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Pathophysiology I > Pathophysiology: Electrolyte Disorders > Flashcards

Pathophysiology: Electrolyte Disorders Flashcards

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1
Q

Hypokalemia [K+] Frequency of occurrence

A
  • ~3% of ambulatory patients
  • ~20% of hospitalized patients
  • ~40% of pts prescribed with thiazide diuretics
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2
Q

Hypokalemia [K+] increases mortality risk in patients with:

A
  • Heart failure (HF)
  • Chronic Kidney Disease (CKD)
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3
Q

Decreased serum [K+] of?

A
  • less than 3.5 mEq/L
  • Severe: ~2-2.5 mEq/L
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4
Q

Causes of Hypokalemia

A
  • Losses
  • transcellular shift
  • inadequate intake
  • pseudohypokalemia
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5
Q

Hypokalemia evaluation Laboratory

A
  • [K+] < 3.5 mEq/L –check magnesium

May also need to evaluate:
• Urine electrolytes
• Acid-Base status

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6
Q

History for Hypokalemia Evaluation: PMH, Medications

A
  • past medical history: cardiac, renal, thyroid
  • medications: insulin, beta-agonists
  • volume loss
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7
Q

Hypokalemia evaluation of physical exam

A
  • EKG: cardiac assessment
  • weakness, paralysis: neurologic assessment
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8
Q

Hypokalemia symptoms

A

DA SIC WALT
- decreased intestinal motility: nausea, vomiting, ileus
- alkalosis
- shallow respirations
- irritability
- confusion, drowsiness
- weakness, fatigue
- Arrythmias
- Lethargy
- Thready pulse

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9
Q

Pseudohypokalemia

A
  • delayed sampling process
  • leukocytosis
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10
Q

Hypokalemia: Pathophysiology MOA: Inadequate Intake

A
  • normal renal physiology continues to excrete K+ even with no K+ intake
  • extreme decreased K+ intake coupled with hypomagnesemia results in significantly worse hypokalemia:
    -> Anorexia nervosa
    -> crash diets
    -> alcoholism (delirium tremens)
    -> intestinal malabsorption
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11
Q

Why does hypomagnesium exacerbate hypokalemia

A
  • Magnesium inhibits K+ secretion in the distal nephron
  • correct magnesium first, then potassium will correct
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12
Q

Hypokalemia: MOA Losses

A
  • GI Losses: vomiting, diarrhea
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13
Q

Hypokalemia: Renal Losses

A

Mi TyPO
- osmotic diuresis
- polydipsia
- mineralocorticoid excess (see meds)
- Type I and Type II Renal Tubular acidosis

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14
Q

Medications that causes Hypokalemia

A
  • Laxatives/Enemas (OTC)
  • Diuretics: (loop, thiazide)
  • Corticosteroids: (dexamethasone, fludrocortisone)
  • Amphotericin B
  • Cisplatin
  • Penicillin antibiotics (high dose): (ticarcillin, carbenicillin, piperacillin)
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15
Q

Medications for Hypokalemia (meds that cause Hypokalemia)

A

BADFIT
B- Beta 2 antagonists
A- Amphotericin B
D- Digoxin
F- Furosemide, foscarnet
I- insulin
T- Thiazides

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16
Q

High dose penicillin examples

A
  • penicillin, piperacillin, ticarcillin
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17
Q

Hypokalemia MOA: High dose penicillin

A
  • increased Na+ delivery to distal tubule
  • results in excretion of K+
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18
Q

Amphotericin B MOA:

A
  • inhibits secretion of H+ in collecting duct causing Mag++ depletion
  • Mag++ depletion causes K+ sweating
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19
Q

Hypokalemia: Aminoglycosides MOA:

A
  • gentamicin, tobramycin, Cisplatin, Foscarnet
  • deplete Mag++ resulting in K+ wasting
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20
Q

Fludrocortisone MOA

A
  • significant retention of Na
  • increase of Na+ leads to decrease of K+
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21
Q

Example of Loop Diuretics

A
  • Furosemide (Lasix) -> “Water Pill”
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22
Q

Loop diuretic inhibits what? and where? and results in what?

A
  • Na, K, Cl in the thick ascending limb
  • resulting in significant Na+ concentration gradient
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23
Q

Loop diuretic delivers Na+ where? Results in what?

A
  • Thick ascending limb
  • reabsorption of Na and increased excretion of K+
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24
Q

Where else does Loop diuretics occur and what happens?

A
  • in the collecting duct
  • enhanced Na+ delivery results in K+ loss in the collecting duct
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25
25% of filtered Na is normally reabsorbed in?
- in the loop of Henle
26
Loop diuretics and Thiazide diuretics
- loss of Na+ & water - hypokalemic metabolic alkalosis - increased Ca2+ loss
27
Thiazide Diuretics MOA:
- hydrochlorothiazide - Inhibits Na, Cl, in the distal convoluted tubule - The lower [Na] results in more calcium reabsorption. - increased delivery of Na+ to the collecting duct
28
How does Thiazide affect calcium reabsorption?
- it inhibits Na in the convoluted tubule - the lower the [Na], the more calcium reabsorption
29
How does Thiazide influence K+?
- increased delivery of Na to the collecting duct - results in reabsorption of Na and increased excretion of K
30
10% of filtered Na is absorbed where?
- distal convoluted tubule
31
Renal Tubular Acidosis (RTA)
- pH issue in blood caused from either K+ or HCO3 - results in hyperchloremic metabolic acidosis with a normal serum anion gap - location: Bownman's capsule
32
Type 1 Renal Tubular Acidosis (RTA)
- location: Distal Tubule - impaired hydrogen ion secretion = increase hydrogen ions in blood - pH urine >5.5 - hypokalemia - renal stones (+ or -)
33
Type 2 Renal Tubular Acidosis (RTA)
- location: proximal tubule - problem with reabsorption of HCO3 - high urine pH initially; later < 5.5 - hypokalemia - bone demineralization (+ or -)
34
Type 4 Renal Tubular Acidosis (RTA)
- problem with aldosteronism - location: distal tubule - decreased aldosterone - secretion or aldosterone - resistance - urine pH <5.5 - HYPERkalemia
35
Type 1 RTA characteristics
CHHAS - hereditary - Cirrhosis - Autoimmune diseases: Sjoren, Systemic Lupus Erythematosis (SLE) - Hypercalciuria - Sickle cell
36
Type 1 RTA Drugs
- Lithium - Amphotericin B
37
Type 2 RTA Etiology
- hereditary - Fanconi's syndrome - Multiple Myeloma - Amyloidosis - Heavy Metal Poisoning
38
Type 2 RTA Drugs
- carbonic anhydrase inhibitors - vitamin D deficiency
39
Type 4 RTA Etiology
- Hypoaldosteronism - Pseudohypoaldosteronism - kidney disease
40
Type 4 RTA drugs
- ACE inhibitors (ACEI) - NSAIDs - Amiloride - Spironolactone - Heparin
41
Renal Tubular Acidosis (RTA) symptoms
- headache, weakness, Nausea, Vomiting - Kussmaul breathing
42
Transcellular Shifts Hypokalemia MOA
- Alkalosis - Beta2-adrenergic stimulation
43
Hypokalemia: Transcellular Shifts associated diseases
- refeeding syndrome - Thyrotoxicosis - Delirium tremens - select drug intoxications
44
Transcellular shifts Hypokalemia associated Medications
- insulin - Beta2-sympathomimetics - decongestants - Amphotericin B - increased activity Na/K ATPase pump
45
Albuterol Xanthines - theophyllin
- Beta2 agonist medications
46
Thyrotoxicosis
- increased sensitization of Na/K ATPase pump
47
Alkalemia
- transcellular shift in hypokalemia - exchange of H+/K+ in buffering system - vomiting, diarrhea, metabolic alkalosis
48
Refeeding syndrome
- shift to carbohydrate metabolism - ex: insulin release
49
Frequency of occurrence of Hyperkalemia [K+]
- 1% of healthy ambulatory patients - 10% of hospitalized patients - most common in elderly with impaired renal function - [K+] of >5 mEq/L - severe: [K+] >7 mEq/L
50
Causes of Hyperkalemia
- impaired excretion - transcellular shifts - pseudohyperkalemia - increased intake
51
Characteristics of Hyperkalemia
- often asymptomatic - repeat serum K+ - BUN/SCr - ABG - Serum glucose - rare [K+] intake - crush injury
52
Past Medical History for Hyperkalemia
- Physical Exam (PE): blood pressure (BP), volume status - heart disease, CKD, diabetes
53
Obtain an ECG for Hyperkalemia if:
- [K+] >6 mEq/L - has symptoms
54
Hyperkalemia PMH:
- heart disease, diabetes, CKD
55
Hyperkalemia symptoms
- MURDER - Muscle cramps - Urine abnormalities - Respiratory distress - Decreased cardiac contractility - EKG changes - Reflexes
56
Hyperkalemia Past medical history
- cardiac, renal, diabetes, liver disease
57
Hyperkalemia Medications
- ACE inhibitors - ARB - NSAIDs - K+ sparing diuretic - heparin - trimethoprim - lithium - calcineurin inhibitors - beta-blockers - digoxin - somatostatin
58
Hyperkalemia PE
- EKG: cardiac assessment - Weakness: paralysis -> neurologic assessment
59
Hyperkalemia Laboratory
- Repeat [K+] >5 mEq/L - Chem 7: BUN, CO2, SCr, glucose, Cl, K+, and Na+ - Urine electrolytes - Acid-Base status
60
Common progression of ECG changes in Hyperkalemia
- Peaked T-waves - P-wave flattening - PR-interval prolongation - widening QRS complex - Sine waves
61
Hyperkalemia: Renal Impairment
- AKI - CKD
62
Hyperkalemia: Transcellular shifts
- Rhabdomyolysis - burns - necrosis - transfusion - acidosis - low insulin, hyperosmolality - Drug-induced K+ channel activation - hyperkalemic period paralysis - beta-blockers, digitalis - hemolysis - exercise
63
Pseudohyperkalemia
- hemolysis - IV fluids containing [K+] - familial hyperkalemia - cell hyperplasia (erythro-, thrombo-, leukocytosis)
64
increased [K+] production true Hyperkalemia
- TLS - Crush injury - hemolysis
65
Decreased urinary excretion causes hyperkalemia
- acute or chronic kidney injury - Hypoaldosternonism - Pseudohypoaldosteronism - reduced distal flow/tubular delivery
66
Hypoaldosternonism
- [K+] sparing diuretics, RAAS blockage, heparin, CNI, NSAIDs
67
Causes of Pseudohyperkalemia
- Collection Technique: mechanical trauma, fist clenching, prolonged tourniquet use, delayed processing, cold sample storage, WBC K+ release during pneumatic transport (CLL) - increased Platelets WBC: [K+] release from platelets during clotting process - [K+] release from WBC with fragile membranes - Other: Heparin/EDTA tubes - Post-splenectomy - Familial pseudohyperkalemia
68
Increased intake hyperkalemia
- [K+] supplementation - Foods - RBC transfusion - [K+] salt substitutes - Drug: Penicillin G Potassium
69
Transcellular Shifts MOA: Hyperkalemia
- Na+/K+ ATPase activity results in decreased intracellular [K+] influx - increased [K+] release
70
Transcellular Shifts Hyperkalemia Medications
- Beta blockers - Somatostatin - Succinylcholine - High serum digoxin concentration
71
How is [K+] increased in hyperkalemia?
- cell breakdown/lysis - Hypertonicity - Hyperglycemia - Mannitol infusions - ALL these cause H2O efflux
72
Mannitol
- inhibits Na+ and H2O reabsorption in the proximal tubule, loop of Henle - expands ECF volume - dilutes bicarbonate - creating dilutional acidosis - resulting in hemolysis of RBC - results intracellular volume - hypernatremia risk - occurs predominately during high doses of this drug
73
Impaired Excretion: Hyperkalemia
- acute kidney injury (AKI) - chronic kidney disease - decreased distal renal flow - AKI - CKD - CHF -Cirrhosis
74
Hyperkalemia medications that lower aldosterone
- ACE inhibitors - ARB - Heparin - decreased aldosterone results in increased renin
75
Hyperkalemia medication(s) that increase aldosterone
- [K+] sparing diuretics - NSAIDs
76
Primary renal tubule defects in Hyperkalemia
- sickle cell disease - lupus (SLE) - amyloidosis (injury to distal tubule)
77
Urine [Na+] concentration in Hyperkalemia
- <20 mmol/L - decreased distal flow of Na+ and H2O
78
Disease based Hyperkalemia
MACHINE - Medications: ACEI, ARBs, K+ sparing, NSAIDs - Acidosis: Metabolic, Respiratory - Cellular destruction: Burns, Rhabdomyolosis - Hyperaldosteronism, hemolysis - Intake: excessive - Nephrons: renal failure - Excretion: impaired
79
Drug causes in Hyperkalemia
THANKSC - Trimethoprim - Heparin - ACEI, ARBs - NSAIDs - K+ sparing diuretics - Succinylcholine - Cyclosporine
80
Hypomagnesemia [Mag++] Epidemiology
- serum concentrations are NOT reliable index of total body magnesium concentrations - 42% hospitalized pts with hypokalemia have hypomagnesemia - ~65% in intensive care patients - increases mortality risk in pts in: Critically ill patients - serum [Mag++] of <1.8 mEq/L - severe: [Mag++] ~<1.25 mEq/L
81
Causes of Hypomagnesemia
- decreased intake - endocrine related - GI Loss/ Malabsorption - Increased renal loss - Endocrine related - Misc. - Lab range: 1.7 - 2.3 mg/dL
82
Summary of Hypomagnesemia: Physiologic mechanism
- Relax smooth muscles: lungs - Laxative - relax skeletal muscle: leg muscles - NMDA-Calcium blocker - Regulate heart contractility - vasodilation - regulate calcium level
83
Hypomagnesemia clues
- Neuromuscular: Weakness, tremor, muscle fasciculation, positive Chvostek's sign, positive Trousseau's sign, Dysphagia - CNS: depression, agitation, nystagmus, seizures - Cardiac: Arrythmia, ECG changes - Metabolic: hypokalemia, hypocalcemia - must correct Mag++ then K+ will correct
84
History for Hypomagnesemia
- GI diseases - chronic diarrhea - alcohol use/abuse
85
Hypomagnesemia Laboratory
- serum magnesium - consider ordering: K+, Ca++
86
Hypomagnesemia Intake MOA:
- rare except for parenteral nutrition that contains no magnesium - protein-calorie malnutrition - PPI
87
Hypomagnesemia GI Losses MOA:
- severe/ prolonged diarrhea - Crohn's disease - Ulcerative colitis - short bowel syndrome - Celiac disease - Whipple's disease
88
Hypomagnesemia Endocrine causes MOA:
- primary and secondary hyperaldosteronism - SIADH - "Hungry" bones - Diabetes mellitus
89
Hypomagnesemia Misc. MOA:
- Stress - Chronic alcoholism - excessive lactation - heat - extreme exercise - CABG
90
Causes of Hypomagnesemia
- malnutrition - malabsorption - metabolic acidosis - alcoholism - medications - proton pump inhibitors - diuretics (loop, thiazide) - cisplatin: Starts ~3 weeks in; Persistent: avg 5 months - aminoglycosides: may necrosis proximal tubule - amphotericin B - pentamidine: IV administration only
91
Where do Mag++ absorption occurs?
- thick ascending limb - and this is also where medications can impact
92
Proton pump inhibitors (PPIs)
- do NOT impact in thick ascending limb - ex: Lansoprazole, pantoprazole
93
PPIs MOA:
- inhibit Mag++ transporter
94
Loop diuretics in Hypomagnesemia MOA
- decrease Mag++ when Na+ increase
95
Loop diuretics in Hypomagnesemia location
- ascending limb
96
Amphotericin B, Aminoglycosides, Pentamidine
- decrease reabsorption in the distal tubule - decrease reabsorption in the loop of Henle
97
Calcineurin inhibitors examples:
- cyclosporine - tacrolimus - MOA: downregulation of Mag transport proteins in loop of Henle, Distal tubule
98
Epidermal growth factor receptor inhibitors
- cetuximab, panitumumab, mattuzumab - MOA: downregulation of Mag transport proteins in loop of Henle, Distal tubule
99
Hypermagnesemia epidemiology
- common in Stage 4, Stage 5 CKD - very rare - may occur if taking antacids - serum concentrations are NOT reliable index of total body [Mag++] - laboratory measures extra-cellular concentration - caused by renal failure and excessive intake of Mag++ containing antacids
100
Hypermagnesemia causes
- impaired renal function - intake: laxatives - tumor lysis syndrome - ingestion: antacids, Epsom salt - over correction: IV administration
101
Symptoms of Hypermagnesemia
- nausea - vomiting - neurologic impairment - depressed nerve function - skeletal muscle contraction - muscle weakness - bradycardia - hypotension - hypotension - EKG change: prolonged QRS, PR, QT intervals
102
Hypocalcemia epidemiology
- more common in elderly or malnourished - 15-50% incidence in intensive care patients - rarely requires emergent treatment - 40%: bound to plasma proteins, predominately albumin - unbound/ionized is the active form - correct Ca++ - ionized [Ca++] of <4.4mg/dL - total [Ca++] of <8.6 mg/dL
103
Hypocalcemia causes
- alteration in PTH effect - vitamin D deficiency - Medications/Misc.
104
Hypocalcemia symptoms
SPASMODIC - spasm - parethesia - seizures - muscle tone increased (smooth) - orientation impaired, confused - dermatitis - impetigo (rare but serious) - cardiovascular, Chvostek's sign
105
Hypocalcemia past medical history:
- CKD - Vitamin D deficiency - hypoparathyroidism
106
Hypocalcemia medications
- loop diuretics - anticonvulsants - bisphosphonates - calcitonin cinacalcet - antibiotics (INH, rifampin, foscarnet)
107
Hypocalcemia laboratory
- repeat calcium - obtain PTH - consider other labs: Mag, ABG
108
Physical exam Hypocalcemia
- Chvostek's sign: spasm of facial muscle - Trousseau's sign: carpopedal spasm
109
Hypocalcemia MOA
- decreased parathyroid hormone (PTH) dependence - increased PTH dependence
110
Decreased PTH dependence Hypocalcemia
- hypoparathyroidism - hypomagnesemia
111
Increased PTH dependence Hypocalcemia
- vitamin D deficiency - CKD - Sepsis - Tumor lysis syndrome - AKI
112
Hypocalcemia medications MOA
MOA-Chelation: Foscarnet - increased Enzyme processing of Vitamin D: - increased excretion (cinacalcet) - blocked bone resorption - induction of Hypomagnesemia
113
Which medications increase enzyme processing of vitamin D
- Phenobarbital - Phenytoin - Ketoconazole
114
Which medications increase excretion (cinacalcet)
- Furosemide
115
Which medications blocked bone resorption
- Denusomab - Bisphosphonates - Fluoride
116
Induction of Hypomagnesemia
- Aminoglycosides
117
When there is low serum Mag++ in hypocalcemia
Replete & rule out: - GI losses - renal losses - alcoholism - malnutrition - drug-induced
118
During elevated PTH level in Hypocalcemia
Secondary hyperparathyroidism etiologies: - CKD/ESRD - Malabsorption - Vit D deficiency or resistance - Pseudohypoparathyroidism (PTH resistance)
119
Inappropriately Normal/Low PTH level in Hypocalcemia
Evaluate for hypoparathyroidism: - destruction of parathyroid glands (ex: thyroid surgery, autoimmune) - irradiation - infiltrative disease (very rare)
120
Low serum 25-OH Vit in Hypocalcemia
Replete and Rule out: - GI losses - low dietary intake - low sunlight
121
Other causes of hypocalcemia
- acute pancreatitis - sepsis/severe illness - hyperphosphatemia (Ca++ deposited in bone) - large volumes of blood (citrate chelates Ca++)
122
Epidemiology of Hypercalcemia [Ca++]
- Hyperparathyroidism: more common in women, age > 50 years - Cancer causing: dependent on tumor type, occurs in 15-70% - ~15-50% incidence in intensive care patients - total serum [Ca++] of > 10.2 mg/dL - Severe ≥ 13 mg/dL - Crisis ≥ 15 mg/dL
123
Hypercalcemia causes
- increased bone resorption - increased GI reabsorption - tubular reabsorption (renal)
124
Hypercalcemia symptoms
- fatigue/weakness - Polyuria/polydipsia/nocturia - anorexia - depression - anxiety
125
Hypercalcemia signs
- Nephrolithiasis - Acute or chronic kidney disease - severe: ventricular arrythmias - calcification in tissues
126
Hypercalcemia causes (2)
CHIMPANZEE - Calcium supplements - Hyperparathyroidism - Immobilization, iatrogenic - Multiple myeloma, Milk alkali syndrome (ex: lithium) - Parathyroid hyperplasia - Alcohol - Neoplasm (breast or lung cancer) - Zollinger Ellison syndrome - Excessive vitamin D - Excessive vitamin A - Sarcoidosis
127
Hypercalcemia causes (3)
BACKME - Bone pain - Arrhythmias - Cardiac arrest - Kidney stones - Muscle weakness - Excessive urination
128
Hypercalcemia Endocrine disease MOA
- adrenal insufficiency - Hyperthyroidism - Acromegaly
129
Hypercalcemia Medications
- Thiazide diuretics - Lithium - Vit D - Vit A - Calcium - Aluminum/magnesium - antacids - Theophylline - Tamoxifen - Ganciclovir
130
Hypercalcemia Neoplasms MOA
- bone metastasis - breast - lung - head/neck/esophagus - multiple myeloma - lymphoma - leukemia
131
Hypophosphatemia Epidemiology
- rare in ambulatory persons - 18-28%n incidence in critically ill pts - Serum [PO4-] of < 2.7 mg/dL - Severe < 1.5 mg/dL
132
Hypophosphatemia causes
- decreased GI absorption - increased Renal excretion - metabolic causes - medications
133
Hypophosphatemia decreased GI Absorption
- alcoholism - Vit D deficiency - malabsorption - excess intake aluminum based antacids - parenteral nutrition - fasting/starvation
134
Hypophosphatemia: Increased Renal excretion
- Hyperparathyroidism - DKA - Osteomalacia - RTA - ATN - Hypokalemia, hypomagnesium - multiple myeloma - Fanconi syndrome
135
Hypophosphatemia: Metabolic
- Respiratory alkalosis - Hungry bone - DKA - Refeeding syndrome
136
Mild hypophosphatemia
- mostly asymptomatic - MOA: decreased [PO4-] results in increased Hgb for oxygen, creates tighter connection, doesn't release in muscle - decrease phosphate results in decrease in ATP that impacts function of leukocytes, platelets, encephalopathy, cardiomyopathy
137
Hyperphosphatemia causes
- acute phosphate load - transcellular shit - decreased renal shift - pseudohyperphosphatemia - Serum [PO4-] > 4.5 mg/dL
138
Hyperphosphatemia symptoms
- Tetany - seizures - hypotension - calcifications in soft tissue
139
Hyperphosphatemia: decreased renal excretion
- renal failure (acute, chronic) - Hypoparathyroidism - Thyrotoxicosis
140
Hyperphosphatemia: Transcellular shift
- acidosis - leukemia - lymphoma - tissue ischemia
141
Hyperphosphatemia: Acute phosphate load
- phosphate enemas, laxatives - tumor lysis syndrome - Vit D intoxication - Hemolysis: transfusion, rhabdomyolysis
142
Pseudohyperphosphatemia
Endogenous: - hemolysis - hyperlipidemia - hyperbilirubinemia Exogenous: - Amphotericin B - Heparin - Tissue plasminogen activator
143
Calcitonin release
- decreases serum calcium
144
PTH release results in?
- works on bone and kidney to increase serum calcium

Pathophysiology I (4 decks)

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