Histology and cell biology for USMLE Step 1

A cell is studied that secretes large amounts of a peptide hormone. Electron microscopy shows abundant rough endoplasmic reticulum, a prominent Golgi apparatus and numerous membrane-bound dense granules near the apical surface. Which additional feature would you expect if this cell instead secreted a STEROID hormone?

1. Extensive terminal web of actin filaments A feature of absorptive epithelium with a brush border, not of endocrine steroid cells.
2. More rough endoplasmic reticulum still Rough ER is for protein synthesis. Steroids are not translated, so they need no ribosomes.
3. Abundant peroxisomes with catalase Peroxisomes handle very long chain fatty acid beta-oxidation. Their absence or dysfunction causes Zellweger and adrenoleukodystrophy, but they are not the defining steroidogenic organelle.
4. Numerous stored secretory granules Steroids are lipid-soluble and diffuse out as they are made; they are NOT stored in granules. That is why steroid secretion cannot be released in a rapid bolus.
5. Abundant smooth endoplasmic reticulum and lipid droplets, with tubular cristae in the mitochondria correct Correct. Steroidogenic cells, adrenal cortex, Leydig cells, theca and granulosa, need smooth ER for the cytochrome P450 enzymes, cholesterol-rich lipid droplets as substrate, and mitochondria with TUBULAR rather than shelf-like cristae because the first and last steps of steroid synthesis occur inside them.

The point: Read the organelle and name the function. Rough ER plus granules: peptide secretion (plasma cell, pancreatic acinar). Smooth ER plus lipid droplets plus tubular cristae: steroid secretion. Lots of mitochondria and infoldings: active transport (proximal tubule).

Source: USMLE Content Outline — histology and cell biology NBME / FSMB (USMLE programme) · tier 0, exam blueprint / regulator

A 55-year-old woman has painful flaccid blisters and erosions of the oral mucosa and trunk. Nikolsky sign is positive. Direct immunofluorescence shows a reticular, net-like intercellular pattern of IgG within the epidermis. Which structure is the antibody target?

1. Desmoglein in desmosomes correct Correct. Pemphigus vulgaris. Desmosomes hold keratinocytes to each other, so their loss causes acantholysis WITHIN the epidermis: flaccid, easily ruptured blisters, mucosal involvement and a positive Nikolsky sign.
2. Hemidesmosome components BP180 and BP230 Bullous pemphigoid. These anchor basal cells to the basement membrane, so the split is SUBepidermal: tense blisters, usually sparing the mouth, with a LINEAR band of IgG and C3 and a negative Nikolsky sign.
3. Type VII collagen anchoring fibrils Epidermolysis bullosa acquisita and dystrophic epidermolysis bullosa; blisters arise below the lamina densa and scar.
4. Gap junction connexins Gap junctions mediate cell-to-cell communication rather than adhesion; loss does not cause blistering.
5. Tight junction claudins Provide the paracellular seal in simple epithelia. They are not the adhesion structure of stratified squamous epidermis.

The point: Desmoglein = desmosome = pemphigus vulgaris = flaccid, oral, intraepidermal, net-like IF, Nikolsky positive, potentially fatal. Hemidesmosome = pemphigoid = tense, spares mouth, subepidermal, linear IF, Nikolsky negative, milder.

Source: USMLE Content Outline — histology and skin pathology NBME / FSMB (USMLE programme) · tier 0, exam blueprint / regulator

A premature infant born at 27 weeks develops progressive respiratory distress with diffuse ground-glass opacification and air bronchograms. Which cell type is functionally immature, and what does it produce?

1. Goblet cell, secreting mucin Goblet cells are absent from terminal bronchioles and alveoli, and mucus does not affect surface tension.
2. Type I pneumocyte, forming the gas exchange barrier Type I cells cover about 97% of the alveolar surface but are terminally differentiated and secrete nothing.
3. Alveolar macrophage, clearing debris Important in infection and in heart failure cells, but not in surfactant production.
4. Type II pneumocyte, producing surfactant correct Correct. Type II pneumocytes make dipalmitoylphosphatidylcholine, which lowers alveolar surface tension. They are also the stem cell that regenerates the alveolar lining after injury. Maturity is estimated by a lecithin/sphingomyelin ratio above 2.
5. Clara (club) cell, secreting a protective glycoprotein Club cells sit in the terminal bronchioles, degrade toxins and act as a reserve cell, but they do not cause neonatal respiratory distress syndrome.

The point: Type II pneumocytes: surfactant plus alveolar stem cell. Surfactant appears around 26 weeks and is adequate by about 35. Antenatal maternal corticosteroids accelerate it. Maternal diabetes DELAYS it, because fetal insulin antagonises cortisol.

Source: USMLE Content Outline — histology and respiratory physiology NBME / FSMB (USMLE programme) · tier 0, exam blueprint / regulator