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Pathophysiology I > Pathophysiology: Electrolyte Disorders > Flashcards

Pathophysiology: Electrolyte Disorders Flashcards

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
Q

25% of filtered Na is normally reabsorbed in?

A
  • in the loop of Henle
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26
Q

Loop diuretics and Thiazide diuretics

A
  • loss of Na+ & water
  • hypokalemic metabolic alkalosis
  • increased Ca2+ loss
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27
Q

Thiazide Diuretics MOA:

A
  • 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
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28
Q

How does Thiazide affect calcium reabsorption?

A
  • it inhibits Na in the convoluted tubule
  • the lower the [Na], the more calcium reabsorption
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29
Q

How does Thiazide influence K+?

A
  • increased delivery of Na to the collecting duct
  • results in reabsorption of Na and increased excretion of K
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30
Q

10% of filtered Na is absorbed where?

A
  • distal convoluted tubule
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31
Q

Renal Tubular Acidosis (RTA)

A
  • 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
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32
Q

Type 1 Renal Tubular Acidosis (RTA)

A
  • location: Distal Tubule
  • impaired hydrogen ion secretion = increase hydrogen ions in blood
  • pH urine >5.5
  • hypokalemia
  • renal stones (+ or -)
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33
Q

Type 2 Renal Tubular Acidosis (RTA)

A
  • location: proximal tubule
  • problem with reabsorption of HCO3
  • high urine pH initially; later < 5.5
  • hypokalemia
  • bone demineralization (+ or -)
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34
Q

Type 4 Renal Tubular Acidosis (RTA)

A
  • problem with aldosteronism
  • location: distal tubule
  • decreased aldosterone
  • secretion or aldosterone
  • resistance
  • urine pH <5.5
  • HYPERkalemia
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35
Q

Type 1 RTA characteristics

A

CHHAS

  • hereditary
  • Cirrhosis
  • Autoimmune diseases: Sjoren, Systemic Lupus Erythematosis (SLE)
  • Hypercalciuria
  • Sickle cell
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36
Q

Type 1 RTA Drugs

A
  • Lithium
  • Amphotericin B
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37
Q

Type 2 RTA Etiology

A
  • hereditary
  • Fanconi’s syndrome
  • Multiple Myeloma
  • Amyloidosis
  • Heavy Metal Poisoning
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38
Q

Type 2 RTA Drugs

A
  • carbonic anhydrase inhibitors
  • vitamin D deficiency
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39
Q

Type 4 RTA Etiology

A
  • Hypoaldosteronism
  • Pseudohypoaldosteronism
  • kidney disease
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40
Q

Type 4 RTA drugs

A
  • ACE inhibitors (ACEI)
  • NSAIDs
  • Amiloride
  • Spironolactone
  • Heparin
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41
Q

Renal Tubular Acidosis (RTA) symptoms

A
  • headache, weakness, Nausea, Vomiting
  • Kussmaul breathing
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42
Q

Transcellular Shifts Hypokalemia MOA

A
  • Alkalosis
  • Beta2-adrenergic stimulation
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43
Q

Hypokalemia: Transcellular Shifts associated diseases

A
  • refeeding syndrome
  • Thyrotoxicosis
  • Delirium tremens
  • select drug intoxications
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44
Q

Transcellular shifts Hypokalemia associated Medications

A
  • insulin
  • Beta2-sympathomimetics
  • decongestants
  • Amphotericin B
  • increased activity Na/K ATPase pump
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45
Q

Albuterol
Xanthines - theophyllin

A
  • Beta2 agonist medications
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46
Q

Thyrotoxicosis

A
  • increased sensitization of Na/K ATPase pump
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47
Q

Alkalemia

A
  • transcellular shift in hypokalemia
  • exchange of H+/K+ in buffering system
  • vomiting, diarrhea, metabolic alkalosis
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48
Q

Refeeding syndrome

A
  • shift to carbohydrate metabolism
  • ex: insulin release
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49
Q

Frequency of occurrence of Hyperkalemia [K+]

A
  • 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
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50
Q

Causes of Hyperkalemia

A
  • impaired excretion
  • transcellular shifts
  • pseudohyperkalemia
  • increased intake
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51
Q

Characteristics of Hyperkalemia

A
  • often asymptomatic
  • repeat serum K+
  • BUN/SCr
  • ABG
  • Serum glucose
  • rare [K+] intake
  • crush injury
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52
Q

Past Medical History for Hyperkalemia

A
  • Physical Exam (PE): blood pressure (BP), volume status
  • heart disease, CKD, diabetes
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53
Q

Obtain an ECG for Hyperkalemia if:

A
  • [K+] >6 mEq/L
  • has symptoms
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54
Q

Hyperkalemia PMH:

A
  • heart disease, diabetes, CKD
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55
Q

Hyperkalemia symptoms

A
  • MURDER
  • Muscle cramps
  • Urine abnormalities
  • Respiratory distress
  • Decreased cardiac contractility
  • EKG changes
  • Reflexes
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56
Q

Hyperkalemia Past medical history

A
  • cardiac, renal, diabetes, liver disease
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57
Q

Hyperkalemia Medications

A
  • ACE inhibitors
  • ARB
  • NSAIDs
  • K+ sparing diuretic
  • heparin
  • trimethoprim
  • lithium
  • calcineurin inhibitors
  • beta-blockers
  • digoxin
  • somatostatin
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58
Q

Hyperkalemia PE

A
  • EKG: cardiac assessment
  • Weakness: paralysis -> neurologic assessment
59
Q

Hyperkalemia Laboratory

A
  • Repeat [K+] >5 mEq/L
  • Chem 7: BUN, CO2, SCr, glucose, Cl, K+, and Na+
  • Urine electrolytes
  • Acid-Base status
60
Q

Common progression of ECG changes in Hyperkalemia

A
  • Peaked T-waves
  • P-wave flattening
  • PR-interval prolongation
  • widening QRS complex
  • Sine waves
61
Q

Hyperkalemia: Renal Impairment

A
  • AKI
  • CKD
62
Q

Hyperkalemia: Transcellular shifts

A
  • Rhabdomyolysis
  • burns
  • necrosis
  • transfusion
  • acidosis
  • low insulin, hyperosmolality
  • Drug-induced K+ channel activation
  • hyperkalemic period paralysis
  • beta-blockers, digitalis
  • hemolysis
  • exercise
63
Q

Pseudohyperkalemia

A
  • hemolysis
  • IV fluids containing [K+]
  • familial hyperkalemia
  • cell hyperplasia (erythro-, thrombo-, leukocytosis)
64
Q

increased [K+] production true Hyperkalemia

A
  • TLS
  • Crush injury
  • hemolysis
65
Q

Decreased urinary excretion causes hyperkalemia

A
  • acute or chronic kidney injury
  • Hypoaldosternonism
  • Pseudohypoaldosteronism
  • reduced distal flow/tubular delivery
66
Q

Hypoaldosternonism

A
  • [K+] sparing diuretics, RAAS blockage, heparin, CNI, NSAIDs
67
Q

Causes of Pseudohyperkalemia

A
  • 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
Q

Increased intake hyperkalemia

A
  • [K+] supplementation
  • Foods
  • RBC transfusion
  • [K+] salt substitutes
  • Drug: Penicillin G Potassium
69
Q

Transcellular Shifts MOA: Hyperkalemia

A
  • Na+/K+ ATPase activity results in decreased intracellular [K+] influx
  • increased [K+] release
70
Q

Transcellular Shifts Hyperkalemia Medications

A
  • Beta blockers
  • Somatostatin
  • Succinylcholine
  • High serum digoxin concentration
71
Q

How is [K+] increased in hyperkalemia?

A
  • cell breakdown/lysis
  • Hypertonicity
  • Hyperglycemia
  • Mannitol infusions
  • ALL these cause H2O efflux
72
Q

Mannitol

A
  • 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
Q

Impaired Excretion: Hyperkalemia

A
  • acute kidney injury (AKI)
  • chronic kidney disease
  • decreased distal renal flow
  • AKI - CKD - CHF -Cirrhosis
74
Q

Hyperkalemia medications that lower aldosterone

A
  • ACE inhibitors
  • ARB
  • Heparin
  • decreased aldosterone results in increased renin
75
Q

Hyperkalemia medication(s) that increase aldosterone

A
  • [K+] sparing diuretics
  • NSAIDs
76
Q

Primary renal tubule defects in Hyperkalemia

A
  • sickle cell disease
  • lupus (SLE)
  • amyloidosis (injury to distal tubule)
77
Q

Urine [Na+] concentration in Hyperkalemia

A
  • <20 mmol/L
  • decreased distal flow of Na+ and H2O
78
Q

Disease based Hyperkalemia

A

MACHINE
- Medications: ACEI, ARBs, K+ sparing, NSAIDs
- Acidosis: Metabolic, Respiratory
- Cellular destruction: Burns, Rhabdomyolosis
- Hyperaldosteronism, hemolysis
- Intake: excessive
- Nephrons: renal failure
- Excretion: impaired

79
Q

Drug causes in Hyperkalemia

A

THANKSC
- Trimethoprim
- Heparin
- ACEI, ARBs
- NSAIDs
- K+ sparing diuretics
- Succinylcholine
- Cyclosporine

80
Q

Hypomagnesemia [Mag++] Epidemiology

A
  • 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
Q

Causes of Hypomagnesemia

A
  • decreased intake
  • endocrine related
  • GI Loss/ Malabsorption
  • Increased renal loss
  • Endocrine related
  • Misc.
  • Lab range: 1.7 - 2.3 mg/dL
82
Q

Summary of Hypomagnesemia: Physiologic mechanism

A
  • Relax smooth muscles: lungs
  • Laxative
  • relax skeletal muscle: leg muscles
  • NMDA-Calcium blocker
  • Regulate heart contractility
  • vasodilation
  • regulate calcium level
83
Q

Hypomagnesemia clues

A
  • 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
Q

History for Hypomagnesemia

A
  • GI diseases
  • chronic diarrhea
  • alcohol use/abuse
85
Q

Hypomagnesemia Laboratory

A
  • serum magnesium
  • consider ordering: K+, Ca++
86
Q

Hypomagnesemia Intake MOA:

A
  • rare except for parenteral nutrition that contains no magnesium
  • protein-calorie malnutrition
  • PPI
87
Q

Hypomagnesemia GI Losses MOA:

A
  • severe/ prolonged diarrhea
  • Crohn’s disease
  • Ulcerative colitis
  • short bowel syndrome
  • Celiac disease
  • Whipple’s disease
88
Q

Hypomagnesemia Endocrine causes MOA:

A
  • primary and secondary hyperaldosteronism
  • SIADH
  • “Hungry” bones
  • Diabetes mellitus
89
Q

Hypomagnesemia Misc. MOA:

A
  • Stress
  • Chronic alcoholism
  • excessive lactation
  • heat
  • extreme exercise
  • CABG
90
Q

Causes of Hypomagnesemia

A
  • 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
Q

Where do Mag++ absorption occurs?

A
  • thick ascending limb
  • and this is also where medications can impact
92
Q

Proton pump inhibitors (PPIs)

A
  • do NOT impact in thick ascending limb
  • ex: Lansoprazole, pantoprazole
93
Q

PPIs MOA:

A
  • inhibit Mag++ transporter
94
Q

Loop diuretics in Hypomagnesemia MOA

A
  • decrease Mag++ when Na+ increase
95
Q

Loop diuretics in Hypomagnesemia location

A
  • ascending limb
96
Q

Amphotericin B, Aminoglycosides, Pentamidine

A
  • decrease reabsorption in the distal tubule
  • decrease reabsorption in the loop of Henle
97
Q

Calcineurin inhibitors examples:

A
  • cyclosporine
  • tacrolimus
  • MOA: downregulation of Mag transport proteins in loop of Henle, Distal tubule
98
Q

Epidermal growth factor receptor inhibitors

A
  • cetuximab, panitumumab, mattuzumab
  • MOA: downregulation of Mag transport proteins in loop of Henle, Distal tubule
99
Q

Hypermagnesemia epidemiology

A
  • 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
Q

Hypermagnesemia causes

A
  • impaired renal function
  • intake: laxatives
  • tumor lysis syndrome
  • ingestion: antacids, Epsom salt
  • over correction: IV administration
101
Q

Symptoms of Hypermagnesemia

A
  • nausea
  • vomiting
  • neurologic impairment
  • depressed nerve function
  • skeletal muscle contraction
  • muscle weakness
  • bradycardia
  • hypotension
  • hypotension
  • EKG change: prolonged QRS, PR, QT intervals
102
Q

Hypocalcemia epidemiology

A
  • 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
Q

Hypocalcemia causes

A
  • alteration in PTH effect
  • vitamin D deficiency
  • Medications/Misc.
104
Q

Hypocalcemia symptoms

A

SPASMODIC
- spasm
- parethesia
- seizures
- muscle tone increased (smooth)
- orientation impaired, confused
- dermatitis
- impetigo (rare but serious)
- cardiovascular, Chvostek’s sign

105
Q

Hypocalcemia past medical history:

A
  • CKD
  • Vitamin D deficiency
  • hypoparathyroidism
106
Q

Hypocalcemia medications

A
  • loop diuretics
  • anticonvulsants
  • bisphosphonates
  • calcitonin cinacalcet
  • antibiotics (INH, rifampin, foscarnet)
107
Q

Hypocalcemia laboratory

A
  • repeat calcium
  • obtain PTH
  • consider other labs: Mag, ABG
108
Q

Physical exam Hypocalcemia

A
  • Chvostek’s sign: spasm of facial muscle
  • Trousseau’s sign: carpopedal spasm
109
Q

Hypocalcemia MOA

A
  • decreased parathyroid hormone (PTH) dependence
  • increased PTH dependence
110
Q

Decreased PTH dependence Hypocalcemia

A
  • hypoparathyroidism
  • hypomagnesemia
111
Q

Increased PTH dependence Hypocalcemia

A
  • vitamin D deficiency
  • CKD
  • Sepsis
  • Tumor lysis syndrome
  • AKI
112
Q

Hypocalcemia medications MOA

A

MOA-Chelation: Foscarnet
- increased Enzyme processing of Vitamin D:
- increased excretion (cinacalcet)
- blocked bone resorption
- induction of Hypomagnesemia

113
Q

Which medications increase enzyme processing of vitamin D

A
  • Phenobarbital
  • Phenytoin
  • Ketoconazole
114
Q

Which medications increase excretion (cinacalcet)

A
  • Furosemide
115
Q

Which medications blocked bone resorption

A
  • Denusomab
  • Bisphosphonates
  • Fluoride
116
Q

Induction of Hypomagnesemia

A
  • Aminoglycosides
117
Q

When there is low serum Mag++ in hypocalcemia

A

Replete & rule out:
- GI losses
- renal losses
- alcoholism
- malnutrition
- drug-induced

118
Q

During elevated PTH level in Hypocalcemia

A

Secondary hyperparathyroidism etiologies:
- CKD/ESRD
- Malabsorption
- Vit D deficiency or resistance
- Pseudohypoparathyroidism (PTH resistance)

119
Q

Inappropriately Normal/Low PTH level in Hypocalcemia

A

Evaluate for hypoparathyroidism:
- destruction of parathyroid glands (ex: thyroid surgery, autoimmune)
- irradiation
- infiltrative disease (very rare)

120
Q

Low serum 25-OH Vit in Hypocalcemia

A

Replete and Rule out:
- GI losses
- low dietary intake
- low sunlight

121
Q

Other causes of hypocalcemia

A
  • acute pancreatitis
  • sepsis/severe illness
  • hyperphosphatemia (Ca++ deposited in bone)
  • large volumes of blood (citrate chelates Ca++)
122
Q

Epidemiology of Hypercalcemia [Ca++]

A
  • 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
Q

Hypercalcemia causes

A
  • increased bone resorption
  • increased GI reabsorption
  • tubular reabsorption (renal)
124
Q

Hypercalcemia symptoms

A
  • fatigue/weakness
  • Polyuria/polydipsia/nocturia
  • anorexia
  • depression
  • anxiety
125
Q

Hypercalcemia signs

A
  • Nephrolithiasis
  • Acute or chronic kidney disease
  • severe: ventricular arrythmias
  • calcification in tissues
126
Q

Hypercalcemia causes (2)

A

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
Q

Hypercalcemia causes (3)

A

BACKME
- Bone pain
- Arrhythmias
- Cardiac arrest
- Kidney stones
- Muscle weakness
- Excessive urination

128
Q

Hypercalcemia Endocrine disease MOA

A
  • adrenal insufficiency
  • Hyperthyroidism
  • Acromegaly
129
Q

Hypercalcemia Medications

A
  • Thiazide diuretics
  • Lithium
  • Vit D
  • Vit A
  • Calcium
  • Aluminum/magnesium
  • antacids
  • Theophylline
  • Tamoxifen
  • Ganciclovir
130
Q

Hypercalcemia Neoplasms MOA

A
  • bone metastasis
  • breast
  • lung
  • head/neck/esophagus
  • multiple myeloma
  • lymphoma
  • leukemia
131
Q

Hypophosphatemia Epidemiology

A
  • 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
Q

Hypophosphatemia causes

A
  • decreased GI absorption
  • increased Renal excretion
  • metabolic causes
  • medications
133
Q

Hypophosphatemia decreased GI Absorption

A
  • alcoholism
  • Vit D deficiency
  • malabsorption
  • excess intake aluminum based antacids
  • parenteral nutrition
  • fasting/starvation
134
Q

Hypophosphatemia: Increased Renal excretion

A
  • Hyperparathyroidism
  • DKA
  • Osteomalacia
  • RTA
  • ATN
  • Hypokalemia, hypomagnesium
  • multiple myeloma
  • Fanconi syndrome
135
Q

Hypophosphatemia: Metabolic

A
  • Respiratory alkalosis
  • Hungry bone
  • DKA
  • Refeeding syndrome
136
Q

Mild hypophosphatemia

A
  • 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
Q

Hyperphosphatemia causes

A
  • acute phosphate load
  • transcellular shit
  • decreased renal shift
  • pseudohyperphosphatemia
  • Serum [PO4-] > 4.5 mg/dL
138
Q

Hyperphosphatemia symptoms

A
  • Tetany
  • seizures
  • hypotension
  • calcifications in soft tissue
139
Q

Hyperphosphatemia: decreased renal excretion

A
  • renal failure (acute, chronic)
  • Hypoparathyroidism
  • Thyrotoxicosis
140
Q

Hyperphosphatemia: Transcellular shift

A
  • acidosis
  • leukemia
  • lymphoma
  • tissue ischemia
141
Q

Hyperphosphatemia: Acute phosphate load

A
  • phosphate enemas, laxatives
  • tumor lysis syndrome
  • Vit D intoxication
  • Hemolysis: transfusion, rhabdomyolysis
142
Q

Pseudohyperphosphatemia

A

Endogenous:
- hemolysis
- hyperlipidemia
- hyperbilirubinemia

Exogenous:
- Amphotericin B
- Heparin
- Tissue plasminogen activator

143
Q

Calcitonin release

A
  • decreases serum calcium
144
Q

PTH release results in?

A
  • works on bone and kidney to increase serum calcium

Pathophysiology I (4 decks)

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