AN6.1-3 | General Features of lymphatic system — Gate Quiz

Correct! The thoracic duct (the largest lymphatic vessel) drains into the left subclavian vein at its junction with the left internal jugular vein (left venous angle). It drains the entire left side of the body and the right side below the diaphragm.

Thoracic duct → left subclavian vein (at left venous angle). Right lymphatic duct → right subclavian vein. Rule of thumb: Everything except the right upper quadrant (right head/neck/arm/thorax) drains via the thoracic duct.

Incorrect. The thoracic duct drains into the left subclavian vein at the venous angle. The right lymphatic duct (which drains the right head/neck, right arm, and right thorax) drains into the right subclavian vein.

Correct! Lacteals absorb long-chain fatty acids (>12 carbons) packaged with apolipoprotein B-48 as chylomicrons. This lipid-rich lymph is called chyle and appears milky. It enters the thoracic duct and reaches the bloodstream via the left subclavian vein.

Fat absorption route: long-chain FAs → chylomicrons in enterocytes → lacteals → thoracic duct → blood. Short-chain and medium-chain FAs (<12 carbons) bypass lacteals and enter portal blood directly.

Incorrect. Glucose and amino acids are absorbed by intestinal epithelial cells directly into blood capillaries of the portal circulation (not lacteals). Long-chain fatty acids are packaged as chylomicrons and absorbed via lacteals.

Correct! Lymphatic capillary endothelial cells overlap like roof tiles. Anchoring filaments connect these cells to the surrounding collagen matrix. When interstitial pressure rises (oedema), the anchoring filaments pull the cells apart, opening gaps for fluid entry. This is a pressure-activated one-way valve mechanism.

Lymphatic capillary entry: increased interstitial pressure → anchoring filaments pull endothelial cells apart → gaps open → fluid enters. Decreased pressure → cells close → prevents backflow. This is the first valve in the lymphatic system.

Incorrect. Tight junctions would seal the vessel (blood capillary pattern). Semilunar valves prevent backflow in collecting vessels, not at the capillary level. The basement membrane of lymphatic capillaries is discontinuous.

Correct! Lymphangions are contractile units of collecting lymphatic vessels bounded by semilunar valves. The smooth muscle in their wall contracts rhythmically (intrinsic propulsion), generating pressure to drive lymph forward — analogous to a peristaltic pump.

Lymph propulsion mechanisms: (1) Intrinsic — smooth muscle of lymphangion (primary driver); (2) Extrinsic — skeletal muscle pump, respiratory pump, arterial pulsation. Valves prevent backflow. Bed rest impairs extrinsic mechanisms → leg oedema in bedridden patients.

Incorrect. Skeletal muscle, respiratory, and arterial pulsation effects are all external (extrinsic) forces. Smooth muscle contraction of the lymphangion itself is the intrinsic mechanism.

Correct! Blood capillaries leak some plasma proteins (especially albumin) into the interstitium. Lymphatics return these proteins to circulation. When lymphatics are blocked, proteins accumulate in the interstitium, raising local colloid osmotic pressure and drawing water in. The resulting fluid is protein-rich and becomes fibrotic over time — hence non-pitting (as opposed to sodium/water accumulation in cardiac oedema which is protein-poor and pitting).

Lymphoedema = protein-rich oedema → non-pitting → progressive fibrosis. Cardiac/renal oedema = protein-poor, salt-water oedema → pitting (protein does not accumulate). Treatment: compression, physiotherapy; poorly responsive to diuretics (protein remains).

Incorrect. The mechanism of non-pitting lymphoedema is protein accumulation (not removed by failed lymphatics) → increased interstitial oncotic pressure. Cardiac oedema has excess salt-water but normal lymphatic removal of proteins (early).

Correct! Adult Wuchereria bancrofti worms reside in lymphatic vessels and lymph nodes. Their physical presence and the host immune reaction cause obstruction, inflammation, and eventually fibrosis of lymphatics → chronic lymphatic obstruction → lymphoedema → elephantiasis if untreated.

Filariasis lifecycle: mosquito bite → L3 larvae → develop into adult worms in lymphatics → microfilariae released into blood (nocturnal peak) → mosquito ingests microfilariae → cycle continues. Disease = adult worm obstruction → elephantiasis. Treatment: diethylcarbamazine (DEC) or ivermectin + albendazole (MDA programme in India).

Incorrect. The adult worms (not microfilariae) block lymphatics mechanically and by provoking inflammation. Microfilariae are the larval stage that circulate in blood (nocturnal periodicity) and are taken up by mosquitoes.

Correct! A negative sentinel lymph node biopsy indicates the first-draining regional node is free of cancer cells. By convention, this predicts with high accuracy that the remaining axillary nodes are also negative — full axillary dissection (with its risk of lymphoedema) can be safely omitted.

SLNB principle: if the sentinel (first-draining) node is negative → no further dissection. If positive → proceed to axillary node clearance. SLNB has revolutionised breast cancer surgery by dramatically reducing the incidence of arm lymphoedema while maintaining oncological safety.

Incorrect. The rationale of SLNB is to avoid unnecessary axillary dissection in node-negative patients. A negative sentinel node on frozen section is sufficient to proceed without full dissection (reducing lymphoedema risk by 60–70%).

Correct! The sigmoid colon drains venously into the inferior mesenteric vein → portal vein → liver. Portal venous spread is the characteristic route for colorectal cancer liver metastases. The liver is the primary filter of portal blood, so it is the first and most common site of metastasis from GI cancers.

Cancer spread routes: Lymphatics → regional nodes → distant (thoracic duct → lungs). Portal venous spread → liver (GI cancers). Systemic venous spread → lungs. Liver metastases without lymph node involvement = portal venous spread (colorectal, gastric, pancreatic cancer pattern).

Incorrect. Mesenteric/para-aortic lymph node spread would show lymph node enlargement (not seen here). Transcoelomic spread produces peritoneal nodules (carcinomatosis), not liver deposits. Thoracic duct → systemic circulation → pulmonary metastases would be the sequence for lymphatic distant spread.

Correct! The thymus is a primary lymphoid organ where T-lymphocyte precursors undergo maturation, positive selection (must recognise self-MHC), and negative selection (must not react to self-antigens). Mature naive T cells are then released to peripheral lymphoid organs.

Primary lymphoid organs: Thymus (T cell maturation) + Bone marrow (B cell maturation). Secondary lymphoid organs: Lymph nodes + Spleen + Tonsils + MALT (Peyer's patches). Primary = development site; Secondary = response site.

Incorrect. Spleen, lymph nodes, and tonsils are secondary lymphoid organs where immune responses are initiated. Primary lymphoid organs (thymus for T cells, bone marrow for B cells) are where lymphocyte development occurs.

Correct! Inguinal lymph node dissection severs the lymphatic collecting vessels draining the lower limb. This causes secondary lymphoedema — chronic, progressive, non-pitting, protein-rich swelling that is firm due to protein deposition and progressive fibrosis. Normal ABPI excludes arterial disease; non-pitting character distinguishes it from DVT or hypoalbuminaemia.

Post-dissection lymphoedema: unilateral, non-pitting, progressive, starts weeks to months after surgery. Treatment: compression garments, manual lymphatic drainage, skin care. Prevention: minimise dissection extent, preserve lymphatic structures when possible.

Incorrect. DVT would cause acute, tender, pitting swelling with abnormal venous duplex (and ABPI might be affected). Hypoalbuminaemia causes bilateral pitting oedema. Venous insufficiency causes pitting oedema. Non-pitting unilateral post-dissection oedema = lymphoedema.