Six models,
one agent.

SIADH = too much ADH → too much free water retained → dilutional hyponatremia.

For Step 2 CK, think: “water problem, not sodium loss.”

Core mechanism

ADH acts on the collecting duct → inserts aquaporins → kidneys reabsorb free water.

So in SIADH:

• Total body water ↑
• Serum sodium ↓ because it gets diluted
• Serum osmolality ↓
• Urine is inappropriately concentrated

Classic labs

The key Step 2 phrase is:

> Hyponatremia with low serum osmolality, high urine osmolality, and euvolemia

Why urine sodium is high?

Because the body has slightly increased water volume, so it suppresses RAAS and dumps sodium in urine.

But clinically, the patient still looks euvolemic — no edema, no dehydration.

Common causes

High-yield causes:

• Small cell lung carcinoma — ectopic ADH
• CNS disease: stroke, hemorrhage, trauma, infection
• Pulmonary disease: pneumonia, TB
• Drugs:
• SSRIs
• Carbamazepine
• Cyclophosphamide
• MDMA
• Vincristine

Symptoms

Depends on severity and speed of sodium drop.

Mild:

• Nausea
• Headache
• Confusion
• Weakness

Severe:

• Seizures
• Coma
• Brain edema

Treatment for Step 2

#### Mild or asymptomatic SIADH

Fluid restriction

That is the main answer most of the time.

#### Severe symptoms, seizures, or very low Na⁺

Hypertonic saline, usually 3% saline

But correct slowly to avoid osmotic demyelination syndrome.

#### Chronic/refractory SIADH

Options include:

• Salt tablets
• Loop diuretics
• Vaptans, e.g. tolvaptan/conivaptan

Most important differential: hypovolemic hyponatremia

Both can have low sodium, but:

• SIADH: euvolemic, urine Na⁺ high
• Vomiting/diarrhea/dehydration: hypovolemic, urine Na⁺ usually low unless renal salt wasting/diuretics

Exam trap

If a patient has hyponatremia after small cell lung cancer, CNS injury, or SSRI use, and they look euvolemic:

> Pick SIADH and treat with fluid restriction unless they are seizing or severely symptomatic.

One-liner memory hook

SIADH = “Soaked Inside, ADH High”

Too much water retained, sodium gets diluted, urine stays concentrated.

SIADH = too much ADH → too much free-water retention.

So the blood becomes dilute, while the urine stays inappropriately concentrated.

Classic lab pattern

• Low serum Na⁺ → hypotonic hyponatremia
• Low serum osmolality: <275 mOsm/kg
• Urine osmolality >100 mOsm/kg
• Urine Na⁺ >30–40 mEq/L
• Patient appears euvolemic: no edema, no dehydration
• Normal kidney, adrenal, and thyroid function

Common Step 2 causes

• Small-cell lung cancer (ectopic ADH)
• CNS disease: stroke, hemorrhage, infection
• Pulmonary disease: pneumonia, tuberculosis
• Drugs: SSRIs, carbamazepine, cyclophosphamide
• Postoperative pain/nausea

Symptoms depend on severity

• Mild: nausea, headache, confusion
• Severe/acute: seizures, coma

Management

• Mild/chronic: fluid restriction; treat the cause
• Persistent cases: salt tablets, loop diuretic, or a vasopressin antagonist
• Severe symptoms or seizures: carefully give 3% hypertonic saline

Major exam trap

Correct chronic hyponatremia slowly—generally no more than 8 mEq/L in 24 hours—to avoid osmotic demyelination syndrome.

Memory hook:

SIADH = Serum Is diluted, ADH is High.

SIADH = too much ADH when the body doesn’t actually need it.

ADH normally tells the kidneys: “Save water.”

In SIADH, ADH stays on inappropriately → kidneys retain free water → blood gets diluted.

What happens?

• Low serum sodium (dilutional hyponatremia)
• Low serum osmolality
• Concentrated urine despite low blood sodium
• urine osmolality high
• urine sodium usually >40 mEq/L
• Patient is usually euvolemic: no major edema, no dehydration signs

Why no edema?

The initial water retention causes mild volume expansion, so the kidneys dump sodium and water via natriuresis. Net result: sodium stays low, but the patient looks clinically euvolemic.

Classic causes — “SALT”

• Small-cell lung carcinoma
• Antidepressants / anticonvulsants (especially SSRIs, carbamazepine)
• Lung disease (eg, pneumonia)
• Trauma/CNS disease (stroke, meningitis, head injury)

Also think: postoperative state, nausea, pain.

Symptoms

Depend on how low and how quickly sodium falls:

• Mild: nausea, headache, confusion
• Severe/acute: seizures, coma

Step 2 diagnosis pattern

Hyponatremia + low serum osmolarity + inappropriately concentrated urine + euvolemia

→ think SIADH after excluding hypothyroidism and adrenal insufficiency.

Treatment

• Mild/chronic: fluid restriction
• More significant: salt tablets ± loop diuretic; sometimes urea
• Severe symptomatic hyponatremia (seizure, severe confusion): cautious 3% hypertonic saline
• Treat the cause; consider vasopressin antagonists (eg, tolvaptan) in selected resistant cases.

Exam trap: Don’t correct chronic hyponatremia too quickly—risk of osmotic demyelination syndrome.

SIADH = too much ADH when the body doesn’t need it.

ADH normally tells the kidneys: “Hold on to water.”

In SIADH, that signal stays switched on → the patient retains free water → blood gets diluted.

What happens?

• Low serum sodium = dilutional hyponatremia
• Low serum osmolality
• Urine is inappropriately concentrated (ADH is making the kidney retain water)
• Urine sodium is usually high (>40 mEq/L)
• Patient looks euvolemic: no major edema, no dehydration

Classic causes — think “lung, brain, drugs”

• Small-cell lung carcinoma (ectopic ADH)
• CNS disease: stroke, hemorrhage, infection, trauma
• Pulmonary disease: pneumonia, TB
• Drugs: SSRIs, carbamazepine, cyclophosphamide, antipsychotics

Symptoms

Depend on how fast/severe the sodium falls:

• Headache, nausea, confusion
• Seizures/coma if severe or acute

Step 2 diagnosis pattern

> Hyponatremia + low serum osm + concentrated urine + normal volume status = SIADH

Important: rule out hypothyroidism and adrenal insufficiency first.

Treatment

• Mild/chronic: fluid restriction
• Severe symptomatic (seizure, severe confusion): cautious 3% hypertonic saline
• Treat the cause; consider vaptans in selected persistent cases.

Exam trap:

SIADH has hyponatremia but *no edema* because the slight volume expansion triggers sodium excretion, restoring near-normal extracellular volume—while water retention persists.

Memory hook:

SIADH = “Soaked Inside, Apparently Dry/Healthy.”

Water is retained internally, but the exam stem says “euvolemic.”

SIADH — the simple Step 2 CK version

SIADH = too much ADH → water retention → dilutional hyponatremia.

The kidneys retain water even though the body’s overall fluid volume is almost normal.

Classic findings

• Low serum sodium
• Low serum osmolality
• Inappropriately concentrated urine → high urine osmolality
• High urine sodium
• Euvolemic patient: no edema, no major dehydration
• Normal thyroid, adrenal, renal, and cardiac function

Why?

ADH makes the collecting ducts reabsorb water:

> More ADH → more water retained → sodium gets diluted

The extra water is usually not enough to cause obvious edema because the body compensates by excreting sodium.

Common causes

Think “CNS, chest, cancer, drugs”:

• CNS disease: stroke, hemorrhage, meningitis, trauma
• Pulmonary disease: pneumonia, tuberculosis
• Small-cell lung carcinoma: ectopic ADH production
• Medications: SSRIs, carbamazepine, cyclophosphamide, MDMA

Symptoms

Mostly due to cerebral edema from hyponatremia:

• Headache
• Nausea, confusion
• Seizures
• Coma if severe or rapidly developing

Diagnosis: the exam sequence

• Hyponatremia
• Check serum osmolality → low
• Check urine osmolality → inappropriately high
• Check volume status → euvolemic
• Exclude hypothyroidism and adrenal insufficiency

Treatment

• Treat the cause
• Fluid restriction is first-line
• Severe symptomatic hyponatremia → cautious 3% hypertonic saline
• Chronic SIADH may require vasopressin receptor antagonists such as tolvaptan

Major exam trap

Correct sodium slowly—generally no more than about 8 mEq/L in 24 hours—to avoid osmotic demyelination syndrome.

One-line memory hook

> SIADH: Small-cell lung cancer causes “Sodium Is Actually Diluted Here.”

Classic vignette: A patient with small-cell lung cancer has confusion, Na⁺ té, low serum osmolality, concentrated urine, high urine sodium, and no edema or dehydration → SIADH.

SIADH — simple Step 2 CK version

SIADH = too much ADH despite low plasma osmolality.

The kidneys retain free water, so the patient becomes dilutionally hyponatremic.

Classic lab pattern

Why is the urine concentrated?

Normally, low serum osmolality should suppress ADH → dilute urine.

In SIADH, ADH remains active → water retention + concentrated urine.

Common causes

Think “CNS, chest, cancer, drugs”:

• CNS: stroke, hemorrhage, trauma, meningitis
• Chest: pneumonia, tuberculosis
• Cancer: especially small-cell lung carcinoma — ectopic ADH
• Drugs: SSRIs, carbamazepine, oxcarbazepine, opioids, MDMA, cyclophosphamide

Symptoms

Due to cerebral edema from hyponatremia:

• Nausea, headache, confusion
• Seizures or coma if severe/rapid onset

Treatment

• Treat the cause and restrict fluids
• If severe symptoms—seizure, severe confusion, coma:

3% hypertonic saline

• Correct sodium slowly to avoid osmotic demyelination syndrome
• Vaptans, such as tolvaptan, may be used in selected cases but are less commonly the key Step 2 answer.

Exam trap

SIADH is euvolemic hyponatremia.

Compare:

• Heart failure/cirrhosis: hyponatremia + edema → hypervolemic
• Vomiting/diarrhea: hyponatremia + volume depletion → hypovolemic
• SIADH: hyponatremia but no obvious edema or dehydration

One-line memory hook

> Low serum osmolality + concentrated urine + euvolemia = SIADH.

You’re missing carbon monoxide (CO) poisoning.

Why SpO₂ is 99%: pulse oximetry can’t distinguish oxyhemoglobin from carboxyhemoglobin, so it may look falsely normal.

Clues in this vignette

• House fire/smoke inhalation
• Headache + confusion
• Normal-looking SpO₂ despite tissue hypoxia

What to check

• Co-oximetry / ABG with carboxyhemoglobin level

Regular pulse ox and standard ABG PaO₂ can be misleading.

Immediate management

• Give 100% high-flow oxygen immediately.
• Consider hyperbaric oxygen if severe features: loss of consciousness, neurologic symptoms, cardiovascular instability/ischemia, severe acidosis, very high carboxyhemoglobin level, or pregnancy.

Exam trap: PaO₂ can be normal too because dissolved oxygen is normal; the problem is hemoglobin is occupied by CO and the O₂ dissociation curve shifts left.

Carbon monoxide (CO) poisoning.

Standard pulse oximetry cannot distinguish carboxyhemoglobin from oxyhemoglobin, so SpO₂ may falsely read 99% despite severe tissue hypoxia.

• Check carboxyhemoglobin by co-oximetry on blood gas; PaO₂ can also remain normal.
• Give 100% high-flow oxygen immediately—don’t wait for results.
• Consider hyperbaric oxygen consultation for neurologic symptoms, severe acidosis, cardiac ischemia, pregnancy, or markedly elevated COHb.
• In an enclosed-space fire, also consider cyanide toxicity, especially with soot, cardiovascular collapse, or severe lactic acidosis.

If this is a real patient, this is an emergency requiring immediate ED/toxicology management.

You’re missing carbon monoxide (CO) poisoning — pulse oximetry can look falsely normal because it cannot distinguish oxyhemoglobin from carboxyhemoglobin.

In a house-fire patient with headache + confusion, assume CO exposure:

• Give 100% oxygen immediately (non-rebreather; secure airway if needed).
• Check co-oximetry / carboxyhemoglobin level on blood gas—not standard SpO₂.
• Consider hyperbaric oxygen for severe neurologic symptoms, syncope, significant acidosis, pregnancy, or high COHb.
• In an enclosed-space fire, also consider cyanide toxicity, especially with severe lactic acidosis, hypotension, or cardiovascular collapse; hydroxocobalamin may be indicated.

Exam trap: normal SpO₂ does not rule out CO poisoning.

Carbon monoxide poisoning—standard pulse oximetry can look normal because it cannot reliably distinguish oxyhemoglobin from carboxyhemoglobin.

• Clues: enclosed-space fire, headache, confusion, nausea/syncope.
• Check: arterial/venous blood gas with co-oximetry for carboxyhemoglobin; PaO₂ may also be normal.
• Act: give 100% high-flow oxygen immediately; consider hyperbaric oxygen for severe neurologic features, significant COHb elevation, cardiac ischemia, severe acidosis, or pregnancy.
• Also don’t miss: cyanide toxicity in major enclosed-space smoke inhalation—think profound lactic acidosis, hypotension, seizures/cardiovascular collapse; hydroxocobalamin is the usual antidote.

If this is a real patient, treat as an emergency even with a “99%” SpO₂.

You’re missing carbon monoxide (CO) poisoning. A normal pulse oximeter reading can be falsely reassuring because standard SpO₂ cannot distinguish oxyhemoglobin from carboxyhemoglobin—so it may read 99% despite significant tissue hypoxia.

In a house-fire patient with headache and confusion:

• Remove from exposure and give 100% high-flow oxygen immediately.
• Check COHb with co-oximetry—not routine pulse oximetry or standard ABG saturation.
• Obtain ECG, glucose, lactate, electrolytes, blood gas, and assess for trauma/inhalation injury.
• Consider cyanide toxicity if there was an enclosed-space fire plus severe altered mental status, shock, or markedly elevated lactate; discuss empiric hydroxocobalamin with toxicology/emergency specialists.
• Urgent hyperbaric consultation if severe neurologic symptoms, loss of consciousness, ischemia, severe acidosis, pregnancy, or markedly elevated COHb.

If this is a real patient, treat it as an emergency and activate EMS/ED/toxicology support now—don’t wait for the COHb result.

Carbon monoxide (CO) poisoning—the classic trap is that SpO₂ can read 99% despite significant tissue hypoxia, because standard pulse oximeters misread carboxyhemoglobin as oxyhemoglobin.

• Suspect with headache, confusion, dizziness, nausea after fire exposure.
• Check carboxyhemoglobin by co-oximetry; a routine ABG/PaO₂ may also look normal.
• Remove from exposure and give 100% oxygen immediately; involve toxicology/emergency services urgently.
• Consider hyperbaric oxygen consultation for severe neurologic symptoms, loss of consciousness, cardiac ischemia, severe acidosis, pregnancy, or markedly elevated COHb.
• In a severe enclosed-space fire with shock or profound lactic acidosis, also consider cyanide toxicity.

If this is a real patient, treat it as an emergency—don’t be reassured by the SpO₂.

I’ll pull together a focused RA quiz with NEET PG-style clinical and concept traps.I hit a backend permission issue while fetching the question bank, so I can’t load the interactive quiz card right now.

But I can still give you a 10-question NEET PG-style RA quiz directly in chat if you want — with answers hidden first, then explanations after you attempt.

I’ll build a balanced NEET-PG set covering diagnosis, antibodies, extra-articular features, imaging, and treatment traps.I couldn’t retrieve the quiz bank because of a temporary access error. Please try again shortly, and I’ll generate the 10-question rheumatoid arthritis quiz.

I’ll put together a focused NEET PG–style RA set with diagnosis, antibodies, imaging, and treatment traps.I couldn’t access the quiz bank right now. Want me to make a fresh 10-question RA mini-test directly here instead?

I’ll make it exam-style—mixing core concepts with the usual NEET-PG traps.I couldn’t access the question bank right now. Want me to make a fresh 10-question NEET-PG-style RA quiz directly here instead?

I’ll build a 10-question NEET-PG-style set focused on rheumatoid arthritis diagnosis, antibodies, complications, and treatment traps.I couldn’t load the quiz right now because the question bank returned a technical access error. Please try again in a moment—I’ll generate the 10-question rheumatoid arthritis set when it’s available.

I’m building a 10-question, exam-focused rheumatoid arthritis set with a mix of diagnosis, antibodies, complications, and treatment traps.The question bank isn’t returning results right now, so I can’t launch the interactive quiz reliably. I can still give you a 10-question RA quiz directly in chat if you want.The question bank isn’t returning results right now, so I can’t launch the interactive quiz reliably. I can still give you a 10-question RA quiz directly in chat if you want.

I’ll find the most relevant Oncourse lesson for nephrotic syndrome and bring it up.I couldn’t pull up an Oncourse lesson because there are no enrolled course subjects available in your profile right now.

If you want, I can still teach nephrotic syndrome here directly — high-yield style with causes, pathophys, complications, and exam traps.

I’ll find the most focused nephrotic syndrome lesson for a quick, exam-relevant review.I couldn’t find a lesson because no enrolled course subjects are linked to your profile. Enroll in a course or select a subject, then I can pull up the nephrotic syndrome lesson.

I’ll pull up a focused nephrotic syndrome lesson—prioritizing mechanisms, causes, and exam traps.I can’t access any enrolled-course lessons right now. Want me to give you a crisp nephrotic syndrome overview here instead?

I’m finding a focused nephrotic syndrome lesson—start with the core mechanisms, then hit the exam traps.I can’t pull a lesson yet because there isn’t an enrolled course available in your account. If you enroll in a course, I’ll fetch the best nephrotic syndrome lesson straight away.

I’ll pull up the most relevant nephrotic syndrome lesson for focused exam prep.I couldn’t pull up a lesson because no enrolled course subjects are available in your account. Add/enrol in a course, then I can fetch the nephrotic syndrome lesson directly.

I’ll pull up a focused nephrotic syndrome lesson with the core exam patterns and differentiators.I couldn’t pull a lesson because no enrolled course subjects are linked to your account yet. You can still study nephrotic syndrome here—ask me for a quick explanation, flashcards, or a practice quiz.

Tachycardia means an abnormally fast heart rate.

For adults, it’s usually defined as a heart rate >100 beats/min at rest.

Quick exam framing:

• Sinus tachycardia: fast but normal rhythm, often due to fever, anxiety, pain, anemia, hypovolemia, hyperthyroidism, etc.
• Pathological tachyarrhythmias: abnormal fast rhythms like SVT, atrial fibrillation with rapid ventricular response, ventricular tachycardia.

Key idea: tachycardia is a rate finding, not a diagnosis by itself — always ask *why is the heart fast?*

Tachycardia means an abnormally fast heart rate—typically >100 beats/minute in a resting adult.

It may be:

• Physiological: exercise, anxiety, fever, pregnancy
• Pathological: anemia, dehydration, hyperthyroidism, arrhythmias, or heart disease

The threshold varies with age and clinical context.

Tachycardia means an abnormally fast heart rate—usually >100 beats/minute at rest in adults.

It can be normal temporarily (exercise, anxiety, fever, pain), or due to problems such as dehydration, anemia, hyperthyroidism, medications, or an abnormal heart rhythm.

Exam anchor:

• *Tachycardia* = rate >100/min
• *Bradycardia* = rate <60/min

The key next question is whether it is sinus tachycardia (normal rhythm, just fast) or an arrhythmia like SVT/AF/VT.

Tachycardia means an abnormally fast heart rate.

• In most adults at rest: >100 beats/minute (bpm)
• It can be normal temporarily—during exercise, fever, anxiety, pain, dehydration, or pregnancy.
• It can also result from an abnormal heart rhythm, such as supraventricular tachycardia (SVT), atrial fibrillation, or ventricular tachycardia.

Exam hook: *Tachy = fast; cardia = heart.*

If a fast pulse comes with chest pain, fainting, severe breathlessness, or persistent palpitations, it needs urgent medical assessment.

Tachycardia means an abnormally fast heart rate.

• Adults: resting heart rate >100 beats/minute
• It may be normal/physiological—for example during exercise, fever, pain, anxiety, or dehydration.
• Or it may be due to an arrhythmia, such as supraventricular tachycardia, atrial fibrillation, or ventricular tachycardia.

Symptoms can include palpitations, dizziness, breathlessness, chest discomfort, or fainting—but some people have no symptoms.

Exam anchor: tachycardia = rate >100/min in an adult at rest.

Tachycardia means an abnormally fast heart rate.

• Adults: resting heart rate >100 beats/minute
• It may be normal during exercise, fever, pain, stress, or caffeine intake.
• It can also result from problems such as anemia, hyperthyroidism, dehydration, infection, or abnormal cardiac rhythms (arrhythmias).

Common symptoms include palpitations, dizziness, shortness of breath, chest discomfort, or fainting—though some people have no symptoms.

Exam anchor: Tachycardia describes the rate, not necessarily the rhythm. A fast rhythm may be regular or irregular.

Starling forces = the pressures that decide whether fluid leaves capillaries into interstitium or comes back into capillaries.

The 4 forces

• Capillary hydrostatic pressure — Pc
• Pushes fluid out of capillary
• Think: blood pressure inside vessel

• Interstitial hydrostatic pressure — Pi
• Pushes fluid into capillary
• Usually small; can oppose filtration

• Capillary oncotic pressure — πc
• Pulls fluid into capillary
• Due mainly to plasma proteins, especially albumin

• Interstitial oncotic pressure — πi
• Pulls fluid out of capillary
• Due to proteins in interstitial fluid

Net filtration pressure

\[

NFP = (P_c - P_i) - (\pi_c - \pi_i)

\]

Or simply:

Outward forces − inward forces

Clinical high-yield

Edema occurs when filtration increases, like in:

• ↑ Pc: heart failure, venous obstruction
• ↓ πc: nephrotic syndrome, liver failure, malnutrition
• ↑ πi: inflammation, burns
• Lymphatic blockage: filariasis, malignancy, surgery

Memory hook:

Hydrostatic pushes, oncotic pulls.

Starling forces determine fluid movement across capillary walls:

\[

J_v = K_f[(P_c-P_i)-\sigma(\pi_c-\pi_i)]

\]

• \(P_c\): Capillary hydrostatic pressure → pushes fluid out
• \(P_i\): Interstitial hydrostatic pressure → pushes fluid into capillary
• \(\pi_c\): Plasma oncotic pressure → pulls fluid into capillary
• \(\pi_i\): Interstitial oncotic pressure → pulls fluid out

Net filtration pressure:

\[

(P_c+\pi_i)-(P_i+\pi_c)

\]

• Positive → filtration
• Negative → reabsorption

Exam trap: Modern model says most filtered fluid returns via lymphatics, with little sustained reabsorption at the venous end.

Starling forces determine fluid movement across capillary walls:

\[

J_v = K_f \big[(P_c - P_i) - \sigma(\pi_c - \pi_i)\big]

\]

• \(P_c\) = capillary hydrostatic pressure → pushes fluid out
• \(P_i\) = interstitial hydrostatic pressure → pushes fluid in
• \(\pi_c\) = plasma oncotic pressure (albumin) → pulls fluid in
• \(\pi_i\) = interstitial oncotic pressure → pulls fluid out

Easy memory:

Hydrostatic pushes; oncotic pulls.

Clinical link:

• ↑ \(P_c\): heart failure/venous obstruction → edema
• ↓ \(\pi_c\): hypoalbuminemia (nephrotic syndrome, cirrhosis) → edema
• ↑ permeability (\(K_f\), lower \(\sigma\)): inflammation/burns → edema

Starling forces determine fluid movement across capillary walls.

Net filtration =

\[

(\text{Capillary hydrostatic pressure} + \text{Interstitial oncotic pressure})

• (\text{Interstitial hydrostatic pressure} + \text{Capillary oncotic pressure})

\]

• Capillary hydrostatic pressure (Pc): pushes fluid out of capillary.
• Interstitial hydrostatic pressure (Pi): pushes fluid into capillary.
• Capillary oncotic pressure (πc): plasma proteins pull fluid into capillary.
• Interstitial oncotic pressure (πi): interstitial proteins pull fluid out.

Classic pattern:

• Arteriolar end → higher Pc → filtration out
• Venular end → lower Pc, πc dominates → reabsorption in

Exam link: Edema occurs with ↑Pc (heart failure), ↓πc (hypoalbuminemia), ↑capillary permeability, or lymphatic obstruction.

Starling forces determine fluid movement across capillaries:

\[

\text{Net filtration pressure} =

(P_c-P_i)-(\pi_c-\pi_i)

\]

• \(P_c\): capillary hydrostatic pressure → pushes fluid out
• \(P_i\): interstitial hydrostatic pressure → pushes fluid into capillary
• \(\pi_c\): plasma oncotic pressure, mainly albumin → pulls fluid into capillary
• \(\pi_i\): interstitial oncotic pressure → pulls fluid out

Net effect:

• Arterial end: higher hydrostatic pressure → filtration
• Venous end: lower hydrostatic pressure → reabsorption
• Excess filtered fluid returns via the lymphatics

Exam hook:

Hydrostatic pressure pushes; oncotic pressure pulls.

Starling forces determine fluid movement across capillaries:

• Capillary hydrostatic pressure (Pᶜ): pushes fluid out of capillary → filtration
• Interstitial hydrostatic pressure (Pⁱ): pushes fluid into capillary
• Plasma oncotic pressure (πᶜ): albumin pulls fluid into capillary
• Interstitial oncotic pressure (πⁱ): proteins pull fluid out → filtration

Net filtration pressure:

\[

\text{NFP} = (P_c - P_i) - (\pi_c - \pi_i)

\]

• Positive NFP → filtration into interstitium
• Negative NFP → reabsorption into capillary

Exam hook:

Hydrostatic pushes; oncotic pulls. Lymphatics remove excess filtered fluid.