1. In Haemolytic Jaundice, urine is not coloured.[3][2011] 2. Aspirin in low dose prevents intravascular coagulation.[3][2012][2016] 3. Low plasma protein causes oedema.[3][2012] 4. Normal plasma proteins prevent oedema.[3][2014] 5. Anaemia occurs after gastrectomy.[3][2013][2015] 6. Coagulation time is prolonged in obstructive jaundice.[3][2015] 7. Anaemia occurs in chronic renal failure.[3][2016] 8. Bleeding tendency occurs in obstructive jaundice. [3] [2018] Biconcave shape of RBC is advantageous.[2025] 9. RBCs/ Hematocrit in venous blood are larger than in arterial blood. [3] [2018] [2016 supple.] [2022] 10. Coagulation is an example of a positive feedback mechanism. [4] [NEW PATTERN 2021] 11. Low dose aspirin is used in prevention of myocardial infarction. [4] [NEW PATTERN 2021] 12. Relative lymphocytosis occurs in bone marrow depression in adults. [2019 supple.] 13. Cyanide poisoning causes high pO2 in venous blood. [2019 supple.] 14. Level of albumin is the most important factor that contributes to colloidal osmotic tension.[2024] 15. Foetus does not evoke any immunological response in mother. [2024]

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Physiology Essay/Short Answer Questions - Explained

1. In Haemolytic Jaundice, Urine is Not Coloured

TRUE.

In haemolytic (pre-hepatic) jaundice, the excess bilirubin in circulation is unconjugated (indirect bilirubin). Unconjugated bilirubin is:

Water-insoluble
Bound tightly to plasma albumin
Not filtered by the glomerulus - so it cannot appear in urine

This is why haemolytic jaundice is also called acholuric jaundice - "acholuria" means no bile pigments in urine. The S Das textbook confirms: "The circulating excess bilirubin remains unconjugated with glycuronic acid and is attached to albumin. This is not excreted through urine. Hence it is called acholuric jaundice."

However, urobilinogen is increased in urine (due to increased bilirubin load reaching the gut), but it is colourless. The urine is not dark/brown/yellow.

Contrast with obstructive jaundice: Here, conjugated (direct) bilirubin is water-soluble, spills into blood, is filtered by glomerulus, and appears in urine making it dark brown/tea-coloured.

2. Aspirin in Low Dose Prevents Intravascular Coagulation (Thrombosis)

TRUE.

Low-dose aspirin (75-150 mg/day) exerts a selective anti-platelet effect based on differential sensitivity of platelets vs. endothelial cells to COX inhibition:

Cell	COX-1 product	Effect	Aspirin sensitivity
Platelet	Thromboxane A2 (TxA2)	Pro-aggregatory, vasoconstrictor	Very sensitive - platelets are anucleate, cannot synthesise new COX
Endothelial cell	Prostacyclin (PGI2)	Anti-aggregatory, vasodilator	Partially spared - nucleated cells regenerate COX

Mechanism:

Aspirin irreversibly acetylates COX-1, blocking TxA2 synthesis
Platelets are anucleate - they cannot produce new COX enzyme for their entire 7-10 day lifespan
Endothelial cells have nuclei and regenerate COX within hours, preserving PGI2 production
Net result: TxA2 ↓↓ while PGI2 is relatively maintained → platelet aggregation inhibited → thrombosis prevented

The Scott-Brown textbook states: "Aspirin in low dose blocks the formation of thromboxane A2 in platelets for the life of the platelet; however, there is little effect on prostacyclin (because endothelial cells have a nucleus to produce further enzyme to produce more prostacyclin)."

3 & 4. Low Plasma Protein Causes Oedema / Normal Plasma Proteins Prevent Oedema

Both TRUE - two sides of the same coin.

Plasma proteins (primarily albumin, contributing ~80% of oncotic pressure) are the key determinant of plasma colloidal osmotic pressure (COP), also called oncotic pressure (~25-28 mmHg).

Starling's forces at the capillary:

Net filtration = (Pcap - Pif) - (πpl - πif)

Where πpl = plasma oncotic pressure (from proteins)

When plasma proteins fall (hypoproteinaemia):

Plasma COP falls
The balance of Starling forces shifts toward filtration
Fluid moves out of capillaries into interstitium
Oedema results

Common causes of low-protein oedema:

Nephrotic syndrome (protein loss in urine)
Liver cirrhosis (reduced albumin synthesis)
Protein-energy malnutrition (kwashiorkor)
Protein-losing enteropathy

Normal albumin (3.5-5 g/dL) maintains COP and retains fluid within vessels, preventing oedema.

5. Anaemia Occurs After Gastrectomy

TRUE. Multiple mechanisms:

A. Iron Deficiency Anaemia (early, most common)

Gastric acid (HCl) converts Fe³⁺ (ferric) to Fe²⁺ (ferrous) - the absorbable form
Gastrectomy → loss of gastric acid → reduced iron reduction and absorption
Duodenum and proximal jejunum (main iron absorption sites) may be bypassed in Billroth II reconstruction
Presents as microcytic hypochromic anaemia

B. Vitamin B12 Deficiency Anaemia (late, months-years later)

Intrinsic factor (IF) is produced by gastric parietal cells
IF is essential for B12 absorption in the terminal ileum
Gastrectomy → loss of parietal cells → no IF → B12 malabsorption
Body stores of B12 last ~3-5 years, so anaemia is delayed
Presents as megaloblastic (macrocytic) anaemia with neurological complications
Bailey & Love confirms: "Vitamin B12 deficiency occurs after total gastrectomy; however, it may be years before megaloblastic anaemia is clinically apparent. Vitamin B12 supplementation after total gastrectomy is essential."

C. Folate deficiency - may also occur due to dietary changes

6. Coagulation Time is Prolonged in Obstructive Jaundice

TRUE.

The mechanism involves Vitamin K malabsorption:

In obstructive jaundice, bile salts cannot reach the intestine (bile duct is blocked)
Bile salts are required for emulsification and absorption of fat-soluble vitamins (A, D, E, K)
Vitamin K deficiency results
Vitamin K is essential for gamma-carboxylation of clotting factors II (prothrombin), VII, IX, X (the "2, 7, 9, 10" factors) - as well as protein C and S
Without Vitamin K, these factors are non-functional
The coagulation cascade fails → prolonged prothrombin time (PT) and clotting time

Goldman-Cecil confirms: "Vitamin K is absorbed predominantly in the ileum and requires the presence of bile salts. Clinically significant vitamin K deficiency occurs with malabsorption of fat-soluble vitamins secondary to obstructive jaundice."

Clinical application: Patients with obstructive jaundice are given parenteral Vitamin K before any surgical procedure to correct coagulopathy.

7. Anaemia Occurs in Chronic Renal Failure

TRUE. This is normocytic normochromic anaemia with multiple causes:

Primary mechanism - Erythropoietin (EPO) deficiency:

The peritubular fibroblasts of the renal cortex produce 90% of body's EPO
Renal damage → loss of EPO-producing cells → EPO deficiency
EPO stimulates proliferation and differentiation of RBC precursors in bone marrow
Without EPO → reduced erythropoiesis → anaemia

Secondary mechanisms:

Uraemic toxins suppress bone marrow erythropoiesis
Shortened RBC survival (haemolysis due to uraemic environment)
Blood loss (platelet dysfunction, dialysis losses)
Iron and folate deficiency (dietary restriction, dialysis losses)
Hyperparathyroidism causing marrow fibrosis (in advanced CKD)

Treatment: Recombinant human EPO (e.g., epoetin alfa, darbepoetin) is the cornerstone of management, plus iron supplementation.

8. Bleeding Tendency Occurs in Obstructive Jaundice

TRUE - closely related to Q6 above.

The mechanism is the same - Vitamin K malabsorption leading to deficiency of factors II, VII, IX, X. The result is:

Prolonged prothrombin time (PT/INR)
Inability to form stable fibrin clots
Bleeding tendency - may manifest as easy bruising, prolonged bleeding from wounds, haemorrhage

Additionally, in severe/prolonged obstructive jaundice, endotoxaemia can cause DIC (Disseminated Intravascular Coagulation), worsening bleeding.

8b. Biconcave Shape of RBC is Advantageous

TRUE. The biconcave disc shape (7-8 µm diameter, 2 µm thick at edge, 1 µm at center) confers multiple advantages:

1. Maximum Surface Area: Volume Ratio

A sphere of the same volume would have ~25% less surface area
Greater surface area → faster, more efficient gas exchange (O2 loading, CO2 unloading)
Medical Physiology confirms: "The distinctive shape of the RBC provides a much larger surface-to-volume ratio than that of a spherical cell; this maximizes diffusion area and minimizes intracellular diffusion distances for gas exchange."

2. Minimal Diffusion Distance

Maximum intracellular distance to the membrane is only ~0.85 µm
Haemoglobin at the centre is close to the surface → rapid O2 and CO2 exchange

3. Deformability

The biconcave shape allows RBCs to deform and squeeze through capillaries (3-5 µm diameter) narrower than the RBC itself
The membrane has excess area, allowing shape changes without rupture

4. Stability at Low Osmotic Stress

Can swell by ~70% before haemolysing (vs. a sphere which would lyse immediately with any additional volume)

9. RBCs/Haematocrit in Venous Blood are Larger than in Arterial Blood

TRUE. This is due to the chloride shift (Hamburger phenomenon) and CO2 transport:

Mechanism in tissues/venous blood:

CO2 enters RBCs from tissues
CO2 + H2O → H2CO3 (carbonic anhydrase) → H⁺ + HCO3⁻
HCO3⁻ diffuses out of RBC in exchange for Cl⁻ entering (chloride shift)
The net entry of Cl⁻ (and accompanying water by osmosis) increases RBC volume
Also, CO2 itself dissolves within the RBC
Net result: venous RBCs are slightly larger and have higher haematocrit

Additional factor: Venous blood CO2 causes H⁺ to be buffered by Hb, slightly shifting osmotic balance toward the RBC

The difference is small but measurable - venous haematocrit is approximately 1-3% higher than arterial haematocrit.

10. Coagulation is an Example of a Positive Feedback Mechanism

TRUE.

Positive feedback means: the product of a reaction amplifies the reaction itself (opposite of homeostasis/negative feedback).

In coagulation:

Thrombin is the central amplifier
Thrombin, once formed, activates multiple upstream factors:
- Activates Factors V, VIII, XI (positive feedback loops)
- Activates platelets
- Factor V and VIII are cofactors that massively accelerate thrombin's own generation
This creates an explosive, self-amplifying cascade - once initiated, it proceeds rapidly to fibrin clot formation

Harrison's confirms: "After the initial TF-mediated reaction, the coagulation cascade is amplified in a propagation phase by an explosive positive feedback loop of coagulation reactions that occur on adjacent activated platelets."

This is why a small initial signal (tissue injury) produces a rapid, massive response - the hallmark of positive feedback. The feedback is eventually terminated by natural anticoagulants (antithrombin, protein C, TFPI).

11. Low-Dose Aspirin is Used in Prevention of Myocardial Infarction

TRUE - this is the clinical application of the mechanism in Q2.

Mechanism: Selective inhibition of TxA2 in platelets while sparing endothelial PGI2 → reduced platelet aggregation → reduced coronary artery thrombosis
Dose used: 75-150 mg/day (previously 81 mg in USA)
Used in: Secondary prevention of MI (patients who have had a prior MI, unstable angina, or PCI/stenting)
Primary prevention: Now controversial/limited - current guidelines (2019 ACC/AHA) recommend against routine primary prevention use in most adults due to bleeding risk outweighing benefit, except in selected high-risk patients

The Lippincott Biochemistry text states: "This difference is the basis of low-dose aspirin therapy used to lower the risk of stroke and heart attacks by decreasing formation of thrombi."

12. Relative Lymphocytosis Occurs in Bone Marrow Depression in Adults

TRUE.

When bone marrow is depressed (aplastic anaemia, cytotoxic chemotherapy, radiation), the most severely affected cells are those with rapid turnover:

Neutrophils (half-life ~6-8 hours)
Platelets (lifespan ~10 days)
RBCs are affected later (lifespan 120 days)

Lymphocytes, however:

Are largely long-lived cells (memory T and B cells can last decades)
Many circulate and survive independent of ongoing bone marrow production
Are relatively spared in early/moderate marrow depression

Result: Total WBC count falls due to neutropenia, but lymphocytes remain numerically stable → lymphocytes form a higher percentage of WBCs = relative lymphocytosis (even though absolute lymphocyte count may be normal or only mildly reduced).

This is different from absolute lymphocytosis (e.g., CLL, viral infections) where the absolute number increases.

13. Cyanide Poisoning Causes High pO2 in Venous Blood

TRUE. This is a classic and important physiology fact.

Normal oxygen utilization:

Arterial blood delivers O2 to tissues
Tissues extract O2 → venous pO2 falls to ~40 mmHg
Venous blood is dark red (deoxygenated HbO2 → deoxy-Hb)

Cyanide mechanism:

Cyanide (CN⁻) binds to cytochrome c oxidase (Complex IV) of the mitochondrial electron transport chain
This blocks cellular respiration - cells cannot use O2
Tissues are unable to extract/utilise O2

Result:

O2 remains in venous blood unused
Venous pO2 remains high (approaching arterial levels, ~100 mmHg)
Venous blood appears bright red (cherry-red skin/mucosae is a classic sign of cyanide poisoning)
The patient shows signs of hypoxia despite high O2 levels - a histotoxic hypoxia

This is also why pulse oximetry may be falsely normal in cyanide poisoning - HbO2 saturation is maintained, but tissues are starving of usable oxygen.

14. Level of Albumin is the Most Important Factor Contributing to Colloidal Osmotic Tension

TRUE.

Colloidal osmotic pressure (oncotic pressure) is generated by plasma proteins that are too large to cross the capillary membrane. Although the plasma contains many proteins, albumin dominates because:

Quantitative dominance: Albumin = 3.5-5.0 g/dL, constituting ~60% of total plasma protein (total plasma protein ~7 g/dL)
Molecular size advantage: Albumin (MW ~66,000 Da) is smaller than globulins but present in far higher molar concentration - osmotic pressure depends on number of molecules, not mass
Donnan effect: Albumin carries negative charges at physiological pH; this restrains cations (especially Na⁺) within the vessel, adding to the effective osmotic pressure - the Gibbs-Donnan equilibrium
Contribution: Albumin accounts for approximately 75-80% of total plasma oncotic pressure (~21 of 25-28 mmHg total)

Clinical significance: In hypoalbuminaemia (nephrotic syndrome, cirrhosis, malnutrition), even if globulins are normal, oedema occurs because the albumin fraction is lost.

15. Foetus Does Not Evoke Any Immunological Response in Mother

FALSE (or more precisely: partially false / incomplete statement).

The foetus DOES evoke some immune responses, but multiple mechanisms prevent rejection:

Why the foetus SHOULD be rejected:

Expresses paternal MHC (HLA) antigens that are foreign to the mother
Should trigger T-cell mediated immune rejection

Why the foetus is NOT rejected (Immunological tolerance mechanisms):

Trophoblast lacks classical MHC Class I and II molecules - cannot be recognized by cytotoxic T-cells or helper T-cells in the usual way. It expresses non-classical HLA-G, HLA-E, HLA-C
HLA-G expression by trophoblast inhibits NK cell killing and promotes T-regulatory cell (Treg) induction
Decidual T-regulatory cells (Tregs) are expanded at the feto-maternal interface, suppressing effector T-cell responses
Indoleamine 2,3-dioxygenase (IDO) expressed by trophoblast degrades tryptophan, creating a local immunosuppressive environment
Progesterone has immunosuppressive effects, promoting Th2 skewing (tolerance) over Th1 (rejection)
Complement regulatory proteins (CD55/DAF, CD59) on trophoblast prevent complement-mediated lysis
Physical barrier: The trophoblast separates maternal blood from foetal tissues

Evidence that the mother DOES respond:

Mothers develop anti-paternal antibodies (antibodies against paternal HLA)
Rh isoimmunisation (Rh-negative mother forming antibodies against Rh-positive foetal RBCs)
Sensitisation in subsequent pregnancies proves maternal immune recognition

Conclusion: The foetus does evoke some maternal immune responses, but active tolerance mechanisms prevent rejection. The statement is oversimplified/incomplete - a better phrasing is that the foetus employs multiple strategies to evade maternal immune rejection.

Summary Table

#	Statement	Verdict	Key Mechanism
1	Haemolytic jaundice - urine not coloured	TRUE	Unconjugated bilirubin bound to albumin, not filtered
2	Aspirin low dose prevents intravascular coagulation	TRUE	Selective TxA2 inhibition in anucleate platelets
3	Low plasma protein causes oedema	TRUE	Reduced oncotic pressure - Starling forces
4	Normal plasma proteins prevent oedema	TRUE	Maintains oncotic pressure
5	Anaemia after gastrectomy	TRUE	Iron (↓HCl) + B12 deficiency (↓IF)
6	Coagulation time prolonged in obstructive jaundice	TRUE	Vitamin K malabsorption → factor II,VII,IX,X deficiency
7	Anaemia in chronic renal failure	TRUE	EPO deficiency + uraemic marrow suppression
8	Bleeding tendency in obstructive jaundice	TRUE	Same as #6
8b	Biconcave RBC shape is advantageous	TRUE	Max SA:Vol ratio, deformability, diffusion efficiency
9	RBCs/Haematocrit higher in venous blood	TRUE	Chloride shift - water follows Cl⁻ into RBC
10	Coagulation is positive feedback	TRUE	Thrombin activates its own upstream factors
11	Low-dose aspirin prevents MI	TRUE	Anti-platelet aggregation via TxA2 inhibition
12	Relative lymphocytosis in bone marrow depression	TRUE	Neutrophils depleted; long-lived lymphocytes spared
13	Cyanide poisoning - high venous pO2	TRUE	CN inhibits Complex IV → O2 not consumed by tissues
14	Albumin most important for colloidal osmotic tension	TRUE	75-80% of oncotic pressure; high molar concentration
15	Foetus doesn't evoke immune response in mother	FALSE/INCOMPLETE	Rh isoimmunisation proves maternal response; tolerance ≠ no response

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