Anatomy and Physiology – RN Flashcards

Registered nurse level flashcards for Anatomy and Physiology. These emphasize mechanism, integration across systems, and the clinical judgment the mechanism supports.

Cellular and Fluid Concepts

What does the sodium-potassium pump do, and why does it matter clinically?

It uses ATP to move three sodium ions out of the cell for every two potassium ions in, maintaining the resting membrane potential. Every nerve impulse, muscle contraction, and cardiac action potential depends on it, so ATP depletion in shock or hypoxia leads to cellular swelling and loss of excitable tissue function.

Define preload, afterload, and contractility.

Preload is the volume stretching the ventricle at end diastole. Afterload is the resistance the ventricle must overcome to eject. Contractility is the intrinsic force of contraction independent of preload and afterload. Stroke volume is determined by all three.

State the Frank-Starling law and its clinical limit.

Within physiologic limits, greater ventricular stretch produces a more forceful contraction. Beyond that point, in a failing or overstretched ventricle, further volume decreases stroke volume, which is why fluid loading worsens decompensated heart failure.

Explain why hypotonic fluids are contraindicated in traumatic brain injury.

Hypotonic solutions such as 0.45% sodium chloride lower extracellular osmolality, so water shifts into cells, including brain cells. In a fixed cranial vault this increases cerebral edema and intracranial pressure.

Why can a patient with a low serum albumin be visibly edematous and still be intravascularly volume depleted?

Starling forces. Capillary hydrostatic pressure pushes fluid out; plasma oncotic pressure, mostly from albumin, pulls it back. Low albumin lowers oncotic pressure, so fluid stays interstitially and the patient can be edematous while intravascularly depleted.

Cardiovascular

Why does tachycardia worsen myocardial ischemia?

The coronary arteries perfuse during diastole. As heart rate rises, diastole shortens disproportionately, so coronary perfusion and ventricular filling both fall at the moment myocardial oxygen demand is highest.

Contrast the presentation of left-sided and right-sided heart failure and explain the mechanism.

Left-sided failure backs blood into the pulmonary circulation, producing dyspnea, orthopnea, paroxysmal nocturnal dyspnea, crackles, and pink frothy sputum. Right-sided failure backs blood into the systemic venous system, producing jugular venous distention, peripheral edema, hepatomegaly, ascites, and weight gain.

Trace the renin-angiotensin-aldosterone system and name two drug classes that interrupt it.

Reduced renal perfusion triggers renin release, which cleaves angiotensinogen to angiotensin I; angiotensin-converting enzyme converts it to angiotensin II, a potent vasoconstrictor that stimulates aldosterone, causing sodium and water retention and potassium excretion. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers interrupt it, and both can cause hyperkalemia.

Why does compensated shock present with a normal blood pressure?

Baroreceptor-mediated sympathetic activation raises heart rate, contractility, and systemic vascular resistance, maintaining blood pressure until compensation fails. Tachycardia, narrowed pulse pressure, cool clammy skin, restlessness, and falling urine output appear before hypotension.

Neurologic

State the Monro-Kellie doctrine.

The skull is a rigid container holding brain tissue, blood, and cerebrospinal fluid at a fixed total volume. An increase in any component must be offset by a decrease in another, or intracranial pressure rises. Normal adult intracranial pressure is about 5 to 15 mmHg.

What is the earliest and most sensitive sign of increasing intracranial pressure, and what is the late triad?

The earliest sign is a change in level of consciousness. The late finding is the Cushing triad: widening pulse pressure with rising systolic pressure, bradycardia, and irregular respirations, which indicates brainstem compression.

Which cranial nerves must be intact for safe swallowing?

IX (glossopharyngeal) and X (vagus) for the gag reflex and pharyngeal phase, and XII (hypoglossal) for tongue control of the bolus. Impairment of any of these creates aspiration risk.

Describe autonomic dysreflexia and the first nursing action.

An exaggerated sympathetic response to a noxious stimulus below a spinal cord injury at or above T6, causing severe hypertension, pounding headache, bradycardia, flushing above the lesion, and pallor below it. The first action is to sit the patient upright, then find and remove the trigger, most often bladder distention or fecal impaction.

Respiratory and Acid-Base

Distinguish oxygenation from ventilation and give the corresponding measurements.

Oxygenation is oxygen loading onto hemoglobin, measured by PaO2 (80 to 100 mmHg) and oxygen saturation (95% to 100%). Ventilation is carbon dioxide clearance, measured by PaCO2 (35 to 45 mmHg). A patient can be adequately oxygenated on supplemental oxygen while dangerously hypercapnic.

Give the four-step approach to arterial blood gas interpretation.

First, classify the pH (below 7.35 acidosis, above 7.45 alkalosis). Second, evaluate PaCO2 for the respiratory component and bicarbonate for the metabolic component. Third, identify which value explains the pH abnormality; if PaCO2 moves opposite to the pH, the cause is respiratory, and if bicarbonate moves with the pH, the cause is metabolic. Fourth, determine compensation: none, partial (pH still abnormal), or full (pH back in range).

What is ventilation-perfusion mismatch, and give one example of each type?

A mismatch between alveolar ventilation and capillary perfusion. Ventilation without perfusion (dead space) occurs in pulmonary embolism. Perfusion without ventilation (shunt) occurs in pneumonia, atelectasis, and pulmonary edema.

Why does a normal pulse oximetry reading not exclude respiratory failure?

Pulse oximetry measures only hemoglobin saturation. It gives no information about carbon dioxide retention, and it can read falsely normal in carbon monoxide poisoning, and unreliably in poor perfusion, hypothermia, and motion.

Explain the "good lung down" principle and its exception.

Gravity increases perfusion to the dependent lung, so positioning the healthier lung down matches perfusion to the better-ventilated tissue and improves oxygenation. The exception is unilateral lung abscess or hemorrhage, where the affected lung is placed down to prevent spillage into the healthy lung.

Renal, Endocrine, and Electrolytes

List five functions of the kidney and the failure state each produces.

Waste excretion (uremia), fluid and electrolyte regulation (overload and hyperkalemia), acid-base regulation (metabolic acidosis), erythropoietin production (anemia), and vitamin D activation (hypocalcemia with hyperphosphatemia). Renin release adds hypertension.

Why is creatinine a better marker of kidney function than blood urea nitrogen?

Creatinine, normally about 0.6 to 1.2 mg/dL, is produced at a steady rate from muscle and is filtered without significant reabsorption. Blood urea nitrogen, normally about 10 to 20 mg/dL, also rises with dehydration, high protein intake, gastrointestinal bleeding, and corticosteroid use, so it is less specific.

How does insulin affect potassium, and what are the two clinical consequences?

Insulin drives potassium into cells along with glucose. Clinically, insulin with dextrose is a temporizing treatment for hyperkalemia, and potassium must be monitored and replaced during treatment of diabetic ketoacidosis, where the level can fall sharply once insulin is started.

Contrast the electrolyte and hemodynamic profiles of Addison disease and Cushing syndrome.

Addison disease (adrenocortical insufficiency) produces hyponatremia, hyperkalemia, hypoglycemia, hypotension, and hyperpigmentation. Cushing syndrome (cortisol excess) produces hypernatremia, hypokalemia, hyperglycemia, hypertension, immunosuppression, and osteoporosis.

Distinguish diabetes insipidus from the syndrome of inappropriate antidiuretic hormone.

Diabetes insipidus is a deficiency of antidiuretic hormone, producing large volumes of dilute urine, hypernatremia, and rising serum osmolality. The syndrome of inappropriate antidiuretic hormone is excess hormone, producing water retention, concentrated urine, dilutional hyponatremia, and neurologic changes.

Why does a patient develop hypocalcemia after a thyroidectomy?

The parathyroid glands lie on the posterior thyroid and may be injured or removed. Loss of parathyroid hormone reduces bone resorption, renal calcium reabsorption, and vitamin D activation, so serum calcium falls, producing perioral and digital paresthesias, positive Chvostek and Trousseau signs, tetany, and possible laryngospasm.

Why do immobilized patients develop hypercalcemia and renal calculi?

Bone remodeling responds to mechanical stress. Without weight bearing, osteoclastic resorption outpaces osteoblastic formation, releasing calcium into the blood and urine. Urinary stasis in the supine position adds stone risk, which is why mobilization and hydration are therapeutic.

Which electrolyte disturbances mimic each other by causing increased neuromuscular excitability?

Hypocalcemia and hypomagnesemia both cause tetany, twitching, positive Chvostek and Trousseau signs, and hyperreflexia. Refractory hypocalcemia often will not correct until magnesium is replaced. Conversely, hypercalcemia and hypermagnesemia both depress excitability, causing lethargy, weakness, and diminished reflexes.

Hematologic and Gastrointestinal

Why can a severely neutropenic patient have a serious infection with no redness or purulent drainage?

The classic local signs of inflammation are produced by neutrophil migration into tissue. Without neutrophils, the patient cannot generate them, so even a modest temperature elevation may be the only sign of sepsis and constitutes an emergency.

Which clotting factors require vitamin K, and why does liver disease prolong the international normalized ratio?

Factors II, VII, IX, and X are vitamin K dependent and are synthesized in the liver. Hepatic failure impairs synthesis, and biliary obstruction impairs absorption of fat-soluble vitamin K, so both prolong prothrombin time and the international normalized ratio.

Why do prolonged vomiting and prolonged diarrhea produce opposite acid-base disturbances?

Vomiting and nasogastric suction remove hydrochloric acid from the stomach, causing metabolic alkalosis, typically with hypokalemia and hypochloremia. Diarrhea removes bicarbonate-rich intestinal secretions, causing metabolic acidosis.

Why does gastric bypass or gastrectomy cause vitamin B12 deficiency?

Intrinsic factor is secreted by the gastric parietal cells and is required for vitamin B12 absorption in the terminal ileum. Without it, B12 cannot be absorbed regardless of oral intake, producing megaloblastic anemia and neurologic deficits, so parenteral or high-dose replacement is needed.

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