A&P LECTURE (GOOD LUCK)

What is the primary function of the respiratory system (what)?

To supply the body with O₂ and remove CO₂ through ventilation, external respiration (lungs ↔ blood), transport, and internal respiration (blood ↔ tissues)

Who makes surfactant

Type II alveolar epithelial cells (type II pneumocytes).

What does surfactant do

Lowers alveolar surface tension so small alveoli don’t collapse (prevents atelectasis), increases lung compliance (easier to inflate), and helps normal recoil at high volumes.

When is surfactant production sufficient in fetal lungs (when)?

Around weeks 34–36 of gestation (L/S ratio ~2:1 indicates maturity).

How does the L/S ratio indicate fetal lung maturity

Lecithin increases with lung maturity while sphingomyelin stays constant; an L/S ≥ 2:1 usually means mature lungs.

What is lung compliance

A: Compliance = ΔV/ΔP; it’s how easily lungs/thorax expand for a given pressure change. High compliance = easy to inflate; low compliance = stiff lungs.

How does emphysema or aging affect compliance (how)?

Emphysema and aging increase compliance (lungs are easier to expand but lose elastic recoil).

How do pulmonary fibrosis, pulmonary edema, ARDS affect compliance

They decrease compliance (lungs are stiffer — harder to inflate).

What is elastance, and how is it related to compliance

Elastance = recoil (P/V), the inverse of compliance. Higher elastance = more recoil, lower compliance.

Where is intrapleural pressure measured / where (where)?

In the potential space between visceral and parietal pleura (intrapleural space). Normal resting intrapleural pressure is slightly subatmospheric (≈ −3 to −5 cm H₂O).

How do pressure differences cause air to flow during quiet inspiration (how sequence)?

Diaphragm + external intercostals contract → thoracic volume ↑ → intrapleural pressure becomes more negative → lungs expand → alveolar pressure drops below atmospheric → air flows in until pressure equals atmosphere.

What is FRC and what happens at FRC (what/when)?

Functional Residual Capacity = lung volume at the end of a normal exhalation. At FRC, inward lung recoil balances outward chest wall recoil; airway/alveolar pressure = atmospheric; intrapleural pressure is negative.

What is Laplace’s law for alveoli?

Collapsing pressure ∝ surface tension / radius (P ∝ T / r). Smaller alveoli have higher collapsing pressure if surface tension isn’t reduced by surfactant.

What are the main lung volumes (what — include rough values)?

TV ≈ 500 mL (tidal), IRV ≈ 3100 mL, ERV ≈ 1200 mL, RV ≈ 1200 mL.

What are the main lung capacities (what — equations & rough values)?

TLC ≈ 6000 mL (TV+IRV+ERV+RV), VC ≈ 4800 mL (TV+IRV+ERV), IC ≈ 3600 mL (TV+IRV), FRC ≈ 2400 mL (ERV+RV).

What is dead space

Dead space = volume of inspired air not participating in gas exchange. Anatomical dead space ≈ 150 mL (conducting airways). Physiologic dead space = anatomic + alveolar dead space (can increase with disease). AVR = RR × (TV − VD).

How does slow deep breathing affect alveolar ventilation

Slow, deep breaths increase alveolar ventilation (more of each breath reaches alveoli; less wasted in dead space).

What factors determine airway resistance (what)?

Gas viscosity, airway length, airway radius (radius most important — Poiseuille’s law). Medium-sized bronchi are major contributors; small terminal airways have high individual resistance but are numerous & parallel.

What causes bronchoconstriction (what)?

Parasympathetic activity, substance P, adenosine, hypersensitivity (histamine), leukotrienes/prostaglandins.

What causes bronchodilation

Sympathetic stimulation via β₂-adrenergic receptors (agonists cause bronchodilation).

How do obstructive vs restrictive lung diseases change mechanics

Obstructive: ↑ airway resistance → air trapping → increased lung volumes (RV ↑), FEV1/FVC ratio ↓. Restrictive: ↓ compliance → lower TLC and FVC; FEV1/FVC ratio is often normal or ↑ because both FEV1 and FVC drop proportionally.

What is the normal FEV1:FVC ratio and how is it changed in COPD

Normal ≈ 80%; in obstructive disease (e.g., emphysema, chronic bronchitis, asthma) the ratio is <80% (often 60–70% or less).

Which muscles are used in forceful expiration

Abdominals and internal intercostals push the diaphragm up and compress the thorax during active/forceful expiration (e.g., exercise).

Who controls rhythm/drive of breathing

Medullary centers: Dorsal Respiratory Group (DRG — inspiration) and Ventral Respiratory Group (VRG — active during forced breathing). Pontine centers: pneumotaxic (limits inspiration) and apneustic (promotes deep inspiration).

Where are central & peripheral chemoreceptors located and what do they sense

Central chemoreceptors: ventral medulla (sense H⁺ in CSF — reflect CO₂). Peripheral chemoreceptors: carotid & aortic bodies (sense ↓ PO₂, ↑ PCO₂, ↑ H⁺). CO₂ effect (via pH) is the major chemical drive.

How does the body respond to high altitude

Early: ↑ ventilation (hyperventilation) → ↓ PaCO₂ (respiratory alkalosis). Over time: ↑ EPO → ↑ hematocrit, ↑ 2,3-BPG, ↑ mitochondria, renal excretion of HCO₃⁻ for compensation. Pulmonary vasoconstriction can lead to pulmonary hypertension/edema in some.

How does exercise change ventilation and blood gases

Minute ventilation ↑ (first by ↑ TV, then RR). PaO₂ and PaCO₂ remain relatively stable during moderate exercise; CO₂ excretion increases massively to match production. A-a gradient may widen slightly with intense exercise.

What is the Bohr effect

Increased CO₂ and H⁺ (lower pH), higher temperature, and ↑2,3-BPG shift the hemoglobin-oxygen dissociation curve right → less O₂ affinity → easier O₂ unloading in tissues.

How is CO₂ transported in blood

~7–10% dissolved in plasma, ~20–30% bound to hemoglobin (carbamino), ~60–70% as bicarbonate (HCO₃⁻).

How is O₂ transported in blood

~1.5% dissolved in plasma, ~98.5% bound to hemoglobin.

What is the chloride shift

In tissues, HCO₃⁻ leaves RBCs to plasma and Cl⁻ enters RBCs to maintain electroneutrality; reversed in lungs. This facilitates CO₂ transport as bicarbonate.

What is alveolar gas composition (what — PO₂ & PCO₂ approximate)

Alveolar PO₂ ≈ 100–105 mm Hg; PCO₂ ≈ 40 mm Hg (mix of inspired and residual air). Atmospheric PO₂ is ~160 mm Hg before humidification.

Why is tracheal PO₂ < atmospheric PO₂

Because inspired air is humidified (water vapor displaces some partial pressure), lowering PO₂.

What is physiologic shunt

Blood that passes from the right to left side of circulation without being oxygenated in the lungs (e.g., anatomical shunt or areas of perfusion without ventilation). This reduces arterial PO₂.

How does pulmonary vascular resistance (PVR) behave at FRC and why (what/when)?

At FRC PVR is at a minimum because alveolar and extra-alveolar vessel tension is balanced; extremes of lung volume increase PVR.

46-year-old plumber with slowly progressive dyspnea after workplace exposure — what pattern and why?

Likely restrictive lung disease from fibrosis → ↓ compliance (stiff lungs), difficulty with inspiration, ↓ VC/FVC (both decreased), FEV1/FVC ratio often normal or unchanged because both FEV1 and FVC ↓ proportionally.

Infant born at 30 wks with respiratory distress — what’s happening & how treat?

Premature infant lacks sufficient surfactant → ↑ alveolar surface tension → atelectasis and ↓ FRC → neonatal respiratory distress syndrome (NRDS). Treat with exogenous surfactant and supportive ventilation; antenatal corticosteroids before early delivery can speed surfactant production.

Patient with COPD (emphysema) — what spirometry pattern & compliance?

A: Obstructive pattern: ↓ FEV1, FVC may be near normal or ↓, FEV1/FVC ratio < 0.8. Emphysema → ↑ lung compliance (loss of elastin) and air trapping (↑ RV).

Spinal cord injury below C5 — how does breathing look?

Diaphragm (C3–C5) still works → patient can breathe but lacks intercostal muscle function → abnormal breathing pattern and less effective cough/forced inspiration.

What structures make up the GI tract (what — list who/where)?

Oral cavity, pharynx, esophagus, stomach, small intestine, large intestine. Accessory organs: teeth, tongue, salivary glands, liver, gallbladder, pancreas.

What are the four basic functions of the digestive system (what)?

Mechanical processing, digestion (chemical), absorption of nutrients, secretion & excretion (water, acids, enzymes, buffers).

Who composes the enteric nervous system (who) and what’s its role (what/how)?

Myenteric (Auerbach) and submucosal (Meissner) plexuses — they coordinate gut motility and secretion; the ENS can function independently of CNS (but receives modulation from autonomics).

What are the properties of gut smooth muscle (what)?

Unitary (single-unit) smooth muscle in gut — gap junctions allow syncytial contraction, spontaneous basal electrical rhythm (slow waves), calcium mainly from outside cell.

How does smooth muscle contract in gut (how — signaling cascade)?

Ca²⁺ enters → binds calmodulin → activates myosin light-chain kinase (MLCK) → MLCK phosphorylates myosin → crossbridge cycling → contraction.

What is peristalsis vs segmentation (what/how)?

Peristalsis: coordinated propulsive waves moving bolus aborally (relaxation distal, contraction proximal). Segmentation: mixing contractions (circular muscle) that churn contents without net propulsion.

Where is skeletal muscle present in the GI tract (where)?

In the oropharynx, upper esophagus (and external anal sphincter) — voluntary control for swallowing & defecation reflex. Most of esophagus becomes smooth muscle distally.

What are the major digestive enzymes and where are they active (what/where)?

Salivary amylase (mouth), pepsin (stomach, from pepsinogen), gastric lipase, pancreatic amylase/trypsin/chymotrypsin/lipase/nucleases (small intestine), brush border enzymes (maltase, sucrase, lactase).

How are carbohydrates absorbed (how)?

Broken to monosaccharides (glucose, fructose, galactose) then absorbed via active transport (glucose/galactose via SGLT) or facilitated diffusion (fructose).

How are fats absorbed & transported (how)?

Bile salts emulsify fats → lipases break them to fatty acids/monoglycerides → diffuse into enterocytes → reassembled into triglycerides → packaged into chylomicrons → enter lymph (lacteals).

Who secretes pancreatic enzymes and what stimulates secretion (who/what/how)?

Pancreatic acinar cells secrete enzymes (stimulated primarily by CCK and vagal ACh). Ductal cells secrete HCO₃⁻ stimulated mainly by secretin.

What are the phases of pancreatic secretion (what — when & how)?

Cephalic (sight/smell/taste via vagus → small enzyme release), Gastric (food in stomach → vagovagal reflex + gastrin), Intestinal (chyme in duodenum → secretin stimulates HCO₃⁻; CCK stimulates enzymes — major phase).

How is pancreatic HCO₃⁻ secreted (how — basic mechanism)?

CO₂ + H₂O in ductal cells → HCO₃⁻ formed → secreted apically via Cl⁻/HCO₃⁻ exchanger; Cl⁻ recycled via CFTR-like channels. Basolateral Na⁺/K⁺-ATPase and Na⁺/H⁺ exchangers maintain gradients.

What hormones regulate digestion (who & what do they do)?

Gastrin (stimulates HCl & growth); CCK (stimulates pancreatic enzymes, gallbladder contraction, slows gastric emptying); Secretin (stimulates pancreatic HCO₃⁻, inhibits gastric H+); GIP (stimulates insulin, inhibits gastric acid); Motilin (MMC), Somatostatin (inhibitory).

What is the major function of gastrin (what/who)?

Gastrin from G cells (stomach antrum) stimulates parietal cells to secrete HCl, increases gastric motility and mucosal growth.

What does secretin do and when is it released (what/when)?

Secretin from S cells (duodenum) is released when duodenal pH is low (acidic chyme) and stimulates pancreatic duct cells to secrete bicarbonate to neutralize acid and inhibits gastric acid secretion.

What does CCK do and what stimulates it (what/when)?

CCK from I cells is released by fats & amino acids in duodenum → stimulates pancreatic enzyme secretion and gallbladder contraction and slows gastric emptying, promotes satiety.

What is the migrating motor complex (MMC) and which hormone stimulates it (what/who)?

MMC is a cyclic pattern of motility during fasting that clears the gut; motilin (from M cells) stimulates MMC.

What are VIP and somatostatin roles in the gut (what)?

VIP relaxes smooth muscle, stimulates intestinal secretion of water/electrolytes and pancreatic HCO₃⁻, inhibits gastric H⁺. Somatostatin inhibits release of many GI hormones and gastric/pancreatic secretions.

How is gastric acid (HCl) secretion regulated (how — main stimulants & inhibitors)?

Stimulated by ACh (vagus), Gastrin, and Histamine (via H2). Inhibited by somatostatin, secretin, GIP, CCK and low pH feedback. Drugs: atropine blocks ACh, H2 blockers (cimetidine) block histamine.

What cells produce intrinsic factor and why important (who/what)?

Parietal cells produce intrinsic factor for vitamin B12 absorption in the ileum — essential to prevent pernicious anemia.

What stimulates pancreatic enzyme secretion the most (what/who)?

CCK (I cells) — in response to fats and amino acids in the duodenum — is the major stimulant of acinar enzyme secretion.

What is the function of brush border enzymes (what/where)?

Enzymes on enterocyte microvilli (maltase, sucrase, lactase, peptidases) finish carbohydrate and peptide digestion at the luminal surface; essential for final absorption.

What is the main mechanism for water absorption in colon (what/how)?

Active Na⁺ absorption drives passive water uptake; colon reclaims water & electrolytes producing formed feces. (Slide content emphasizes water absorption + bacterial fermentation).

What are the 6 essential digestive activities (what)?

Ingestion, propulsion, mechanical digestion, chemical digestion, absorption, defecation.

Patient with steatorrhea (fatty stools) after pancreatic surgery — what’s the likely deficit & why?

Loss of pancreatic lipase (or lack of bile) → impaired triglyceride digestion → fats not absorbed → steatorrhea. Give pancreatic enzyme replacement and ensure adequate bile flow.

Patient has watery diarrhea, hypokalemia and achlorhydria — suspect VIPoma. What does VIP do?

VIP causes watery diarrhea, stimulates intestinal electrolyte secretion, relaxes smooth muscle, and inhibits gastric acid. VIPoma = VIP-secreting tumor → secretory diarrhea and electrolyte issues.

A patient with low gastric pH shows inhibited gastrin — what mechanism?

Low gastric pH → D cells release somatostatin which inhibits gastrin release (negative feedback to protect duodenum).

After a duodenal ulcer, a patient has impaired HCO₃⁻ secretion — which hormone normally stimulates pancreatic HCO₃⁻?

Secretin from S cells in response to acidic duodenal chyme stimulates pancreatic ductal bicarbonate secretion.

Newborn with failure to thrive and severe watery diarrhea — think defect in enterocyte brush border enzymes (e.g., lactase deficiency). What happens?

Undigested sugars in lumen cause osmotic diarrhea; treat by removing offending sugar (e.g., lactose-free formula) and supportive care. (Slides emphasize brush border enzyme roles.)yea

What is the average intrapleural pressure at rest?

About –5 cm H₂O at the end of a normal expiration (negative to keep lungs expanded).

What happens to intrapleural pressure during inspiration?

It becomes more negative (≈ –7 or –8 cm H₂O), allowing alveoli to expand and air to flow in.

Why does intrapleural pressure never equal alveolar pressure in a healthy lung?

Because the pleural membranes are airtight; the slight vacuum keeps lungs stuck to the thoracic wall.

What are the two opposing forces that balance at FRC?

Inward elastic recoil of lungs vs. outward elastic recoil of chest wall.

What happens to FRC in obesity, pregnancy, or lying supine?

FRC decreases (due to decreased chest wall expansion).

Why can’t residual volume (RV) be measured by simple spirometry?

Because it’s the air that remains in the lungs after maximal exhalation — it can’t be exhaled.

What methods can measure RV or FRC?

Helium dilution, nitrogen washout, or body plethysmography.

What does a low VC but normal TLC suggest?

Obstructive disease (air trapping increases RV, lowering VC but keeping TLC normal or high).

What does a low TLC indicate?

Restrictive disease (low compliance or limited expansion).

What is the normal alveolar-arterial (A–a) O₂ gradient?

Normally <10–15 mmHg; increased in V/Q mismatch, diffusion limitation, or shunt.

What determines alveolar PO₂?

Inspired O₂, alveolar ventilation, and O₂ consumption rate (via the alveolar gas equation).

Why does CO₂ diffuse faster than O₂?

CO₂ is ~20x more soluble in plasma than O₂.

What is the Haldane effect?

Oxygen binding to hemoglobin decreases hemoglobin’s affinity for CO₂ — helps CO₂ unloading in lungs.

What is the most important stimulus for ventilation under normal conditions?

CO₂ levels (via H⁺ changes detected by central chemoreceptors).
📂 From: Lung PPT

How does anemia affect PaO₂ and O₂ saturation?

PaO₂ and SaO₂ are normal, but total O₂ content is decreased (less Hb).

What is the effect of carbon monoxide on O₂ transport?

CO binds Hb with 200× higher affinity than O₂, reducing O₂ binding capacity and shifting the dissociation curve left (less unloading).

Where is the apneustic center located and what does it do?

In the lower pons; promotes prolonged inspiration (inhibited by pneumotaxic center).

Where is the pneumotaxic center located and what does it do?

In the upper pons; limits inspiration and increases respiratory rate.

What happens in metabolic acidosis to ventilation?

Peripheral chemoreceptors sense low pH → hyperventilation → lowers CO₂ (compensates).

What is Cheyne–Stokes breathing and when does it occur?

Cyclic apnea and hyperventilation — often seen in heart failure or brain injury.

A mountain climber develops respiratory alkalosis after rapid ascent — what renal compensation occurs?

Kidneys excrete bicarbonate and retain H⁺ to normalize pH.

What type of epithelium lines most of the GI tract?

Simple columnar epithelium (with mucus-secreting goblet cells).

What is the main neurotransmitter for gut relaxation?

Nitric oxide (NO).

What neurotransmitter stimulates GI motility and secretion?

Acetylcholine (ACh).

How does the swallowing reflex work?

Initiated by bolus touching pharynx → vagal & glossopharyngeal afferents → medulla → skeletal muscle coordination → upper esophageal sphincter relaxes.

What prevents reflux between stomach and esophagus?

The lower esophageal sphincter (LES) and diaphragmatic crura (act as a physiological sphincter).

What is the composition of saliva?

99.5% water, plus mucins, amylase, lipase, and lysozyme.

Which cells in the stomach secrete mucus and bicarbonate?

Mucous neck and surface epithelial cells — protect mucosa from acid.

What cell type secretes pepsinogen?

Chief (zymogenic) cells.

What triggers pepsinogen → pepsin activation?

Acid (H⁺) in the stomach lumen.

What does intrinsic factor do?

Binds vitamin B12 to allow absorption in the ileum.