Q1. What are general reaction patterns in pathology?
A. Specific genetic mutations causing disease
B. Common ways tissues and organs respond to injury or disease
C. Unique symptoms experienced by patients
D. Types of bacteria causing infections
Q2. Which of the following best characterizes acute inflammation?
A. A delayed immune response without redness or swelling
B. An immediate tissue response with redness, heat, swelling, pain, and loss of function
C. A chronic process involving tissue destruction and repair simultaneously
D. Formation of granulomas in response to persistent stimuli
Q3. What is diapedesis in the context of inflammation?
A. The process of white blood cells multiplying in the bloodstream
B. The movement of white blood cells out of blood vessels to injured tissue
C. The destruction of bacteria by neutrophils
D. The swelling of blood vessels during inflammation
Q4. Which immune cells are among the first to arrive at the site of acute inflammation?
A. Lymphocytes
B. Macrophages
C. Neutrophils
D. Eosinophils
,Q5. What role does chemotaxis play in inflammation?
A. It causes blood vessels to dilate
B. It directs immune cells toward higher concentrations of chemical signals at injury sites
C. It triggers programmed cell death in immune cells
D. It causes swelling by fluid accumulation
Q6. How does apoptosis differ from necrosis?
A. Apoptosis is uncontrolled cell death causing inflammation; necrosis is programmed and orderly
B. Apoptosis is a programmed, orderly cell death; necrosis is uncontrolled cell death causing inflammation
C. Both are uncontrolled forms of cell death
D. Both are programmed and non-inflammatory
Q7. Which morphological change is typical of apoptosis?
A. Cell swelling and rupture
B. Cell shrinking and fragmentation into apoptotic bodies
C. Formation of giant multinucleated cells
D. Accumulation of fatty deposits in cells
Q8. What is nuclear fragmentation in apoptosis?
A. The nucleus enlarges and dissolves completely
B. The nucleus breaks into smaller, membrane-bound pieces called apoptotic bodies
C. The nucleus remains intact but the cell swells
D. The nucleus fuses with other cells to form giant cells
Q9. What role do caspases play in programmed cell death?
A. They promote inflammation by releasing cytokines
, B. They are enzymes that break down cellular proteins leading to apoptosis
C. They repair damaged DNA in cells
D. They stimulate cell proliferation during tissue repair
Q10. The mitochondrial pathway of apoptosis is also known as:
A. The extrinsic pathway
B. The intrinsic pathway
C. The necrotic pathway
D. The inflammatory pathway
Q11. What is a granulomatous reaction?
A. A type of acute inflammation dominated by neutrophils
B. A chronic inflammation characterized by clusters of macrophages surrounded by lymphocytes
C. A process of smooth muscle proliferation in blood vessels
D. The formation of fatty plaques in arteries
Q12. Giant cells in granulomatous inflammation are:
A. Large cells formed by fusion of multiple macrophages with multiple nuclei
B. Enlarged neutrophils that engulf bacteria
C. Single macrophages that have swollen due to lipid accumulation
D. Endothelial cells that have proliferated excessively
Q13. Increased cell size is a key feature of:
A. Hyperplasia
B. Hypertrophy
C. Necrosis
, D. Apoptosis
Q14. Which of the following conditions affect the heart and blood vessels by impairing blood
circulation?
A. Diabetes mellitus and anemia
B. Coronary artery disease, heart failure, and hypertension
C. Asthma and chronic bronchitis
D. Osteoporosis and arthritis
Q15. What components make up the atheromatous plaque structure?
A. Only cholesterol crystals
B. Lipid-rich core, inflammatory cells, and a fibrous cap
C. Purely fibrous tissue without lipids
D. Necrotic tissue and calcium deposits only
Q16. Smooth muscle proliferation in atherosclerosis involves:
A. Decrease in smooth muscle cells in the vessel wall
B. Increase in smooth muscle cell number migrating from media to intima, contributing to plaque growth
C. Transformation of smooth muscle cells into macrophages
D. Apoptosis of smooth muscle cells in the artery wall
Q17. What characterizes idiopathic hypertrophic subaortic stenosis?
A. Thinning of the left ventricular free wall causing reduced contraction
B. Abnormal thickening of the interventricular septum obstructing blood flow
C. Dilation of the aortic root leading to valve insufficiency
D. Inflammation of the pericardium causing fluid accumulation