement

A

Oral: KCL elixir 20mmol/15ml, K lyte 25mmol/pack, slow K 8 mmol/tab, Micro K 8mmol/tab
IV: 10mmol/hr KCl if peripheral, 40mmol/hr if central

64
Q

What electrolyte needs to be replaced with potassium

A

Magnesium
Unless the hypoK patient receives Mg the K will not move intracellularly

65
Q

List 5 causes of hypernatremia

A

Hyponatremia + dehydration: heatstroke, increased losses ex. burns/sweating, GI losses ex. diarrhea, vomiting, GI suction, osmotic diuresis ex. glucose, mannitol
Hyponatremia with hypotonic losses (low total body water): diabetes insipidus, hypothalamic dysfunction, supreasellar tumors, renal disease, drugs (amphotericin, phenytoin, lithium, aminoglycosides), sickle cell
Hypernatremia + increased salt: salt tab ingestions, salt water ingestions, saline infusions, IV sodium bicarb, hyperaldosteronism, Cushing’s, hemodialysis, Conn’s syndrome

66
Q

List 5 causes of diabetes insipidus

A

Central: idiopathic, familial, cancer, hypoxic encephalopathy, infiltrative disorders, SVT, anorexia
Nephrogenic: chronic renal insufficiency, polycystic kidney disease, lithium toxicity, hypercalcemia, hypokalemia, sickle cell

67
Q

What is the presentation of diabetes insipidus

A

polydipsia, polyuria, and dilute urine.

68
Q

How do you calculate the TBW deficit

A

Deficit = normal TBW - current TBW
= normal TBW - (normal TBW x 140/Na)
= normal TBW x (1 - 140/Na)
= [lean weight x (0.6 in men, 0.5 in women)] x (1 - 140/Na)
- Eg: 70 kg female w/ Na 160
- Deficit = 70x0.5 x (1 - 140/160) = 4.375 L

69
Q

What is a safe correction rate in hypernatremia

A

acute (no more than 1mol/hr), chronic (no more than 0.5 mmol/hr’ max 8-10/24 hours)

70
Q

List 10 causes of hyponatremia

A

See photo causes of hyponatremia

71
Q

Which causes of hyponatremia present with a high urine sodium

A

Etiologies where the hyponatremia is ultimately due to an issue with the kidney’s ability to retain sodium ex. SIADH, renal failure, recent diuretics

72
Q

What is the sodium concentration of 3%, 0.9% NS, ringers and 1/2 normal saline

A

3% - 513
0.9% - 154
Ringers - 130
1/2 NS - 77

73
Q

List 3 risk factors for osmotic demyelination

A

Na < 105, hypo-K, alcoholism, liver disease, malnutrition

74
Q

List 5 causes of hypocalcemia

A

Low phosphate
Low Mag
Low Vit D

MTP
Hypoparathyroidism
Rhabdo
Tumor lysis

75
Q

List 5 causes of hypermagnesemia

A

Stuff with Mag in it
Laxatives
Diasylate
Antacids
Supplements

Cant leave
Narcotics, lithium, TSL
bowel obstruction, anti cholinergics

76
Q

List 5 symptoms of hypermagnesemia

A

Nausea, somnolence, muscles weakness, loss of DTR, hypotension, respiratory insufficiency, heart block

77
Q

What ECG findings are associated with hypermag

A

QRS widening, QT or PR prolongation, heart block, cardiac arrest

78
Q

What is the management of hypermag

A

Stop magnesium, fluids, dialysis, calcium IV (antagonizes magnesium)

79
Q

What ECG findings are associated with hypomag

A

Arrhythmias, long QT and short PR, ST depression, flattening and widening of T waves, Can turn into TdP

(similar findings to hypoK and hypoCa)

80
Q

List 5 causes of hyperphosphatemia

A

Decreased excretion: renal failure
Shift: rhabdo, tumor lysis, acidosis, DKA
Increased reabsorption: hypoparathyroidism, vitamin D, thyrotoxicosis, drugs
Increased intake: enemas, oral or IV

81
Q

What electrolyte abnormality is associated with hyperphosphatemia

A

Hypocalcemia

THINK TUMOR LYSIS

82
Q

List 5 causes of hypophosphatemia

A

Insulin
Refeeding
Hungry bone
Vit D low
Diarrhea
ETOH

83
Q

Which electrolyte abnormalities can cause prolonged QtC

A

Hypokalemia, hypocalcemia, hypomagnesemia, hypermagnesemia

84
Q

*3 Diagnostic criteria for DKA (same for peds)

A
  • Ketonuria (serum ketones also seems reasonable)
  • Glucose > 11 mmol/L
  • pH < 7.3
  • Serum bicarbonate < 18 mmol/L
85
Q

*2 severe metabolic complications from IV insulin

A

• Hypokalemia
• Hypoglycemia

86
Q

*4 precipitants for (pediatric) DKA

A

6 I’s – Infection, Infarction, Intoxication, Intraabdominal process, Initial diagnosis, Insulin misuse (both forgetfulness as well as non-adherence)

87
Q

*4 management steps for cerebral edema

A

• Standard maneuvers for elevated ICP
- Elevate head of bed to 30 degrees
- 20% Mannitol over 10-20 min
- Check Na, If low: 3ml/kg of 3% NS over 10-20 min
• Stop/slow insulin infusion
• If intubated, hyperventilate

88
Q

*5 management points in DKA

A

IV fluids
Insulin drip
Replete electrolytes
Search for precipitant
Monitor closely

89
Q

*3 reasons why not to give bicarb

A
  • Exacerbation of electrolyte deficits such as hypokalemia
  • Delaying clearing of ketosis
  • Paradoxical worsening of acidosis in the CSF due to suppression of respiratory compensations and preferential permeability of the blood- brain barrier to CO2
90
Q

*ABG vs VBG: If VBG: ph, CO2, HCO3- are these higher or lower on ABG

A

pH - similar or very slightly lower on VBG
CO2 - similar or slightly higher on VBG
HOC3 - similar or slightly lower on VBG

91
Q

How can a patient in DKA have a normal pH

A

Ketoalkalosis has been reported in cases of excessive vomiting
Winter’s formula: PaCO2 = [1.5 * serum bicarb] + (8 +/-2) can be used to see if there are multiple acid-base disorders

92
Q

How can a patient with DKA have no ketones in their urine?

A

Urine ketone dipsticks measures acetoacetate but not beta hydroxybutyrate. Free fatty acids -> acetoacetate and beta hydroxybutyrate. The ratio of acetoacetate to beta hydroxybutyrate is ~1:3 but may be as high as 1:30 in which case the urine may be falsely negative

93
Q

What is the starting dose of insulin in DKA

A

IV insulin 0.05-0.1U/kg/hr
NEVER bolus

94
Q

How do you correct sodium for glucose in DKA

A

For every 10mmol/L rise in glucose >8 add 3

95
Q

List 5 risk factors for the development of cerebral edema

A

Pt: age < 5y, new onset DM, sick appearance, greater acidosis (lower pH/CO2, more severe dehydration (high Hct/BUN), longer duration of Sx
Tx: bolus insulin, early insulin infusion (before 1h of IVF), NaHCO3

96
Q

What is the starting fluid bolus in peds DKA

A

10ml/kg of IVNS

97
Q

List 5 causes of hypoglycemia

A

Drugs: sulfonylureas, quinolone, beta blockers, AceI, quinine
Increases insulin: exogenous or endogenous (tumor)
Infection, illness
Metabolic: liver/renal failure, adrenal insufficiency, Type 1 diabetes, alcoholism
- Critical sample is used to help diagnosis the underlying cause of hypoglycemia, includes things like cortisol, free fatty acids, ammonia, gas, insulin, lactate, beta hydroxybutyrate
Environmental: accidental, inadequate food intake

98
Q

How do you supplement glucose in hypoglycemia

A

Rule of 50s
- 5ml/kg of 10% dextrose
- 2ml/kg of 25% dextrose
OR 1 mg IM glucagon (s/e of N/V)(onset of action several hours)

99
Q

What is HHS

A

Hyperglycemia >33.3 and hyperosmolarity >320 mOsm/kg and dehydration found in patients with poorly controlled T2DM and some trigger
Severe hyperglycemia causes as osmotic diuresis and dehydration
Non ketotic state; anion gap should be normal and pH >7.30

100
Q

List 10 long term complications of diabetes

A

Macrovascular complications: CAD, CVD, PVD
Microvascular: peripheral neuropathy (incld autonomic neuropathy), nephropathy, retinopathy
Nonvascular: infections, dermatologic changes, sexual dysfunction

101
Q

List 3 ways to diagnose diabetes

A

Fasting glucose >7.0
2h OGTT >11.1
HbAIC >6.5%
Random PG >11.1

Think 7/11

102
Q

List 5 medications used in the treatment of diabetes

A

Decrease sugar absorption: Alpha-glucosidase inhibitor (ex. acarbose)
Insulin sensitizers: Biguanide (ex. Metformin), GLP analogues (ex. liraglutide), Thiazolidinediones (ex. rosiglitazone)
Insulin releasers: DPP4 inhibitors ex. sitagliptin/Januvia, secretagogues/sulfonylureas (ex. glyburide, gliclazide)
Increased sugar loss: SGLT2 inhibitors (ex. empagliflozin)
Insulin

103
Q

Which diabetic medications can cause hypoglycemia

A

Sulfonylureas, insulin

104
Q

Which diabetic medications can cause euglycemic DKA

A

SGLT2 inhibitors (ex. empagliflozin)

105
Q

*Causes of rhabdo (from a tox question)

A

Prolonged immobilization
Excessive muscle activity (can be high or low intensity!)
Muscle ischemia (Rhabdo occurs after reperfusion!)
Temperature extremes
Heat stroke, neuroleptic malignant syndrome, and malignant hyperthermia
Electrical current (High-voltage electrical injury, including lighting, poses the highest risk)
Post-repeated cardioversion
Electrolyte abnormalities (hypoK+, hypoPhos, HypoNa+ / HyperNa+)
Illicit drugs (opioids, antipsychotics, benzodiazepines, amphetamines, ecstasy, LSD, and synthetic cannabinoids)
Medications (Statins, antipsychotics)
Infections
Metabolic myopathies - Inborn errors of metabolism – appear in children
Connective tissue disorders - polymyositis, dermatomyositis, and Sjögren’s syndrome.
Rheumatologic disorders – SLE
Endocrine disorders – hypothyroidism
Biologic toxins - snakebite, bee stings
Other + unknown (Post-succinylcholine, post caffeine overdose, and others!)

106
Q

List 4 pathologic processes in rhabdo

A

Muscles become unable to use ATP, leading to a breakdown in Na/K pumps and disruption of chemical gradients leading to cell destruction
- Increase in intracellular calcium leads to mitochondrial dysfunction
Disruption in the delivery of oxygen, glucose, and nutrients to the skeletal muscle
Increases in metabolic demands that surpass oxygen abilities
Direct myocyte damage

107
Q

List 5 complications of rhabdo

A

Compartment syndrome: influx of electrolytes leads to accumulation of extracellular fluids leading to local edema and raised pressure, causing further ischemia
Electrolyte disorders: hyperkalemia, metabolic acidosis, hyper phosphate, hypocalcemia (binded by phosphate) and then hypercalcemia once mobilized from phosphate, hyperuricemia
Third spacing and hypovolemia
Hepatic dysfunction
AKI due to myoglobin casts in tubules causing obstruction
DIC

108
Q

What CK is typically seen in rhabdo

A

5x normal limit; 1000

109
Q

What will the urine show in a patient with rhabdo

A

positive blood but no blood cells on examination

110
Q

*4 medications with mechanism used in thyroid storm

A

“Proptotic Polly wait is Dying….Propranolol, PTU, wait 1 hr, Iodine and Dex”

  1. Symptomatic treatment
    - Beta Blockers - propranolol 0.5-2mg IV, metoprolol, esmolol - blocks peripheral T4–>T3 conversion
  2. Block synthesis of thyroid hormone
    - PTU 600-1000mg PO load (1st line) OR Methimazole (preferred in liver failure)
  3. Block release of thyroid hormone
    - KI or 10 drops Lugol’s sol’n (iodine load); must wait an hour after PTU is given
  4. Block conversion of T4 to T3. Additional benefit of treating any concomitant adrenal insufficiency.
    - Steroids (hydrocortisone 300mg IV load then 100mg IV or dex)
111
Q

*List three non-pharmacologic management strategies for thyroid storm

A

Cooling (controversial)
NG tube (to give PTU if unable to tolerate PO)
IVF
Tylenol
Rosen also mentions benzos and cholestyramine.
Admission
Endocrinology consult

112
Q

*What are 4 medications that can precipitate thyroid storm?

A

Amiodarone
Lithium
Contrast load
Interferon alpha
Imatinib (tyrosine kinase inhibitors) (chemo)
ARTs

A LA CC-ART (“À La Carte”)
Amio

Lithium
Alpha ((interferon)

Chemo
Contrast
ART

113
Q

*What are 3 lab abnormalities in thyroid storm (non-thyroid labs)?

A

Hepatic failure
Hyperglycemia
Hypercalcemia
Leukocytosis
Mild anemia

114
Q

*Which antipyretic is contraindicated in thyroid storm and why

A

Aspirin should be avoided in thyrotoxic patients because it decreases the protein binding of T 4 and T 3 (therefore increasing t4 and t3 into the circulation)

115
Q

*List five cutaneous manifestations of hypothyroidism

A

Coarse, brittle hair
Alopecia
Dry skin, decreased perspiration
Pallor, cool hands and feet
Coarse, rough skin
Yellow tinge from carotenemia
Thin, brittle nails
Lateral thinning of the eyebrows

116
Q

*2 cardiovascular findings of hypothyroidism

A
  • Low/normal systolic blood pressure
  • Slow pulse to sinus bradycardia
  • Decreased exercise capacity
  • Dyspnea on exertion
  • Sinus bradycardia
  • Long QT with increased ventricular arrhythmia
  • Chest pain, accelerated coronary disease
  • Diastolic heart failure
  • Pericardial effusion
  • Peripheral edema
117
Q

Describes the HPA axis as it related to thyroid function

A

TRH (hypothalamus) -> TSH (pituitary) -> T3/T4 from thyroid
T3 is the active product. T4 is converted to T3

118
Q

What are the possible effects of iodine in a patient with thyroid disease

A

Generally iodine is a substance for thyroid hormone
Wolff-Chaikoff effect: Excess iodide can inhibit the release of T3/T4 by inhibiting the release of thyroid hormone from the gland by blocking iodide trapping
Jod-Basedow effect: Iodide load can induce hyperthyroidism in some patients with multimodal loiter and occult Grave’s disease

119
Q

Interpret the following thyroid function tests

A

see photo

120
Q

List 5 causes of hyperthyroidism

A

Primary - hormone overproduction:
- Autoimmune: Graves (will have a positive TSI; most common cause)
- Overproduction: Toxic nodular goiter (secretes T3/T4), toxic adenoma
- Inflammatory: Thyroiditis, trauma causing injury to a gland, drug induced (amiodarone, lithium), post infectious/viral, autoimmune Hashimoto’s, postpartum
- Exogenous thyroid: toxicosis factitia (ingestion of too much thyroid hormone)
Secondary: Pituitary thyroid hormone receptor resistance, ectopic thyroid tissue

121
Q

List 10 sx of hyperthyroidism

A

Cardiac; tachycardia, arrhythmias (afib, palpitations), widened pulse pressure
Hypermetabolic: heat intolerance, sweating
GI: weight loss, increased appetite, diarrhea
Psych/neuro: anxiety, restlessness, hyperkinesis, confusion, tremors
Systemic: amenorrhea, fine hair, sweating, proximal muscle weakness, fatigue
HEENT: large goiter, exophthalmos

122
Q

What is the management of thyroiditis

A

NSAIDs for inflammation and pain control
Prednisone if refractory

123
Q

What is the diagnostic criteria for thyroid storm

A

Marked pyrexia (40-41 C), extreme tachycardia, altered mental status
Other common sx include CHF, afib, nausea/vomiting/diarrhea, unexplained jaundice with elevated liver enzymes, hyperglycemia

124
Q

List 5 etiologies of hypothyroidism

A

Primary: inadequate production, autoimmune (Hashimoto’s), ablative (from Grave’s), drugs (iodine deficiency, amiodarone, lithium), infiltrative disease, neoplasm, pregnancy,
Secondary: insufficient stimulation to the thyroid gland i.e. low TSH from the pituitary; adenoma, hemorrhage (Sheehan’s syndrome), sarcoidosis

125
Q

List 10 symptoms of hypothyroidism

A

↓HR/SBP (vs high DBP, HTN; reflex from low CO, high PVR)
Nonspecific: fatigue, weakness, weight gain, constipation, menorrhagia, cold intolerance, infertility, high TGs
Neuro/Psych: depression, memory/cognition abNs, carpal tunnel
HEENT: goiter, altered taste, hoarseness
MSK: arthralgias, proximal weakness
Derm: goiter, hand/foot edema, thickened skin, coarse/brittle hair/nails, facial changes (edema, broad nose, swollen lips, macroglossia, flat expression)

126
Q

What is the clinical presentation of myxedema coma

A

High TSH and low T4/T3
hypothermia, refractory hypotension, hypoventilation, bradycardia, myxedema facies (puffy eyelids and lips), altered LOC

127
Q

What is the treatment of myxedema coma

A

IV T4 levothyroxineat 4 mcg/kg (typically 200-400 mcg)
IV hydrocortisone 100mgIV for suspected concurrent adrenal insufficiency

128
Q

Describe the HPA axis as it relates to the adrenal glands

A

Hypothalamus secretes Corticotropin Releasing Hormone CRH and Arginine Vasopressin (AVP) -> pituitary secretes Adrenocorticotropic Hormone (ACTH) in a pulsatile fashion -> adrenal gland -> releases glucocorticoids aldosterone, sex hormones, catecholamines

129
Q

Describe parts of the adrenal gland and the hormones they produce

A

Cortex
- Glomerulosa -> Aldosterone (mineralocorticoid that regulates volume through the Na+/K+ transporters)
- Fasciculata -> Cortisol
- Reticularis -> Sex hormones
Medulla: epinephrine and norepinephrine

130
Q

What is Cushing’s syndrome

A

Glucocorticoid excess due to increased ACTH (ex. Pituitary adenoma) or long term glucocorticoids
Presents with a metabolic syndrome: hypertension, glucose intolerance, hirsutism, weakness
Dx with free urine cortisol

131
Q

What is the clinical presentation of congenital adrenal hyperplasia

A

Enzyme deficiency cause un-oppressed ACTH stimulation leading to hypertrophy
Low cortisol, low aldosterone, increased adrenal androgens
Most often presents with salt wasting (hyperkalemia, hyponatremia), virilization/ambiguous genitalia, poor weight gain, hyperpigmentation in the first few weeks of life

132
Q

What is the clinical presentation of adrenal insufficiency

A

Hyperkalemia, hyponatremia, hypoglycemia, hypotension
- No cortisol: hypoglycemia, fatigue, weakness, depression, nonspecific GI symptoms
- No aldosterone: salt wasting (salt cravings and hyponatremia), hyperkalemia, hypovolemia, hypotension, orthostatic intolerance
- No catecholamines: hypotension that does not respond to fluids

133
Q

List 2 acute and chronic causes of primary and secondary adrenal insufficiency

A

Primary (high ACTH, low cortisol)
Acute etiology
- Adrenal hemorrhage: meningococcemia/sepsis (Waterhouse–Frederiksen), trauma, anticoagulation
- Etomidate: inhibits adrenal enzyme converting deoxycortisol to cortisol (primary?)
Chronic etiology
- Autoimmune adrenalitis (Addison’s; most common in developed countries): isolated or as syndrome (eg: polyglandular autoimmune syndrome)
- Infection: HIV (direct involvement or d/t CMV, MAC, TB, PJP, - Metastatic cancer: breast, lung, melanoma
- Infiltrative: sarcoid, amyloid, hemochromatosis
- Congenital: CAH, adrenoleukodystrophy, ACTH resistance
- Iatrogenic: bilateral adrenalectomy; etomidate, ketoconazole, rifampicin

Secondary (low pituitary ACTH, low cortisol):
Acute etiology
- TBI
- Pituitary apoplexy: hemorrhage into pituitary tumor, visual Sx, HA
- Critical illness (relative insufficiency): sepsis, trauma, pancreatitis, liver failure
- Pituitary tumor: primary, metastatic
- Congenital: empty sella syndrome
- Iatrogenic: pituitary surgery/radiation

134
Q

Why is skin pigmentation seen in primary adrenal insufficiency

A

High ACTH stimulates other hormones ex. melanocytes causing the skin pigmentation

135
Q

What are two ways to diagnose adrenal insufficiency

A

Morning cortisol level - this is when cortisol is the highest
- <50-100 dx confirmed, >500 dx excluded, 100-500 need more testing
ACTH stim test: A normal physiologic response is an increase in cortisol with exogenous supply
- 250mg of ACTH measure give cortisol at 0min, 30 mins, and 60 mins

136
Q

What is the treatment of adrenal insufficiency

A

Fluids + steroids (hydrocortisone or dex)

137
Q

What is Sheehan’s syndrome and 4 main clinical manifestations

A

Post partum hemorrhage causing that leads to pituitary schema and necrosis
= 4 manifestation are :
1- Lactation failure
2- Amenorrhea
3- Adrenal Insufficiency
4- Central Hypothyroidism

KChan Saves the World (24 decks)

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