Rectum and anal canal
The last 15 cm of gut is a storage tank with a two-part valve on the end, and a line drawn across the canal — the dentate line — that decides whether a problem there bleeds silently or hurts like nothing else; almost every anorectal complaint, and every drug on this page, comes back to sphincter pressure, stool consistency, or which side of that line you are on.
What it normally does
The rectum is normally empty. Stool arriving stretches the wall, and that stretch does two jobs at once. It tells you something has arrived (rectal sensation, carried up the pelvic splanchnic nerves, S2-4), and it triggers a local enteric reflex that relaxes the internal sphincter for a few seconds (rectoanal inhibitory reflex, RAIR) so the exquisitely sensitive lining just below the dentate line can taste the contents and tell gas from liquid from solid (sampling). If the moment is wrong, the rectum relaxes to take the volume (accommodation), the urge fades, and you can wait.
Explains why a rectum kept chronically loaded stops reporting that it is full, and why liquid stool can leak out past a hard mass while the internal sphincter is sitting reflexly open — overflow incontinence. It is also why someone who cannot sample reliably finds that passing wind becomes a gamble.
Two sphincters, two nervous systems. The internal anal sphincter is the thickened continuation of the bowel's own circular smooth muscle: involuntary, contracted all day and all night, and responsible for most of the resting closure pressure (roughly 55-70% of a resting pressure of about 40-70 mmHg on manometry, with normal ranges varying by technique). The external anal sphincter is skeletal muscle supplied by the inferior rectal branch of the pudendal nerve (S2-4), and the puborectalis sling is skeletal muscle supplied by direct sacral branches (S3-4, the nerve to levator ani) with a variable pudendal contribution: you can consciously clamp them shut, but maximal squeeze fatigues within about a minute. Puborectalis also hooks the anorectal junction forwards into a bend (the anorectal angle), which is a mechanical barrier in its own right.
Explains why continence fails in two quite different patterns — leaking without knowing (internal sphincter) versus knowing and not making it (external sphincter) — and why a drug that relaxes smooth muscle can heal a fissure without touching voluntary squeeze.
The dentate line sits about 2 cm inside the anal verge, where hindgut endoderm meets proctodeal ectoderm, and everything changes across it. Above: columnar (then transitional) lining, autonomic (visceral) innervation with no somatic pain fibres, venous drainage by the superior rectal vein into the portal system, lymph upwards to internal iliac nodes (and, from the rectum above, along the superior rectal vessels to inferior mesenteric nodes). Below: squamous anoderm, supplied by the inferior rectal branch of the pudendal nerve and as pain-sensitive as any skin on the body, venous drainage into systemic inferior rectal veins, lymph to the superficial inguinal nodes.
Explains why one lump bleeds happily without hurting and another is agony, why an internal haemorrhoid can be banded in clinic without anaesthetic, why a rectal tumour can grow for months painlessly, and why you check the groins for nodes in disease below the line.
Muscle alone does not seal the canal. Three spongy vascular cushions sit in the submucosa (classically left lateral, right anterior, right posterior), fill with blood and press together like a washer, adding perhaps 15-20% of resting pressure and making the seal gas-tight. They are normal anatomy in everyone, fed by small arteriovenous connections off the superior rectal artery, and slung in place by fibromuscular tissue that frays with age and straining. They are not varicose veins.
Explains why haemorrhoidal bleeding is bright red and arterial-looking rather than dark, why treatment targets prolapse and straining rather than 'veins', and why portal hypertension produces anorectal varices — a different lesion, common at endoscopy in cirrhosis but rarely the cause of bleeding — not haemorrhoids.
What goes wrong
Straining, hard stool, long sits on the toilet and the pressure of pregnancy shear the fibromuscular tissue holding the cushions up. The cushions slide down, engorge, and the mucosa over them gets dragged into the canal and abraded by passing stool. Bleeding comes from arteriovenous cushion tissue above the dentate line, so it is bright red and painless — there are no somatic pain fibres up there. Pain appears only when somatic territory is involved: a cushion prolapsing out past the line, or a clot in the external plexus below it (thrombosed external haemorrhoid).
Painless bright red bleeding with prolapse = internal, above the dentate line. Sudden severe pain with a tender blue lump = thrombosed external, below it. Never pin anaemia or a change in bowel habit on haemorrhoids without excluding cancer.
You would find: Bright red blood coating the outside of the stool or dripping into the pan after defecation, painless, with itch or a lump that comes down and goes back. Graded I (bleeds only) to IV (permanently prolapsed, irreducible). A tense purple tender lump appearing at the anal verge over a few hours is a thrombosed external haemorrhoid. Iron-deficiency anaemia from haemorrhoids alone is uncommon — that finding sends you looking elsewhere.
A hard stool splits the anoderm, usually in the posterior midline (about 90%); an anterior midline fissure is the other common site and is seen in up to a quarter of women. The tear is in somatic territory so it hurts badly; pain drives the internal anal sphincter into spasm; the raised resting pressure squeezes shut the very vessels feeding that spot, and the posterior midline is the worst-perfused part of the canal. Ischaemia stops it healing, the next stool tears it open again, and fear of defecation makes the stool harder still. Pain, spasm, ischaemia — a self-feeding loop.
Fissure = pain, spasm, ischaemia. Everything that works lowers sphincter pressure: soft stool first, then a chemical sphincterotomy. Lateral internal sphincterotomy is the surgical version and heals over 90%, but it permanently trades resting pressure for a small risk of incontinence — which is why it is not the first move in a woman with an obstetric history.
You would find: Tearing pain on defecation like passing glass, then a deep ache for minutes to hours afterwards, with a streak of blood on the paper. The patient guards and often will not tolerate a digital examination — inspection by gently parting the buttocks does the work. Chronic fissure: a sentinel skin tag at the outer end and white internal sphincter fibres visible in the base. A fissure off the midline (lateral), multiple, ragged or painless is not an ordinary fissure — think Crohn disease, HIV or other immunosuppression, syphilis, tuberculosis, or anal cancer.
- Faecal incontinence from sphincter or pudendal nerve injury← from “Two sphincters, two nervous systems. The inter…”
Obstetric injury is the commonest structural cause in women: a third or fourth degree tear involves the external sphincter (fourth degree extending through the anal epithelium), and forceps, a large baby or a long second stage stretch the pudendal nerve. Anal surgery does it mechanically — sphincterotomy or fistula surgery divides internal sphincter. Years of straining add a stretch neuropathy on top. Which sphincter fails sets the symptom: lose internal sphincter and you lose resting pressure, so stool escapes without warning; lose external sphincter or puborectalis and you feel the urge perfectly well but cannot hold it.
Passive leak = internal (smooth) sphincter. Urge leak = external (striated) sphincter. Loose stool turns a marginal sphincter into an incontinent one, so the first intervention is firming the stool, not operating.
You would find: You have to ask — almost nobody volunteers it. Sort it into passive soiling (staining underwear, unaware) versus urge incontinence (running and not making it). On examination: a patulous anus that opens as you part the buttocks suggests internal sphincter loss; a weak voluntary squeeze on a finger suggests external. The delivery was often 20-30 years earlier, and symptoms surface when the reserve finally runs out. Around one in twenty Australian adults is affected, and far more in residential aged care.
- Faecal impaction with overflow incontinence← from “The rectum is normally empty. Stool arriving s…”
Hard stool sits in the rectum and does not leave. Chronic distension blunts rectal sensation and keeps the internal sphincter reflexly relaxed (a sustained rectoanal inhibitory response), so the canal sits open. Liquid stool from above tracks around the mass and out. The patient describes diarrhoea and incontinence; the disease is constipation.
New faecal incontinence in an older person is impaction until a rectal examination says otherwise. Clear the rectum from below and the 'diarrhoea' stops.
You would find: Older, immobile, on opioids or anticholinergics. The 'diarrhoea' is small volume, near continuous, often with no urge before it. The diagnosis is made with a gloved finger, not a stool chart. Missing it and prescribing an antidiarrhoeal makes it worse.
- Rectal cancer presenting as haemorrhoids← from “The dentate line sits about 2 cm inside the an…”
The rectum above the dentate line has no somatic pain fibres. A tumour there ulcerates and bleeds without hurting, which is exactly what an internal haemorrhoid does — the symptom cannot distinguish them. Low rectal tumours are also within reach of an examining finger, so a digital rectal examination is part of assessing any rectal bleeding.
'Haemorrhoids' is a diagnosis you make after looking, feeling and excluding the alternatives. If you cannot see the bleeding source, scope it.
You would find: Red flags that make 'haemorrhoids' unsafe: blood mixed through the stool rather than coating it, change in bowel habit, tenesmus (the feeling of never finishing), weight loss, iron-deficiency anaemia, a mass on digital examination, or new symptoms over about 40. Australia has one of the highest colorectal cancer rates in the world; the National Bowel Cancer Screening Program mails an immunochemical faecal occult blood test every two years to people aged 50-74, and since July 2024 people aged 45-49 can request their first kit. Aboriginal and Torres Strait Islander people take part in screening less often, are diagnosed at a later stage and survive it less well — so bleeding in that setting is a reason to examine and refer, not to reassure. Screening is for people without symptoms; anyone with rectal bleeding needs assessment regardless of a recent negative kit.
What we give, and how it works
Open a drug to see what it binds, what that does to the cell, and what you then see in the patient.
- Binds
- No receptor. Macrogol is an inert polymer that holds water in the lumen by osmosis. Lactulose is a disaccharide humans cannot absorb, fermented by colonic bacteria into short-chain acids that do the same osmotic job. Psyllium is a fibre that gels with water and adds bulk.
- Which does
- Water stays in the lumen instead of being absorbed. Stool volume rises and consistency softens, and the extra distension stimulates propulsion.
- So you see
- A soft, formed stool passes without splitting the anoderm or shearing the cushions, so the pain-spasm-ischaemia loop of a fissure is broken and most acute fissures heal on stool softening and analgesia alone.
- And the same mechanism causes
- Water pulled into the lumen has to go somewhere: bloating, cramping and osmotic diarrhoea if pushed too far, and in a frail patient dehydration and electrolyte disturbance. Lactulose produces noticeably more wind and bloating than macrogol, because the gas is made by the same bacterial fermentation that produces the effect.
- Handling
- Effect takes a day or two, so tell the patient that before they abandon it.
Catches people out: Psyllium taken without enough fluid makes stool bulkier and harder — the opposite of what you wanted. And a stimulant laxative sent into an already impacted rectum causes cramping pain without shifting the plug: clear from below first.
- Binds
- Glyceryl trinitrate is a nitric oxide donor, and nitric oxide is the transmitter the non-adrenergic non-cholinergic nerves actually use to relax this sphincter — the drug is replacing a native signal. NO activates soluble guanylate cyclase inside the smooth muscle cell. Diltiazem instead blocks L-type calcium channels in the same muscle.
- Which does
- cGMP rises, protein kinase G activates myosin light chain phosphatase and lowers cytosolic calcium, so the myosin lets go. Resting anal pressure falls.
- So you see
- Pressure down means the posterior midline is perfused again, and the fissure heals over about 6-8 weeks. Be honest about the size of the gain: in the trials roughly half of chronic fissures heal on topical GTN against about a third on placebo, and late recurrence after stopping approaches half — which is why the stool has to stay soft either way.
- And the same mechanism causes
- Headache, in a fifth to a third of people, and often bad enough that they stop. Same mechanism, different vessels: enough nitric oxide is absorbed to dilate meningeal and cerebral arteries, exactly as GTN does when given for angina — and for the same reason it can cause postural dizziness. That also makes it dangerous with a phosphodiesterase-5 inhibitor (sildenafil, tadalafil), which blocks cGMP breakdown: the two stack the same pathway and can drop blood pressure profoundly.
- Handling
- In Australia the 0.2% GTN rectal ointment is the registered product; topical diltiazem is at least as effective with far fewer headaches but has to be compounded, so it is usually the second stop rather than the first.
Catches people out: Warn about the headache before the patient starts, or they will stop on day two and the fissure will still be there in six weeks.
- Binds
- The local anaesthetic blocks voltage-gated sodium channels from inside the axon. The corticosteroid binds the glucocorticoid receptor and changes transcription, cutting inflammatory mediator production in the surrounding skin.
- Which does
- No sodium influx means no action potential, so the pain and itch signal never leaves the anoderm; the steroid damps the inflammation and the itch that goes with it.
- So you see
- A few days of comfort while the acute problem settles. Note the anatomy sets the ceiling: it can only numb tissue with somatic nerves, which is the anoderm and skin below the dentate line. An internal haemorrhoid was never painful, and no ointment shrinks a prolapsing cushion — that is rubber band ligation or surgery.
- And the same mechanism causes
- Prolonged steroid thins perianal skin (atrophy), and thin skin fissures and itches more, so the drug reproduces the symptom it was given for. Topical local anaesthetics applied repeatedly to inflamed skin can sensitise — cinchocaine and the ester anaesthetics are well-recognised contact allergens (lidocaine much less so): an ointment that worked for a week and then began to burn and itch is more likely allergic contact dermatitis than worsening haemorrhoids.
Catches people out: One to two weeks, not months. Perianal itch treated blindly with steroid for months is a standard way to make a simple problem chronic — and to sit on top of an undiagnosed fissure, fungal infection, or anal cancer.
- Binds
- Peripheral mu-opioid receptors on enteric neurons. Loperamide is a P-glycoprotein substrate and is pumped back out at the blood-brain barrier, so at normal doses it produces essentially no central opioid effect — a peripheral opioid by pharmacokinetics, not by receptor selectivity.
- Which does
- Less acetylcholine released from myenteric neurons means fewer propulsive contractions and slower transit, so the colon has longer to absorb water. Anal resting pressure rises a little on top of that.
- So you see
- Stool becomes firm and predictable, and a weakened sphincter that could never hold liquid can hold a formed stool. This is the highest-yield drug in incontinence, and it is worth being clear about why: it changes the stool, it does not repair the sphincter.
- And the same mechanism causes
- Constipation, then impaction, then overflow incontinence — the same mechanism carried too far recreates the exact symptom you were treating. At very high doses (misuse for opioid effect) enough drug escapes P-glycoprotein to block cardiac ion channels — hERG potassium channels, prolonging the QT interval, and sodium channels, widening the QRS — causing fatal arrhythmias.
Catches people out: Examine the rectum before starting it in an older person with new incontinence: if the rectum is loaded, loperamide makes things worse. Avoid it in acute infective colitis or an inflammatory bowel disease flare, where slowing the colon risks toxic megacolon.
Draw the dentate line and hang the whole page off it. Above: no pain fibres, portal drainage, internal iliac nodes — so an internal haemorrhoid bleeds bright red and painlessly, and so does a rectal cancer. Below: pudendal nerve, systemic drainage, inguinal nodes — so a fissure and a thrombosed external pile are agony. Then the two sphincters: internal is smooth muscle, always on, most of the resting pressure, and failing it means leaking without knowing; external is striated, pudendal, voluntary, fatigues, and failing it means urge you cannot hold. Every drug here follows: soft stool for the fissure and the cushions, GTN to relax the internal sphincter (and the headache comes free with the mechanism), loperamide to firm the stool in incontinence (and impaction with overflow is the same mechanism gone too far). Last line, and it is the one that fails students and harms patients: new rectal bleeding is not haemorrhoids until you have looked and felt.
Now test whether it stuck
Reading this through is not the same as being able to reconstruct it. Every question in the bank is free, with a full debrief on each option.