Respiration

Respiration is the pathway by which atmospheric O₂ enters the body and CO₂ leaves it. The PMDC MDCAT 2026 syllabus lists one subtopic here — the human respiratory system — with three outcomes: the functions of its main parts, gas exchange in the lungs, and the effect of smoking. Expect 3-4 MCQs.

PMC Table of Specifications. Focus topic — Human Respiratory System. Sub-areas to nail: the parts of the tract and what each does, why the alveolus is an ideal gas-exchange surface, and how smoking damages that surface.

Human Respiratory System

The human respiratory tract is a continuous tube from the nose to the alveoli. It is split into a conducting zone (no gas exchange) and a respiratory zone (gas exchange occurs).

Pathway of air

Nose / mouth → pharynx → larynx (with vocal cords and epiglottis) → trachea → right and left primary bronchi → secondary & tertiary bronchi → bronchioles → terminal bronchioles → respiratory bronchioles → alveolar ducts → alveoli.

Functions of the main parts

Parts of the human respiratory system and what each does
Part	Function
Nasal cavity	Warms, moistens and filters incoming air; hairs and ciliated mucous membrane trap dust; houses the olfactory receptors.
Pharynx	Common passage for air and food.
Larynx (voice box)	Contains the vocal cords for sound production. The epiglottis closes it during swallowing so food enters the oesophagus, not the trachea.
Trachea	Kept permanently open by C-shaped cartilage rings; its ciliated, mucus-secreting epithelium sweeps trapped particles upward to the pharynx.
Bronchi	Carry air into each lung; branch repeatedly. Cartilage decreases and smooth muscle increases as they narrow.
Bronchioles	No cartilage — smooth muscle regulates their diameter and so the distribution of air.
Alveoli	The site of gas exchange: O₂ diffuses into the blood and CO₂ diffuses out.
Diaphragm & intercostal muscles	Change the volume of the thoracic cavity, drawing air in and pushing it out.
Pleura	Double membrane with pleural fluid between the layers; reduces friction as the lungs move.

Alveoli — the gas-exchange unit

Each lung contains ~300 million alveoli, giving a total surface area of ~70 m². Features that make them ideal exchange surfaces:

One-cell-thick squamous epithelium → very short diffusion distance (<1 µm).
Dense pulmonary capillary network → large area for diffusion and a steep gradient maintained by blood flow.
Surfactant (made by Type II alveolar cells) lowers surface tension and prevents collapse during expiration. Surfactant deficiency in premature babies causes respiratory distress syndrome.

Gas exchange in the lungs

Exchange is passive diffusion down partial-pressure gradients across the thin alveolar–capillary membrane. Deoxygenated blood arriving from the pulmonary artery has a low pO₂ and a high pCO₂; alveolar air is the reverse. So O₂ diffuses alveolus → blood and CO₂ diffuses blood → alveolus, and the blood leaving in the pulmonary vein is oxygenated. Breathing keeps replacing the alveolar air, which keeps the gradients steep.

Effect of smoking on the respiratory system

Tobacco smoke contains ~4,000 chemicals; three matter most for MDCAT:

Tar: A sticky mixture of carcinogens. It paralyses and destroys the cilia of the tracheal and bronchial epithelium, so mucus and trapped particles are no longer swept upwards. Mucus accumulates, provoking "smoker’s cough" and repeated infections.
Nicotine: The addictive component. It is a stimulant that causes vasoconstriction and raises heart rate and blood pressure.
Carbon monoxide (CO): Binds haemoglobin about 250 times more strongly than O₂, forming carboxyhaemoglobin and cutting the oxygen-carrying capacity of the blood.

Long-term consequences follow directly from this damage:

Chronic bronchitis — persistent inflammation and over-production of mucus in the airways.
Emphysema — alveolar walls are broken down, so the many small alveoli merge into fewer large air spaces. Surface area for gas exchange falls sharply and elastic recoil is lost, leaving the patient breathless.
Lung cancer — carcinogens in tar cause mutations in bronchial epithelium; smoking is by far its leading cause.

Memory aid. "Thin, wet, wide, windy" — the four things every good gas-exchange surface needs: a thin wall, a moist lining, a large surface area, and a good blood/air supply to keep the diffusion gradient steep. The alveolus scores on all four; emphysema destroys the third.

Worked MCQs

Five MCQs covering the high-yield testing patterns for the human respiratory system.

Q1. The trachea is prevented from collapsing by:

Complete rings of bone
C-shaped rings of cartilage
Rings of smooth muscle
Its ciliated epithelium

Incomplete, C-shaped cartilage rings hold the trachea permanently open while leaving the posterior wall soft, so the oesophagus behind it can bulge as a bolus passes. Bronchioles, by contrast, have no cartilage — only smooth muscle.

Q2. Which structure prevents food from entering the trachea during swallowing?

Vocal cords
Soft palate
Epiglottis
Uvula

The epiglottis is a flap of elastic cartilage that folds down over the glottis as the larynx rises during swallowing, directing the bolus into the oesophagus. The vocal cords produce sound; the soft palate closes off the nasal cavity.

Q3. Gas exchange in the human lung takes place by:

Active transport across alveolar cells
Simple diffusion down partial-pressure gradients
Osmosis through the alveolar wall
Facilitated diffusion using carrier proteins

O₂ and CO₂ cross the alveolar–capillary membrane passively, each moving from higher to lower partial pressure. No ATP and no carrier is involved — which is why a thin wall, a large surface area and a steep gradient are the things that determine the rate.

Q4. Surfactant secreted by type II alveolar cells functions to:

Increase the diffusion distance for oxygen
Trap inhaled dust particles
Lower surface tension and stop the alveoli collapsing
Bind oxygen for transport to the blood

The moist alveolar lining would otherwise generate enough surface tension to pull the tiny alveoli shut on expiration. Surfactant lowers that tension. Premature babies who have not yet made enough surfactant develop respiratory distress syndrome.

Q5. Emphysema in a long-term smoker reduces gas exchange mainly because:

The trachea becomes blocked with mucus
Alveolar walls break down, so the surface area for diffusion falls
Haemoglobin is destroyed by tar
The epiglottis no longer closes properly

Destruction of alveolar walls merges many small alveoli into a few large air spaces, so total surface area collapses and elastic recoil is lost. Tar separately paralyses and destroys cilia (causing smoker’s cough), and carbon monoxide separately reduces the blood’s oxygen-carrying capacity — but the emphysema itself is a surface-area problem.

Quick Recap

Air pathway: nose → pharynx → larynx → trachea → bronchi → bronchioles → alveoli (~300 million, surface area ~70 m²).
Nose warms, moistens and filters; epiglottis guards the larynx; trachea is held open by C-shaped cartilage and cleared by cilia; bronchioles have smooth muscle but no cartilage.
Alveoli are the gas-exchange site: one-cell-thick wall, moist lining, huge area, dense capillary network.
Surfactant from type II cells lowers alveolar surface tension and prevents collapse.
Exchange is passive diffusion: O₂ alveolus → blood, CO₂ blood → alveolus, down partial-pressure gradients.
Smoking: tar destroys cilia (smoker’s cough, infections) and is carcinogenic; nicotine is the addictive stimulant; CO forms carboxyhaemoglobin.
Smoking-related damage: chronic bronchitis, emphysema (lost alveolar surface area), lung cancer.

Test yourself. Take a timed practice test or browse topic-wise MCQs to lock these concepts in.