CASE STUDIES LAB
Goals:
To use your physiology knowledge and critical thinking skills to analyze patient cases.
Background:
Case studies allow in-depth exploration of physiology in a format that is applicable to your future career as a health care professional. In this lab, you will work in a group to research and analyze several patient cases.
Electrolyte physiology
Electrolytes
are ions that perform a number of body functions. Some ions play a role in the
transmission of electrical impulses. Others help stabilize protein structures.
Many of the ions contribute to osmotic pressure across cell membranes.
Electrolytes that play important roles in the body are sodium (Na+),
potassium (K+), calcium (Ca2+), chloride
(Cl–), phosphate (PO43-),
and magnesium (Mg2+). Health care practitioners must understand
electrolyte balance because it is critical to patient health, and indicates
whether a patient can function normally, and/or function safely. The following
lists common electrolyte imbalances, their causes, consequences, and
mechanisms.
Sodium function: Main extracellular fluid cation, maintains extracellular fluid concentration, primary determinant of extracellular osmolality, transmits nerve and muscle impulses
Hyponatremia
Causes:
- Hypovolumetric hyponatremia –vomiting, diarrhea, diuretics
- Hypervolumetric hyponatremia – excess water accumulation (excess drinking, edema), kidney failure
- Adrenal gland insufficiency
Consequences: lethargy, confusion, diminished reflexes, fatigue, nausea, vomit, seizures, coma, orthostatic hypotension and tachycardia (if hypovolumetric), pitting edema (if hypervolumetric)
Mechanism : cells are in a hypotonic solution, so they gain water, swell, and no longer function well
Hypernatremia
Causes:
- Hypovolumetric – drinking too little water, excessive sweating, diuretics, diabetes, vomit, diarrhea, kidney disease
- Hypervolumetric – hyperaldosteronism, drinking seawater
- Diabetes insipidus
Consequences: irritability, confusion, seizure, coma, hypotension, tachycardia, weakness
Mechanism: cells are in a hypertonic solution, so they lose water, crenate, and no longer function well
Potassium function: Major intracellular cation, helps maintain intracellular osmolality, regulates cell excitability, affects membrane potential
Hypokalemia
Causes: starvation, diuretics, vomiting, diarrhea, kidney disease, excessive sweating, hyperaldosteronism
Consequences: weakness, hyporeflexia, paresthesia, dysrhythmias, cardiac arrest
Mechanism: low potassium causes hyperpolarization of cells, making it harder to produce action potentials, including in the heart
Hyperkalemia
Causes: kidney disease, adrenal insufficiency, ACE inhibitors, dehydration, excessive potassium supplements, diuresis
Consequences: confusion, numbness, weakness, flaccid paralysis, dysrhythmias, cardiac arrest
Mechanism: high potassium
depolarizes cells, making repolarization difficult or impossible, including in
the heart
Chloride function: Main extracellular anion, helps maintain extracellular osmolality, associated directly with sodium and inversely with bicarbonate
Hypochloremia
Causes: defective renal tubular absorption, vomiting, diarrhea
Consequence: not many symptoms due to hypochloremia alone, but symptoms due to associated disorders – irritability, hyperreflexia, cramping
Hyperchloremia
Causes: dehydration, sweating, vomiting, diarrhea, kidney failure, diuretics, excessive intake of NaCl, diabetes insipidus
Consequences: not many symptoms due to hyperchloremia alone, but symptoms due to associated disorders – lethargy, reduced consciousness, weakness, edema, tachypnea, hypertension, tachycardia
Calcium function: Bone and tooth density, activates some enzymes, affects cell membrane permeability and threshold of some channels, needed for muscle contraction and signaling at chemical synapse
Hypocalcemia
Causes: hypoparathyroidism, eating disorders, osteoporosis treatment, kidney failure, vit D deficiency, alkalosis
Consequences: confusion, irritability, seizures, dysrhythmias, fatigue, paresthesia, hyperreflexia, muscle cramps
Mechanism:
- Neuromuscular – calcium usually inhibits some V-gated sodium channels, lowering the threshold for depolarization. When Ca++ is low, sodium channels reach threshold more easily, and neurons and muscles fire action potentials more easily
- Alkalosis – blood H+ and Ca2+ compete for albumin carriers. As blood H+ decreases, more albumin binding sites are freed up, Ca2+ binds, and less Ca2+ is available
Hypercalcemia
Causes: Hyperparathyroidism, cancer, immobility, severe dehydration, excessive supplements
Consequences: dysrhythmias, asystole, coma, lethargy, weakness, diminished reflexes, nausea, vomiting
Mechanism: Ca2+ usually inhibits some V-gated sodium channels, lowering the threshold for
depolarization. When Ca2+ is high, sodium channels are farther from
threshold, and neurons and muscles fire fewer action potentials
Phosphate function: major intracellular anion, promotes energy storage and cell membrane structure, binds calcium, serves as a buffer
Hypophosphatemia
Causes: use of antacids, alcohol withdrawal, malnourishment, hyperparathyroidism
Consequences: same as hypercalcemia plus instability of cell membranes, left shift of oxyhemoglobin dissociation curve
Mechanism:
- Calcium related effects- phosphate binds calcium, so when phosphate is low, more calcium is free
- Instability of membranes – low phosphate, low phospholipids and ATP
- L shift: decreased production of 2,3 DPG
Hyperphosphatemia
Causes: decreased renal function, hypoparathyroidism, or extensive cell destruction (hemolysis, crush injuries etc.)
Consequence: same as hypercalcemia
Mechanism:
- Calcium related effects- phosphate binds calcium, so when phosphate is high, more calcium is bound
Magnesium function: contributes to enzyme and metabolic processes, modifies nerve impulse transmission and skeletal muscle response
Hypomagnesemia
Causes: alcoholism, starvation, diarrhea, diuretics, decreased intestinal absorption
Consequences: irritability, hyperreflexia, spasms, seizures, paresthesia, dysrhythmias, nystagmus
Mechanism:
- Neuromuscular – magnesium competitively inhibits calcium influx into the presynaptic nerve channels via the voltage-dependent calcium channel and thus decreases neurotransmitter release, so low magnesium increases neurotransmitter release
Hypermagnesemia
Causes: kidney failure, taking magnesium-containing medications like some antacids and laxatives, hemolysis (RBC contain high Mg2+)
Consequences: diaphoresis, nausea, vomit, lethargy, weakness, flaccidity, brachycardia, apnea, hypotension, cardiac arrest
Mechanism:
- Neuromuscular – magnesium competitively inhibits calcium influx into the presynaptic nerve channels via the voltage-dependent calcium channel and thus decreases neurotransmitter release
Case 1
Cindy Brown is a 80 year old widow who was brought into the emergency room one evening by her brother. Early in the day, Mrs. Brown had seen bright red blood in her stool. She continued with her daily activities: she cleaned her house in the morning, had lunch with her daughter, and volunteered at the local library. However, the bleeding continued all day, and she started feeling light-headed. By dinnertime she decided to ask her brother for help. Mrs. Brown does not smoke or drink alcoholic beverages. She takes aspirin, as needed, for arthritis.
In the emergency room, Mrs. Brown is confused and anxious. Her skin is pale, cool, and moist. Her pulse is 106, regular, and weak. Her respirations are 22, regular, normal volume, and unlabored. Her blood pressure is 90/60 supine. The nurse takes a standing blood pressure as well, and it is 75/45. Her hematocrit is 29%.
A colonoscopy shows that the bleeding came from a herniation in the colonic wall. Mrs. Brown’s physician orders a normal saline infusion, which the nurse starts, and a blood sample to be drawn to be typed to prepare for a blood transfusion. Mrs. Brown receives two units of whole blood, and is admitted for observation. She is instructed not to take aspirin.
Questions:
- Describe the body’s sequence of events that led to Mrs. Brown becoming light-headed and needing to seek help.
- Discuss the physiological reason for each of the signs that you assessed (skin, pulse, respiration, blood pressure, hematocrit).
- Discuss the rationale behind each of the treatments provided (normal saline, blood transfusion, no aspirin).
- Had her blood loss been more severe, Mrs. Brown might have received a low dose of dopamine. Why is low-dose dopamine helpful in the treatment of hypovolemic shock?
Case 4
Seth Johnson is a 54 year old college physics professor with a history of coronary artery disease who was admitted to the hospital for increasing lower extremity edema, abdominal swelling, and shortness of breath. Professor Johnson noted a 30-pound weight gain over the past month, and during the past week he has had three-pillow orthopnea.
Professor Johnson is in moderate respiratory distress in the hospital. His skin is cool, pale, and clammy. His pulse is 95, irregular, and weak. His respirations are 28, regular, adequate volume, labored, with bilateral rales. His blood pressure is 140/80. His abdomen is enlarged, and lower extremities are remarkable for pitting edema. His physician orders laboratory tests, results are as follows:
Plasma Na+: 133 mEq/L (normal 136-140 mEq/L)
Plasma K+: 6.0 mEq/L (normal 3.5-5.3 mEq/L)
Plasma Cl–: 93 mEq/L (normal 98-108 mEq/L)
Plasma HCO3–: 16 mEq/L (normal 24 mEq/L)
Plasma Creatinine: 3.7 mg/dLL (normal 0.7-1.5 mg/dL)
Plasma PO43-: 6.8 mg/dL (normal 2.7-4.5 mg/dL)
pCO2: 36 mmHg (normal 40 mmHg)
Blood urea nitrogen: 101 mg/dL (normal 7-22 mg/dL)
pH: 7.25
SpO2: 96%
Upon evaluation of the findings, Professor Johnson’s physician diagnoses him with both congestive heart failure and acute renal failure.
Questions:
- Discuss Professor Johnson’s signs and symptoms in the context of his diagnoses (edema, weight gain, skin, pulse, respiration, shortness of breath, blood pressure).
- Discuss Professor Johnson’s electrolyte levels in the context of his diagnoses (Na+ K+ PO43-). Why are these findings common in acute renal failure? When a health care practitioner reads these values, what might they expect in terms of his behavior or ability to move? (Hint for PO43-: it binds with calcium, so the effects of high phosphate are similar to those of low calcium)
- Why are congestive heart failure and renal failure often found together?
- Which acid-base disorder does he have? What caused it? What is the compensation? (identify laboratory values)
