Perineal body

Location

• Female: between the posterior vaginal opening and the anus
• Male: between the bulb of the penis and the anus
• It lies just anterior to the anal canal at the junction of the urogenital and anal triangles.

Muscular attachments

• Bulbospongiosus
• Superficial transverse perineal muscles
• Deep transverse perineal muscles
• External anal sphincter
• Fibers of levator ani, especially puborectalis/pubococcygeus contributions

Functions

1. Supports the pelvic floor by acting as a central muscular anchor.
2. Helps maintain the position of the vagina, rectum, and other pelvic viscera.
3. Contributes to urinary and fecal continence through its relationships with the pelvic floor and external anal sphincter.
4. Resists widening of the vaginal outlet and supports the posterior vaginal wall.

Clinical importance

• Pelvic-organ prolapse
• Perineal descent
• Anal sphincter dysfunction or fecal incontinence, particularly if an obstetric anal sphincter injury is present

Perineal body: anatomical explanation

Position

• In females: between the posterior edge of the vaginal opening and the anus.
• In males: between the bulb of the penis and the anus.
• It is just posterior to the perineal membrane and connects to the posterior end of the urogenital hiatus of the levator ani.

Structures attaching to it

Functional significance

• Coordinates forces generated by the pelvic-floor and perineal muscles
• Supports the posterior vaginal wall in females
• Helps maintain the integrity of the pelvic floor
• Contributes indirectly to urinary and fecal continence through its association with the pelvic floor and external anal sphincter

Clinical relevance

Iron metabolism

Overview

Dietary iron
     ↓
Duodenum absorbs iron
     ↓
Ferroportin exports iron into plasma
     ↓
Transferrin carries Fe3+ in blood
     ↓
Bone marrow uses iron for hemoglobin synthesis
     ↓
Red blood cells circulate for about 120 days
     ↓
Macrophages phagocytose old RBCs and recycle iron
     ↓
Ferroportin releases recycled iron back to transferrin

Liver stores excess iron as ferritin/hemosiderin
     ↑
Hepcidin controls ferroportin at intestine, macrophages, and liver

1. Absorption

Heme iron

• Found in meat, poultry, and fish.
• Absorbed as heme and subsequently broken down within enterocytes to release iron.
• Generally absorbed more efficiently than non-heme iron.

Non-heme iron

• Usually dietary ferric iron (Fe³⁺) from plant and fortified foods.
• It must be reduced to ferrous iron (Fe²⁺) at the intestinal brush border.
• Divalent metal transporter 1 (DMT1) transports Fe²⁺ into the enterocyte.

• Increases: vitamin C, gastric acid, iron deficiency, increased erythropoiesis, hypoxia.
• Decreases: phytates, polyphenols/tannins in tea or coffee, calcium in some settings, and inflammatory states.

1. Stored as ferritin and lost when the enterocyte is shed.
2. Exported into blood through ferroportin.

2. Transport in blood

• Each transferrin molecule can carry two Fe³⁺ ions.
• Transferrin delivers iron particularly to erythroid precursors in bone marrow via transferrin receptor 1.
• Cellular uptake occurs by receptor-mediated endocytosis.

3. Utilization

• Myoglobin in skeletal and cardiac muscle
• Cytochromes and other electron-transport enzymes
• Catalase, peroxidases, and other iron-containing enzymes

4. Recycling

• Senescent erythrocytes are phagocytosed by macrophages in the spleen, liver, and bone marrow.
• Hemoglobin is broken down.
• Heme is processed, releasing iron.
• Iron is either stored as ferritin or exported by ferroportin to bind plasma transferrin again.

5. Storage

• Hepatocytes
• Macrophages of liver, spleen, and bone marrow
• Skeletal muscle, to a lesser degree

Storage forms

• Ferritin: soluble, readily mobilized storage protein. Serum ferritin generally reflects iron stores but also rises as an acute-phase reactant.
• Hemosiderin: insoluble aggregated storage form, more prominent with iron excess.

6. Hepcidin: the master regulator

Mechanism

High hepcidin
     ↓
Less ferroportin on cell surface
     ↓
Less iron released from enterocytes, macrophages, and hepatocytes
     ↓
Low plasma iron availability

• Decreases intestinal iron absorption
• Traps recycled iron inside macrophages
• Reduces release of stored hepatic iron
• Lowers serum iron and transferrin saturation

Hepcidin increases with

• High body iron stores
• High transferrin saturation
• Inflammation, especially IL-6-mediated inflammation
• Infection

Hepcidin decreases with

• Iron deficiency
• Anemia
• Hypoxia
• Increased erythropoietic drive, partly through erythroferrone released from erythroblasts

7. Clinical correlations

Iron studies: common patterns