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 Wrong. A dense mesh of actin filaments at the cell surface (terminal web) is a feature of absorptive lining cells with a brush border, not of hormone-secreting steroid cells.
2. More rough endoplasmic reticulum still Wrong. Rough ER is used for making proteins. Steroids are not built from a genetic code, they are not translated, so steroid-making cells do not need extra ribosomes.
3. Abundant peroxisomes with catalase Wrong. Peroxisomes break down very long chain fatty acids (beta-oxidation). When they are missing or not working, this causes Zellweger syndrome and adrenoleukodystrophy, but peroxisomes are not the organelle that defines a steroid-making cell.
4. Numerous stored secretory granules Wrong. Steroids dissolve easily in fat (lipid-soluble) and simply diffuse out of the cell as soon as they are made. They are NOT stored in granules like peptide hormones are. This is why steroid hormones cannot be released all at once in a sudden burst.
5. Abundant smooth endoplasmic reticulum and lipid droplets, with tubular cristae in the mitochondria correct Correct. Cells that make steroid hormones, like the adrenal cortex, Leydig cells, and the theca and granulosa cells of the ovary, need plenty of smooth ER to hold the cytochrome P450 enzymes, cholesterol-rich lipid droplets as raw material, and mitochondria with TUBULAR, rather than shelf-like, folds called cristae, because the first and last steps of making steroids happen inside the mitochondria.

The point: Learn to read the organelles and name the function. Rough ER plus granules means peptide hormone secretion, as in plasma cells or pancreatic acinar cells. Smooth ER plus lipid droplets plus tubular mitochondrial cristae means steroid hormone secretion. Lots of mitochondria plus membrane folds means active transport, as in the kidney's 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. This is pemphigus vulgaris. Desmosomes are the structures that hold skin cells (keratinocytes) to each other. When antibodies attack desmoglein, the cells separate WITHIN the epidermis (acantholysis), causing floppy blisters that break easily, mouth involvement, and a positive Nikolsky sign, where light rubbing makes the skin slide off.
2. Hemidesmosome components BP180 and BP230 Wrong. Antibodies against hemidesmosome parts BP180 and BP230 describe bullous pemphigoid. These structures anchor the deepest skin cells to the basement membrane, so the split happens BELOW the epidermis (subepidermal): tense blisters that usually spare the mouth, with a straight, LINEAR band of IgG and C3, and a negative Nikolsky sign.
3. Type VII collagen anchoring fibrils Wrong. Antibodies against type VII collagen anchoring fibrils describe epidermolysis bullosa acquisita and dystrophic epidermolysis bullosa. Blisters form below the lamina densa layer and heal with scarring.
4. Gap junction connexins Wrong. Gap junctions, made of connexins, let cells communicate with each other, they do not hold cells together. Losing them does not cause blistering.
5. Tight junction claudins Wrong. Tight junctions, made of claudins, seal the space between cells in simple, single-layer tissues. They are not the structure that holds together the multi-layered (stratified squamous) skin.

The point: Remember: desmoglein and desmosomes go with pemphigus vulgaris, floppy blisters, mouth involvement, a split within the epidermis, a net-like pattern on immunofluorescence, a positive Nikolsky sign, and it can be life-threatening. Hemidesmosomes go with pemphigoid, tense blisters, sparing the mouth, a split below the epidermis, a straight-line pattern on immunofluorescence, a negative Nikolsky sign, and it is 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 Wrong. Goblet cells are not found in the terminal bronchioles or alveoli, and mucus does not affect surface tension anyway.
2. Type I pneumocyte, forming the gas exchange barrier Wrong. Type I pneumocytes cover about 97% of the alveolar surface, but they are fully specialized (terminally differentiated) cells that secrete nothing.
3. Alveolar macrophage, clearing debris Wrong. Alveolar macrophages matter in infection, and they show up as 'heart failure cells' in heart failure, but they play no role in making surfactant.
4. Type II pneumocyte, producing surfactant correct Correct. Type II pneumocytes make dipalmitoylphosphatidylcholine (surfactant), which lowers surface tension inside the air sacs (alveoli). They also act as the stem cell that regrows the alveolar lining after injury. Lung maturity is estimated using a lecithin/sphingomyelin ratio above 2.
5. Clara (club) cell, secreting a protective glycoprotein Wrong. Club (Clara) cells sit in the terminal bronchioles, break down toxins, and act as backup (reserve) cells, but they are not what causes newborn respiratory distress syndrome.

The point: Type II pneumocytes make surfactant and act as the alveolar stem cell. Surfactant starts appearing around 26 weeks and is usually enough by about 35 weeks. Giving the mother corticosteroids before birth speeds this up. Maternal diabetes DELAYS surfactant production, because the baby's own insulin works against cortisol.

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