1
Q
What is the most abundant intracellular cation?
A
K
2
Q
Importance of potassium?
A
Cell metabolism, neuromuscular and cardiac electrical transmission
3
Q
Etiology of K imbalances
A
Renal dysfunction
Dietary
Meds side effects (diuretics)
4
Q
Causes of hypokalemia
A
- Loss: renal excretion via diuretics, vomiting, diarrhea, hyperaldosteronism, hypomag
- Shift: insulin, dobutamine, epi
5
Q
S/s of hypokalemia
A
- Weakness, fatigue, constipation, palpitations
- EKG: flat T, ST depression, U waves
6
Q
Tx of mild hypokalemia
A
PO KCl (K-Dur, K-Lor, K-Tab)
7
Q
Tx of mod-severe hypokalemia
A
IV KCl at 10 mEq/hr
8
Q
10 mEq of KCl raises serum K by:
A
0.1 mEq/L
9
Q
Causes of hyperkalemia
A
- Absolute: renal insufficiency, meds (ACE, ARB, digoxin)
- Pseudo: DKA, hemolysis
10
Q
S/s of hyperkalemia
A
- Weakness, cramping, paresthesias
- EKG: peaked T, wide QRS, loss of P, sine wave
11
Q
Sine wave on EKG is a late sign of:
A
Hyperkalemia
12
Q
What is a late sign of hyperkalemia?
A
Sine wave on EKG
13
Q
Tx of hyperkalemia
A
- ALWAYS on cardiac monitor
- Ca gluconate (stabilize myocytes)
- Regular insulin
- Albuterol nebulizer
- Lasix
- Na polystyrene sulfonate (Kayexalate)
- Dialysis
14
Q
Importance of Na in the body
A
Indirect measure of free water in serum
15
Q
Define osmolarity
A
Concentration of solutes per L of solution
- HIGH = fluid depletion
- LOW = fluid retention
16
Q
Etiology of Na imbalances
A
- Hormonal (SIADH)
- Free water excess or loss
17
Q
Causes of hyponatremia
A
- Hypovolemic: diuretics, DM, adrenal insufficiency, sweat, burns, vomiting, diarrhea
- Hypervolemic: CHF, cirrhosis, nephrotic synrome, preg, excess IVF
- Euvolemic: SIADH, Ca, water intoxication
18
Q
S/s of hyponatremia
A
HA, N/V, lethargy, confusion, seizure, coma
19
Q
What are the symptoms of hyponatremia determined by?
A
Degree and rapidity of development
20
Q
Causes of hypernatremia
A
- Hypovolemic: sweating, vomiting, diarrhea, DI
- Hypervolemic: excess IV hydration, hyperaldosteronism
21
Q
Tx of mild (asymp) hyponatremia
A
Fluid restriction
22
Q
Tx of mod-severe hyponatremia
A
- Acute/severe: 3% hypertonic saline 100 ml over 10 min
- Chronic: 0.5 ml/kg/hr or less
23
Q
Why is correction of chronic hyponatremia slow?
A
Avoid central pontine myelinolysis (flaccid paralysis, seizures)
24
Q
S/s of hypernatremia
A
AMS, seizures, hyperreflexia, spasticity, lethargy
25
Tx of hypernatremia
Gradual correction w/hypotonic or isotonic fluids (to avoid cerebral herniation)
26
Importance of Ca in body
- Blood coagulation
- Nerve conduction
- Osteoclast bone activity
- APs for muscle contractions
27
Etiologies of Ca imbalance
Regulated via PTH, calcitonin (thyroid), calcitriol (kidneys)
28
What Ca level is most accurate?
Ionized Ca level
29
Causes of hypocalcemia?
Hypothyroid
HypoPTH
Thyroidectomy
CKD
30
S/S of hypocalcemia
- Paresthesias, hyperreflexia, tetany, Chvostek/Trousseau
| - EKG: QT prolonged leading to Torsades
31
Tx of hypocalcemia
- Asymp: oral Ca carbonate (or citrate)
- 10% Ca gluconate IV
- Replace Mg 1st if deficient
32
Causes of hypercalcemia
- HyperPTH
- Bone cancer
- Prolonged immobilization
33
S/s of hypercalcemia
- Stones, bones, moans, psychic groans and fatigue overtones
| - EKG: short QT
34
Tx of mild-mod hypercalcemia
Increased oral hydration or IVF with or w/o diuretic
35
Tx of mod-severe hypercalcemia
Bisphosphonates IV OR calcitonin IM/SC OR dialysis
36
Importance of Mg in the body
- Energy metabolism and neuromuscular transmission
| - Necessary in facilitating replacement of K and Ca
37
Etiologies of Mg imbalance
- GI absorption
- Renal excretion
- Tubular reabsorption
38
Causes of hypomagnesemia
- Alcoholism (poor diet, decreased intestinal absorption, increased renal excretion)
- Vomiting
- Diarreha
39
S/s of hypomagnesemia
Lethargy, confusion, tremors, seizures, paresthesias, hyperreflexia
40
Tx of mild/chronic hypomagnesemia
Mg oxide PO 1-2x a day
41
Tx of mod/symptomatic hypomagnesemia
Mg sulfate IV over 15-60 mins
42
Causes of hypermagnesemia
- Renal failure
- Supratherapeutic replacement
- Antacid abuse
43
S/s of hypermagnesemia
- Hyporeflexia
- Bradycardia
- Hypotension
- Cardiac arrest
44
Tx of hypermagnesemia
- Stop any Mg supplements
| - Give loop diuretics, CaCl IV, dialysis
45
What conditions use Mg therapeutically?
- Asthma
- AF, torsades, dig toxicity
- Preeclampsia
- Migraine/cluster HAs
- Constipation
46
MOA of Mg therapy in asthma?
Pulm smooth muscle relaxation at bronchial level (improves FEV1)
47
MOA of Mg therapy in AF/torsades/dig tox?
Prolongs sinus node recovery time and reduces AV node/accessory pathway conductions
48
MOA of Mg therapy in preeclampsia?
- Ca antagonist effect for seizure activity or to slow uterine contractions
- Stimulates PG release, potent vasodilatory effect for BP control
49
MOA of Mg therapy in migraine/cluster HAs?
Decrease vasospasm and pain transmitting chemicals
50
MOA of Mg therapy in constipation?
Osmotic effect - causes H2O retention in GI lumen
51
What is the normal BUN:Cr ration?
10-20:1
52
Elevated BUN alone indicates?
```
RBC hemolysis (GIB)
Excess protein intake
Corticosteroids
```
53
Elevated BUN and Cr with ratio over 20:1 indicates?
Prerenal azotemia (dehydration)
54
Elevated BUN and Cr with ration less than 20:1 indicates?
Azotemia (CKD, GN, post-renal obstruction)
55
Abnormalities of Cl and CO2 MC reflect:
Compensations of acid-base secondary to pulm (respiratory) or renal (metabolic) disorders
56
Causes of hypochloremia
- Primary metabolic alkalosis (GI losses)
| - Compensated respiratory acidosis
57
Causes of hyperchloremia
- Primary metabolic acidosis (excess NS)
| - Compensated resp alkalosis
58
Causes of hypobicarbonatemia
- Primary met acidosis (renal failure)
| - Compensated resp alkalosis
59
Causes of hyperbicarbonatemia
- Metabolic alkalosis (hypovolemia)
| - Compensated chronic resp acidosis
60
CV effects of acidosis
Decreased contractility
| Hypotension
61
Metabolic effects of acidosis
Insulin resistance
| Hyperkalemia
62
Neuro effects of acidosis
Somnolence
| Coma
63
Respiratory effects of acidosis
Compensatory hyperventilation resulting in respiratory muscle fatigue
64
What is the use of anion gap?
Used to determine a metabolic acidosis state and to figure out its etiology (esp in setting of AMS or unknown exposures)
65
How to calculate anion gap
AG = Na - (Cl+HCO3)
| Normal is 8-16
66
DDx of an elevated anion gap acidosis?
- MUDPILES (methanol, uremia, DKA, propylene glycol, isoniazid, lactic acidosis, ethylene glycol, salicylates)
- GOLDMARK (glycols, oxoproline, lactate, D-lactate, methanol, aspirin, renal failure, ketoacidosis)
67
Etiologies of euglycemic ketoacidosis
- Fasting diabetic
- Hypertriglyceridemia
- Low carb/high fat diet
- Gestational DM
68
How does a fasting diabetic develop euglycemic ketoacidosis?
Depletion of their glycogen stores which ultimately results in decreased glucose production
69
How does hypertriglyceridemia cause euglycemic ketoacidosis?
Causes volume displacement that can result in patient's glucose level to appear normal or near-normal
70
How does a low carb/high fat diet cause euglycemic ketoacidosis?
Decreases insulin levels and increases glucagon
71
How does gestational DM cause euglycemic ketoacidosis?
- Glucose utilization by fetus
- Decreased carb intake from hyperemesis
- Insulin levels that prohibit glycogenolysis but still alter glucagon:insulin ration
72
Treatment of euglycemic ketoacidosis
Aggressive administration of NS solution, insulin, maintaining K levels, treating underlying conditions
73
What is the only means by which ketoacidosis can be reversed?
Insulin therapy - but induces an intracellular shift of K resulting in hypokalemia
74
How is insulin therapy used to treat ketoacidosis?
- Reverses it but induces hypokalemia
| - Treatment should be coupled with glucose and potassium
75
Etiology of alcoholic ketoacidosis
- Abd pain and/or vomiting causes decreased dietary intake (starvation)
- Development of increased ketoacid production
- Body decreases insulin to combat starvation
76
Treatment of alcoholic ketoacidosis
- ABCDEs
- Hydration with D5NS
- Bicarb (ONLY for severe acidosis and if not responding to D5NS)
77
How to treat someone who comes into ED with AMS and unclear etiology?
```
DONT
Dextrose (if hypoglycemic)
O2
Naloxone
Thiamine
```
78
Onset of salicylate toxicity?
May begin 4-6 hrs after ingestion in a young infant, 24 hr or more in adolescent/adult
79
Pathophys of salicylate toxicity
- Inhibits Krebs cycle and AA synthesis which triggers fatty acid metabolism leading to ketonemia
- Respiratory alkalosis
- Renal insufficiency possible
80
Earliest signs of salicylate toxicity
N/V, diaphoresis, tinnitus
81
Treatment of salicylate toxicity
- ABCs
- Dextrose w/AMS
- Gastric lavage and charcoal if early presentation
- Na bicarb
- Dialysis
82
Describe pathophys of starvation/fasting and how to treat it
- Similar to alcoholic ketoacidosis but less severe ketonemia
- Treatment with D5NS, counseling
83
Pathophys of uremia
- Chronic decline in tubular functions of kidney
- H excretion reduced
- HCO3 excretion increased
- Attempted buffering releases Ca salts from bone and their excretion in urine
84
Treatment of uremia
Na bicarb to keep serum HCO3 greater than 20, nephrology consult
EM - Exam 2
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