A 2-year-old boy has a history of recurrent bacterial infections, especially of his skin. When he has an infection, pus does not form. His mother reports that, when he was born, his umbilical cord took 5 weeks to detach. He is ultimately diagnosed with a defect in a molecule in the pathway that results in neutrophil extravasation. Which of the following correctly pairs the defective molecule with the step of extravasation that molecule affects?

LFA-1 (integrin); tight adhesion

Two weeks after undergoing low anterior resection for rectal cancer, a 52-year-old man comes to the physician because of swelling in both feet. He has not had any fever, chills, or shortness of breath. His temperature is 36°C (96.8°F) and pulse is 88/min. Physical examination shows a normal thyroid and no jugular venous distention. Examination of the lower extremities shows bilateral non-pitting edema that extends from the feet to the lower thigh, with deep flexion creases. His skin is warm and dry, and there is no erythema or rash. Microscopic examination of the interstitial space in this patient's lower extremities would be most likely to show the presence of which of the following?

Neutrophilic, protein-rich fluid

Lymphocytic, hemosiderin-rich fluid

Protein-rich, glycosaminoglycan-rich fluid

An 8-year-old boy is shifted to a post-surgical floor following neck surgery. The surgeon has restricted his oral intake for the next 24 hours. He does not have diarrhea, vomiting, or dehydration. His calculated fluid requirement is 1500 mL/day. However, he receives 2000 mL of intravenous isotonic fluids over 24 hours. Which of the following physiological parameters in the boy’s circulatory system is most likely to be increased?

Interstitial hydrostatic pressure

A 48-year-old male dies in the intensive care unit following a severe Streptococcus pneumoniae pneumonia and septic shock. Autopsy of the lung reveals a red, firm left lower lobe. What would you most likely find on microscopic examination of the lung specimen?

Alveolar exudate containing neutrophils, erythrocytes, and fibrin

Eosinophilia in the alveolar septa

Vascular dilation and noncaseating granulomas

A 4-year-old Caucasian boy is brought by his mother to the pediatrician with a red and swollen elbow. He was playing outside a few days prior to presentation when he fell and lightly scraped his elbow on the sidewalk. He was born at 34 weeks' gestation and was in the neonatal ICU for 2 days. His temperature is 102.1°F (38.9°C), blood pressure is 105/65 mmHg, pulse is 110/min, and respirations are 20/min. On exam, he has a swollen, erythematous, fluctuant, and exquisitely tender mass on his right elbow. There is expressible purulence coming from his wound. A peripheral blood smear in this patient would most likely reveal which of the following findings?

Neutrophils with abundant peroxidase-positive granules

Absence of dark blue cytoplasmic staining upon nitroblue tetrazolium administration

Neutrophils with peroxidase-negative granules

Neutrophils with pale cytoplasm without granules

Macrocytic erythrocytes and acanthocytes

Vascular changes in inflammation for USMLE Step 2 CK: High-Yield Pathology Lessons

Vasodilation & Permeability - Leaky Pipes Open

Phase 1: Vasodilation
- Brief, transient vasoconstriction (neurogenic) followed by vasodilation.
- Mediators: Histamine, Prostaglandins, Nitric Oxide (NO).
- Results in ↑ blood flow (hyperemia), causing Rubor (redness) and Calor (heat).

Phase 2: Permeability
- Hallmark of acute inflammation, leading to protein-rich exudate & edema (Tumor).
- Mechanisms:
  - Endothelial cell contraction (Immediate, transient): Most common; mediated by histamine, bradykinin, leukotrienes in post-capillary venules.
  - Direct endothelial injury (Immediate, sustained): Severe insults like burns or toxins.
  - Leukocyte-mediated injury: Late response.
  - Increased transcytosis: Via VEGF.

⭐ Histamine-mediated endothelial contraction is the principal mechanism of the immediate transient phase of increased vascular permeability, primarily affecting post-capillary venules.

Stasis & Leukocyte Margination - Cellular Traffic Jam

Stasis: A direct result of ↑ vascular permeability.
- Loss of protein-rich fluid (exudate) leads to ↑ blood viscosity and hemoconcentration (↑ RBCs).
- This dramatically slows blood flow, especially in post-capillary venules.
Leukocyte Margination: The hemodynamic consequence of stasis.
- As blood flow slows, heavy leukocytes fall out of the central axial stream and move towards the vessel periphery.
- This peripheral positioning allows neutrophils to tumble along and interact with the endothelial surface, a prerequisite for adhesion.

Leukocyte extravasation in inflammation

⭐ Pavementing: A severe manifestation of margination where the endothelial surface becomes so densely lined with leukocytes that it resembles a cobblestone pavement. It is a hallmark of florid acute inflammation.

Edema & Fluid Dynamics - The Fluid Shift

Fluid movement across capillaries is governed by Starling forces: the balance between hydrostatic pressure (pushes fluid out) and plasma colloid oncotic pressure (pulls fluid in).
Exudate: Inflammatory edema.
- Caused by ↑ vascular permeability from mediators like histamine.
- Endothelial gaps allow protein and cells to leak into the interstitium, causing a large ↑ in interstitial oncotic pressure ($\oldsymbol{\pi_i}$).
- Characteristics: High protein (>2.9 g/dL), high specific gravity (>1.020), cellular. Appears cloudy.
Transudate: Non-inflammatory edema.
- Caused by altered Starling forces, not permeability changes.
- Common causes: ↑ hydrostatic pressure (heart failure) or ↓ oncotic pressure (liver disease, nephrotic syndrome).
- Characteristics: Low protein (<2.5 g/dL), low specific gravity (<1.012), acellular. Appears clear.

⭐ Light's Criteria are used clinically to differentiate pleural exudates from transudates, critical for diagnosing the cause of a pleural effusion. 📌 EXudate = EXiting protein & cells due to inflammation.

Vasodilation (via histamine, NO) and increased blood flow cause redness and heat.

Increased vascular permeability is the hallmark of acute inflammation, leading to protein-rich exudate and swelling.

The most common mechanism is endothelial cell contraction (gaps), a rapid, reversible process mediated by histamine and bradykinin.

Direct endothelial injury causes immediate, sustained leakage in severe injuries.

Loss of fluid leads to stasis, concentrating RBCs and promoting leukocyte margination.

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