Hereditary mucoepithelial dysplasia (HMD), or simply mucoepithelial dysplasia, is a rare autosomal dominant multiepithelial disorder causing systemic maldevelopment of the epithelia and mucous membranes that line the surface of tissues and structures throughout the body, particularly affecting systems affiliated with mucosa, which includes the respiratory, digestive, urinary, reproductive and immune systems. The disorder is attributed to improper formation of desmosomes and gap junctions, which prevents proper cornification of the epithelial layer of the skin.

Desmosomes are extracellular protein structures responsible for cellular adhesion, whereby cells of the same type are held closely together. Gap junctions are specialized channels located within the cell membrane of many animal cell types, which serve as gateways that connect the cytoplasmic interior of two adjacent cells, allowing the passage of small molecules such as ions, nucleotides, second messengers and others. The movement and exchange of small molecules between cells is an important part of intracellular communication processes like cell signaling.

Hepatic microvascular dysplasia (HMD or MVD) or portal atresia is a disorder where mixing of venous blood and arterial blood in the liver occurs at the microscopic level. It occurs most commonly in certain dog breeds such as the Cairn and Yorkshire terriers although any dog breed may be at risk.

This disease may also be found in cats.

HMD is sometimes misdiagnosed as Portosystemic vascular anomaly (PSVA) or a "Liver Shunt" (portosystemic shunt). HMD can be diagnosed with an MRI, using a tracing dye in the subject's blood, and observing the flow of blood through the subject's liver and surrounding areas (stomach, intestine) for anomalies. It can also be diagnosed using a bile-acid level test; or more accurately, a "fasting-blood ammonia levels" test. Symptoms include stunted growth in the first 6–9 months, vomiting, seizures, and hydro-encephalitic episodes (from ammonia concentrating in the blood). HMD is usually treated non-surgically with antibiotics (metronidazole) and stool-softeners (lactulose).

Acute respiratory distress syndrome (ARDS) has some similarities to IRDS. Transient tachypnea of the newborn presents with respiratory distress syndrome in the preterm newborn.

Infant respiratory distress syndrome (IRDS), also called neonatal respiratory distress syndrome (NRDS), respiratory distress syndrome of newborn, or increasingly surfactant deficiency disorder (SDD), and previously called hyaline membrane disease (HMD), is a syndrome in premature infants caused by developmental insufficiency of pulmonary surfactant production and structural immaturity in the lungs. It can also be a consequence of neonatal infection. It can also result from a genetic problem with the production of surfactant associated proteins. IRDS affects about 1% of newborn infants and is the leading cause of death in preterm infants. The incidence decreases with advancing gestational age, from about 50% in babies born at 26–28 weeks, to about 25% at 30–31 weeks. The syndrome is more frequent in infants of diabetic mothers and in the second born of premature twins.

IRDS is distinct from pulmonary hypoplasia, another leading cause of neonatal death that involves respiratory distress.