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Diffusion: what is it, what happens when net movement stops, occurs where
movement of molecules from an area of high concentration to an area of low concentration. Net movement of molecules stops when the concentrations are equal in both areas. It occurs in liquids, gases, and solids
Simple diffusion requires —
no external energy
facilitated diffusion: involves the use of —, what happens, and explain if need energy or not
Facilitated Diffusion: involves the use of a protein carrier in the cell membrane. The protein carrier combines with a molecule. esp. one too large to pass easily through the cell membrane and helps move the molecule across the membrane from high → low conc.
Passive and needs no energy - ex. Glucose movement into cell → the large glucose molecule must combine with a carrier molecule to be able to cross the cell membrane and enter the cells
Active Transport: what happens here, is energy needed, example
1. What is Active Transport?
The "Uphill" Battle: Unlike diffusion, active transport moves molecules against their concentration gradient (from an area of low concentration to high concentration).
Energy Required: Because it's moving against the natural flow, it cannot happen on its own—it requires cellular energy (ATP) to force the molecules across.
2. The Energy Source: ATP
The Fuel: The energy used for this process is ATP (adenosine triphosphate).
Where it comes from: ATP is generated right inside the cell's "powerhouse," the mitochondria.
3. Classic Example: The Sodium-Potassium Pump
The Setup: Cells need to maintain very specific balances of sodium (Na) and potassium (K) between the inside (ICF) and outside (ECF) of the cell.
The Action: The sodium-potassium pump constantly uses ATP to actively push sodium out of the cell and pull potassium in, keeping those crucial concentration differences stable.
osmosis: how does it move, is enery needed, osmolarity vs osmolality, isotonic, hypotonic, and hypertonic fluids how does it affect cells
1. Osmosis & How Water Moves
Movement down a gradient: Water naturally flows across a semi-permeable membrane from an area with a low amount of dissolved stuff (solutes) to an area with a high amount of solutes.
Water seeks to dilute: Think of water as trying to balance things out—it always moves toward the higher concentration of solutes to try and dilute them.
No energy needed & when it stops: Osmosis is passive (uses no energy) and keeps going until the concentrations on both sides are equal, or until counter-pressure (hydrostatic pressure) builds up and physically stops the water flow.
Osmotic pull: Any dissolved substance trapped by a membrane will pull water toward it; the higher the concentration of that substance, the stronger its "pull" (known as osmotic pressure).
2. Osmolarity vs. Osmolality
Osmolarity: Measures the concentration of dissolved molecules per liter of solution (mOsm/L).
Osmolality: Measures the concentration of dissolved molecules per kilogram of water (mOsm/kg). This is the preferred measurement doctors use to check the concentration of blood plasma, urine, and other body fluids.
3. How Fluid Concentrations Affect Cells
Cell impact: The concentration of the fluid sitting outside your cells (ECF) directly controls which way water moves and whether your cells stay healthy.
Isotonic fluids: If the fluid outside has the same concentration as the inside of the cell, they are balanced (isotonic), and water stays put with no net movement.
Hypotonic fluids: If the outside fluid has fewer solutes than the cell (hypoosmolar), water rushes into the cell to try and dilute the inside—causing the cell to swell up and potentially burst.
Hypertonic fluids: If the outside fluid has more solutes than the cell (hyperosmolar), water is pulled out of the cell to dilute the outside fluid—causing the cell to shrivel up and potentially die.
explain filtration, hydrostatic pressure and how it works in the capillaries
What is Filtration? The movement of water and dissolved substances through a membrane driven by pressure.
Hydrostatic Pressure: This is simply the pushing force of fluid against a wall. In your body, it is your blood pressure generated by your heart.
How it works in capillaries: As blood flows from the heart into the tiny capillary beds, this pressure pushes water and nutrients out of the blood vessels and into the surrounding tissue (interstitial space).
what is oncotic pressure and how it works
What is Oncotic Pressure? Also called colloid osmotic pressure, this is the pulling force created by large molecules (proteins, like albumin) dissolved in the blood.
How it works: Because your blood has a high concentration of proteins while the tissue spaces have very few, these proteins act like a sponge—they attract water and pull fluid back into the blood vessels from the tissues.
fluid movement depends on what: explain on the arterial end and at the venous end
Fluid movement depends on a balance between four main pressures (two that push out, two that pull in):
At the Arterial End (Entering the capillary bed):
Capillary hydrostatic pressure (the push from blood pressure) is higher than the pulling pressure.
Result: Fluid is pushed out of the capillaries and into the tissues to deliver nutrients.
At the Venous End (Leaving the capillary bed):
As blood moves along, blood pressure drops. Now, plasma oncotic pressure (the protein pull) is higher than the pushing pressure.
Result: Fluid is pulled back into the capillaries, carrying waste products away to be filtered out by the body.
A proper, healthy adult needs fluid intake of —mL → comes from —
2000 to 3000
food/water
what are 2 ways we loose water
Insensible Loss: We constantly lose water without realizing it through invisible evaporation from our skin and lungs, which also helps control body temperature.
Extra Loss: Higher metabolism (from fever or exercise) increases water loss through sweat and breathing, meaning you need to drink more to replace it.
explain the Hypothalamic-Pituitary Regulation
The Sensors: If your body gets dehydrated or your blood becomes too concentrated (high osmolality), specialized sensors (osmoreceptors) in the hypothalamus trigger two actions:
Thirst: Makes you feel thirsty so you drink water.
ADH Release: Signals the posterior pituitary gland to release ADH (Antidiuretic Hormone).
The Kidney Effect: ADH tells the kidneys' tubes to become more permeable to water, meaning your body reabsorbs water back into the blood instead of peeing it out.
Renal Regulation: the kidneys filter what and how much using — hormones, what happens when kidney is damaged?
Filtering & Reabsorbing: Your kidneys filter your entire plasma volume many times a day, reabsorbing 99% of it and producing about 1.5 liters of urine daily.
Fine-Tuning: Using hormones like ADH and aldosterone, the kidneys adjust what gets reabsorbed or excreted to keep blood volume, electrolytes, and acidity balanced.
Kidney Failure: When kidneys are severely damaged, they can't balance fluids, leading to dangerous fluid buildup (edema), high potassium, and acid imbalances.
Corticosteroids: are hormones that do what and released by who and what are the 2 branches from it
Corticosteroids: Hormones released by the adrenal glands help control water and electrolytes:
Glucocorticoids: Fight inflammation and raise blood sugar.
Mineralocorticoids (like aldosterone): Tell the kidneys to hold onto sodium and get rid of potassium.
Natriuretic Peptides: are what that release __ when. and these peptides act as what
Special heart cells (cardiomyocytes) release hormones like ANP when the heart stretches from high blood pressure or too much fluid volume.
The Counter-Attack: These peptides act as the opposite of the RAAS (Renal-Angiotensin-Aldosterone System)—they force the kidneys to dump extra sodium and water into the urine, which lowers blood volume and blood pressure.
VOLEMIA → reffers to
specifically refers to the volume of blood circulating in your blood vessels
Hypovolemia: is what and what is a result of hypovolemia
Hypovolemia: Loss of extracellular fluid exceeding intake - LOOSiNG MORE FLUID THAN YOU ARE RECIEVING (e.g., hemorrhage, GI losses, excessive diuresis) → Lower circulatory blood volume, lower venous return, lower cardiac output, lower tissue perfusion
hypovolemia: causes, appears as, management, monitor
Can be caused by vomiting, diarrhea, hemorrhage, excessive sweating, diuretics, burns, dehydration
Appears as weight loss, dry mucous membranes, poor skin turgor, lower urine output, concentrated urine, weaker/thready pulse, tachycardia, low BP (orthostatic hypotension), thirst, weakness, confusion, flat veins
Management: Oral fluids, IV fluids (0.9%, lactated Ringer's), blood products
Monitor: I/O, daily weight, BP, orthostatic BP, electrolytes, urine output
Hypervolemia: is what and what happens
Excess of fluid → too much NA+ and water retained can cause inc. ECF, inc. hydrostatic pressure; fluid moves into tissues
hypervolemia: causes, appears as, manamgement
Caused by renal and heart failure, excess IV fluids, corticosteroids, sodium retention
Appears as: weight gain, edema, bounding pulse, high BP, vein distention, crackles, possible ascites, pulmonary edema (fluid enters lungs → impaired gas exchange)
Management: fluid restriction, sodium restriction, diuretics, daily weights, 1/0 tracking, lung sounds assessment, assess for edema, monitor O2 levels, treat underlying cause of retention
how does the term extracellular fit into natremia
Natremia refers specifically to the concentration of sodium (Na+) in your blood.
Because sodium is the main electrolyte found in the extracellular fluid (ECF)—the fluid outside of your cells—the term "natremia" is fundamentally an extracellular measurement.
natremia: what does it mean, what is sodiums job, how does it affect the neuro, parallell osmolality changes, major roles
Natremia (Extracellular): This simply means the level of sodium in the fluid outside your cells (the ECF).
Sodium's jobs: It controls water balance, helps nerve cells talk to each other, and makes muscles contract.
Think neuro effects! Because sodium dictates how brain cells and nerves work, any sodium imbalance directly affects your brain and mental state.
Parallel osmolality changes: Sodium imbalances almost always match changes in your body's fluid concentration (osmolality).
Major roles: Sodium controls ECF volume, creates nerve signals, contracts muscles, and helps keep blood and body fluids at the right acid-base balance.
hyponatremia: what is it, what happens to the cells and specifically which ones
What it is: The ECF has too little sodium compared to water, making the fluid "hypotonic" (diluted).
Cell swelling: Because the outside fluid is diluted, water rushes into the cells, causing them to swell.
Brain danger: The most dangerous part is cerebral edema (brain cells swelling inside the skull).
hyponatremia causes
Causes (Low Sodium): Losing salt through vomiting, diarrhea, sweating, or diuretic medications.
Causes (Too Much Water): Diluting the blood with too much water, conditions like SIADH (holding onto too much water), heart failure, or kidney problems.
hyponatremia sympoms
Headaches, nausea, feeling sluggish (lethargy), confusion, irritability, muscle cramps, seizures, dropping level of consciousness (LOC), coma, and trouble concentrating
hyponatremia: manamgent if caused by fluid excess and fluid loss
Management if caused by fluid excess: Restrict fluids, give diuretics to pee out extra water, or use saline. Warning: Never fix sodium too fast, or it can cause a dangerous brain injury called osmotic demyelination syndrome.
Management if caused by fluid loss: Give fluids that contain sodium (isotonic IV fluids), have the patient eat more salt or take salt tablets, stop diuretics, and give medications that block ADH.
Hypernatremia: what is it, and what happens to the cells
What it is: The ECF becomes "hypertonic" (too concentrated with salt).
Cell shrinking: Water is sucked out of the cells to try and dilute the salty ECF, causing the cells to shrivel and dehydrate—especially brain cells.
hypernatremia causes
Causes: Losing pure water (through fever, heavy sweating, diabetes, or not drinking enough) or taking in too much salt. It can also be caused by hyperaldosteronism (an overactive adrenal hormone that makes the body hold onto way too much salt and water).
hypernatremia symptoms
Symptoms: Intense thirst (the body's main alarm system), dry/sticky mouth, flushed skin, low urine output, muscle twitching, seizures, coma, restlessness, and confusion. (Note: Elderly people lose their sense of thirst easily, making them much more vulnerable to hypernatremia).
hypernatremia management
Management: Treat the root cause, not just the symptom! If they are dehydrated, replace water slowly using oral fluids or hypotonic IV solutions (never too fast). If they have too much sodium, dilute them with sodium-free IV fluids and give diuretics to flush out the salt.
Magnesium: what does it support, where does it live, and what is a key clinical pearl, and what is the myoneural junction
What it does: Magnesium is a powerhouse mineral. It supports ATP (energy) production, nerve function, muscle contraction and relaxation, heart rhythm, blood sugar control, blood pressure regulation, and DNA/protein synthesis.
Where it lives: About 50-60% is stored in bones, 30% inside cells, and only 1% in the extracellular fluid (ECF). It is absorbed in the gut and filtered out by the kidneys.
Key Clinical Pearl: Magnesium is not included on a standard Basic Metabolic Panel (BMP)—you have to specifically order a magnesium panel!
The Myoneural Junction: Magnesium acts directly on the junction where nerves meet muscles, which is why imbalances heavily affect reflexes and muscle activity.
Hypomagnesemia: what does it do to the nervous system, sympoms, effect on cardiac, causes, what to monitor, treatments
The Rule: Low magnesium makes the nervous system and muscles hyper-excitable (similar to low calcium).
Symptoms: Tremors, muscle cramps, hyperreflexia, positive Chvostek and Trousseau signs, seizures, confusion, vertigo, and unique irritability.
Cardiac Danger: Can cause serious heart rhythms like Torsades de pointes and ventricular fibrillation.
Causes: Diarrhea, malnutrition, GI fluid loss/NG suction, certain antibiotics, chronic alcohol use, diuretics, and proton pump inhibitors (PPIs).
What to Monitor: Magnesium levels, blood pressure, breathing (respiratory status), and deep tendon reflexes.
Treatments:
Increase dietary intake or use oral magnesium for mild cases.
IV Magnesium Sulfate for severe cases.
Crucial safety note: Infusing IV magnesium too fast causes hypotension (low blood pressure), which spikes the patient's fall risk!
Hypermagnesemia: what does it do , symptoms, what are life threating symptoms, causes, treatments
The Rule: When magnesium is too high, everything is depressed and slowed down. It most commonly happens when the kidneys fail to clear it out.
Symptoms: Hypotension, bradycardia (slow heart rate), extreme lethargy, sluggish or absent deep tendon reflexes, muscle weakness, facial flushing, and paralysis.
Severe/Life-Threatening: Respiratory depression, respiratory arrest, and cardiac arrest.
Causes: Renal failure combined with taking magnesium-containing medications (like antacids or laxatives), or getting too much IV magnesium.
Treatments:
Prevention first: Stop magnesium drugs and restrict dietary magnesium.
IV fluids and diuretics (if kidneys work) to flush it out.
Dialysis if the patient is in renal failure.
IV Calcium Gluconate: Given for severe toxicity because calcium acts as an antidote that directly blocks and opposes the effects of excess magnesium.
Kalemia - what is it and where does it live, what are the sources
What it is & Where it lives: Potassium lives mostly inside cells (ICF). It controls nerve impulses, muscle contractions, and heart rhythm. Even tiny changes in potassium can cause massive problems, especially for the heart!
Sources: Protein-rich foods, fruits, veggies, salt substitutes, and supplements. Regulated by the kidneys.
Hypokalemia - what does this mean for potassium , what is the rule
Potassium levels too low, “Everything simply slows down”
Low serum potassium caused by
Loop diuretics, thiazide diuretics, vomiting, diarrhea, NG suction, poor intake; alkalosis can shift K+ into cells, and the serum level of K+ falls; low magnesium causes low potassium because it allows for more potassium to be excreted through the urine; decreased dietary levels of potassium (rare)
Hypokalemia Causes: losses and shifts
Losses: Loop diuretics, thiazide diuretics, vomiting, diarrhea, and NG suction.
Shifts & Deficiencies: Alkalosis (causes potassium to shift into cells, making serum levels fall), low magnesium levels (which allow more potassium to be wasted and excreted through the urine), and poor dietary intake (though dietary deficiency is rare).
Clinical Manifestations (Symptoms): Hypokalemia
Muscle weakness, fatigue, paresthesia, and leg/calf cramps.
Decreased GI motility (leading to constipation, nausea, and paralytic ileus).
Weak respiratory muscles resulting in slow breathing, a weak pulse, and hyperglycemia.
Cardiac Symptoms: Cardiac dysrhythmias (these are the most serious and life-threatening manifestations).
how does hypokalemia relate to EKG changes
EKG Changes:
Flattened T-waves (which can lead to bradycardia).
ST segment depression.
Prominent U-waves.
Clinical Management & Critical Safety Rules hypokalemia
Potassium Replacement: Administered via oral or IV routes.
CRITICAL IV SAFETY:
Never push potassium IV bolus!
IV potassium must be diluted and infused using an infusion pump at a controlled rate.
The infusion rate should never exceed 10 mEq/hr.
IV potassium causes severe venous irritation ("it burns"). To minimize discomfort, utilize the largest-bore IV or central line possible and infuse it as slowly as clinically appropriate.
Hyperkalemia The Core Rule
When potassium is too high, it creates severe neuromuscular and cardiac hyperexcitability/dysregulation.
Hyperkalemia Causes: renal, med, cell destruction, shift
Renal Issues: Renal failure (patients with kidney failure frequently struggle with life-threatening cardiac dysrhythmias due to potassium dysregulation).
Medications: ACE inhibitors, ARBs, potassium supplements, and potassium-sparing diuretics.
Cell Destruction: Tissue destruction, severe burns, and rhabdomyolysis.
Shifts: A shift of potassium from the ICF out into the ECF.
Acid-Base Connection: Hyperkalemia
Acidosis: Increases hydrogen ions (H+) in the blood, which causes hydrogen to enter cells while pushing potassium out into the ECF, resulting in hyperkalemia.
Clinical Manifestations (Symptoms) hyperkalemia
Muscle weakness, paresthesia (numbing/tingling of the skin), and paralysis.
Hyperactivity/speeding up of GI tract muscles leading to abdominal cramping and diarrhea.
Fatigue, tetany (prolonged, sustained muscle contractions), and dysrhythmias.
EKG Changes hyperkalemia
Tall, peaked T-waves (early sign).
As it worsens: prolonged PR intervals, widened QRS complexes, loss/flattening of P-waves, and dangerous ventricular dysrhythmias.
Treatments & Interventions hyperkalemia: cardiac protection, cellular shifting, removal from body, supportive care
Cardiac Protection: Administer Calcium gluconate or calcium chloride to stabilize the cardiac membrane against high potassium.
Cellular Shifting:
Insulin + Dextrose (Insulin drives potassium from the ECF back into cells; dextrose is given simultaneously to prevent dangerous hypoglycemia).
Beta-2 agonists or Sodium Bicarbonate (also shift potassium into cells).
Removal from the Body:
Potassium-binding medications: Remove potassium through the GI tract, such as sodium polystyrene sulfonate (Kayexalate).
Diuretics: Increase renal potassium excretion, provided kidney function permits (e.g., thiazide diuretics).
Dialysis: Used for severe hyperkalemia, especially in patients with acute or chronic renal failure.
Supportive Care: Stop all oral and IV potassium intake, and increase water intake if appropriate.
Hyperkalemia monitor what
Monitoring Requirement: Use continuous ECG monitoring. Any patient experiencing a potassium imbalance requires continuous cardiac monitoring.
Calcemia (Calcium): where does it live, where we get it, where is it stored, explain ionized (free) calcium
Where it lives & what it does: Calcium is mostly found outside cells (extracellular). It builds bones and teeth, makes muscles contract, transmits nerve signals, helps blood clot, and pumps the heart.
Where we get it: Our main source is food, but it requires Vitamin D to actually be absorbed by the body.
Forms in the body: Calcium is stored in bones and floats in blood plasma. The ionized (free) calcium is the active form that does the work. Blood pH and a blood protein called albumin can change these calcium levels.
Balance of Calcium controlled by what hormones and how
Parathyroid Hormone (PTH): Raises blood calcium by pulling it out of bones/teeth, absorbing more from food in the gut, and having the kidneys reabsorb it.
Calcitonin: Lowers blood calcium by pushing it back into bones, flushing it out in the urine, and blocking gut absorption.
Check and balance: what does this mean in relation to the 2 hormones
PTH and calcitonin work as direct opposites to keep calcium steady.
Hypocalcemia the core rule
The Core Rule: Low calcium makes nerves and muscles hyper-excitable ("things speed up").
SymptomsHypocalcemia
Symptoms: Numbness and tingling (especially around the mouth/perioral), muscle cramps, severe muscle spasms (tetany), overactive reflexes (hyperreflexia), seizures, high-pitched breathing noises (laryngeal stridor), trouble swallowing (dysphagia), and heart rhythm issues (dysrhythmias).
where can hypocalcemia appear at
Symptoms: Numbness and tingling (especially around the mouth/perioral), muscle cramps, severe muscle spasms (tetany), overactive reflexes (hyperreflexia), seizures, high-pitched breathing noises (laryngeal stridor), trouble swallowing (dysphagia), and heart rhythm issues (dysrhythmias).
Special Diagnostic Tests:
Chvostek’s Sign: Tap the facial nerve; if the facial muscles twitch, it's a positive sign of hypocalcemia.
Trousseau’s Sign: Pump up a blood pressure cuff above systolic pressure; if the hand cramps into a claw, it's positive.
EKG Changes: Prolonged QT interval.
Causes of hypocalcemia
Low PTH (not releasing stored calcium), Vitamin D loss, low magnesium, multiple blood transfusions, blood alkalosis, and losing too much calcium.
Management of hypocalcemia
Eat calcium-rich foods, take oral calcium and Vitamin D supplements, and give IV calcium gluconate only in urgent/emergency situations.
Hypercalcemia the core rule
High calcium makes nerves and muscles slow and sluggish
Hypercalcemia can appear as what symptoms then what severe symptoms
Symptoms: Muscle weakness, fatigue, extreme tiredness (lethargy), slow reflexes, constipation, nausea, kidney stones, confusion, and heart dysrhythmias.
Severe Symptoms: Bone pain (from calcium moving out of bones into blood), hallucinations, seizures, coma, bone fractures, kidney stones (nephrolithiasis), peeing a lot (polyuria), and dehydration
Hypercalcemia Possible causes
Overactive parathyroid glands (hyperparathyroidism, responsible for 2/3 of cases), being immobile for too long, taking in too much calcium, taking thiazide diuretics, and certain cancers (kidney, breast, prostate, ovarian, blood/hematologic, and lung cancers).
Treatments of Hypercalcemia
Bisphosphonates: The gold standard medication to slow down bone breakdown.
Calcitonin: Used in some cases to send calcium back into bones or flush it out in urine.
Hydration & Flushing: Isotonic saline IV fluids and loop diuretics to promote kidney excretion and prevent kidney stones.
Lifestyle/Diet: Low-calcium diet, stopping any medications that cause high calcium, increasing weight-bearing exercise (to push calcium back into bones), and drinking extra fluids (IV or oral, including cranberry or prune juice) to generate urine and prevent stones.