PATHOPHYSIOLOGY PARK PRACTICE SOLUTION 2026 SOLVED ITEMS CONFIRMED A+, Exams of Biomedicine

PATHOPHYSIOLOGY PARK PRACTICE SOLUTION 2026 SOLVED ITEMS CONFIRMED A+

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2025/2026

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PATHOPHYSIOLOGY PARK PRACTICE
SOLUTION 2026 SOLVED ITEMS CONFIRMED
A+
◉ Some cancer-causing viruses are able to protect the cells that they
transform from undergoing apoptosis by interfering with the action
of the apoptosis promoter called:
a. TNF-alpha.
b. Fas.
c. p53.
d. IL-2.
e. INF-beta. Answer: C
◉ Which of the following diseases is thought to be related to free
radical damage?
a. osteoarthritis
b. detached retina
c. cerebral aneurysm
d. cancer. Answer: D
◉ Which of the following enzymes, released from dying cells, may
indicate problems in the liver?
pf3
pf4
pf5
pf8
pf9
pfa
pfd
pfe
pff
pf12
pf13
pf14
pf15
pf16
pf17
pf18
pf19
pf1a
pf1b
pf1c
pf1d
pf1e
pf1f
pf20
pf21
pf22
pf23
pf24
pf25
pf26
pf27
pf28
pf29
pf2a
pf2b
pf2c
pf2d
pf2e
pf2f
pf30
pf31
pf32
pf33

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PATHOPHYSIOLOGY PARK PRACTICE

SOLUTION 2026 SOLVED ITEMS CONFIRMED

A+

◉ Some cancer-causing viruses are able to protect the cells that they transform from undergoing apoptosis by interfering with the action of the apoptosis promoter called: a. TNF-alpha. b. Fas. c. p53. d. IL-2. e. INF-beta. Answer: C ◉ Which of the following diseases is thought to be related to free radical damage? a. osteoarthritis b. detached retina c. cerebral aneurysm d. cancer. Answer: D ◉ Which of the following enzymes, released from dying cells, may indicate problems in the liver?

a. alanine aminotransferase b. aspartate aminotransferase c. alkaline phosphatase d. all of the above e. none of the above. Answer: D ◉ Researchers hypothesize that the disappearance of dopamine- generating cells in the midbrain in Parkinson's Disease may be related to oxidative stress due to a decrease in the amount of glutathione in the midbrain. The best explanation for this theory is which of the following? a. DNA synthesis requires glutathione for optimal development. b. Dopamine synthesis requires glutathione to prevent free radical production. c. Free radicals produced via dopamine synthesis are neutralized by glutathione. d. Glutathione is needed for entry of dopamine into the cerebral circulation.. Answer: C ◉ Which of the following is(are) true regarding aging? a. may involve an increase in autoantibodies b. may result from damage accumulation c. both are true d. neither is true. Answer: C

signs are objective or measurable ◉ outcomes. Answer: cure, remission, chronicity, or death ◉ primary prevention. Answer: Efforts to prevent an injury or illness from ever occurring. ◉ secondary prevention. Answer: - focuses on early identification of individuals or communities experiencing illness, providing treatment, and conducting activities that are geared to prevent worsening health status

  • examples: communicable disease screening and case finding; early detection and treatment of diabetes; exercise programs for older adult clients who are frail ◉ Tertiary prevention. Answer: - aims to prevent the long-term consequences of a chronic illness or disability and to support optimal functioning
  • examples: prevention of pressure ulcers as complication of a spinal cord injury; promoting independence for the client who has traumatic brain injury ◉ Atrophy. Answer: Decrease or shrinkage in cellular size.Most common in skeletal muscle, heart, secondary sex organs, and brain.

◉ Physiologic atrophy. Answer: occurs with early development. Ex. Thymus gland gets physiologic atrophy during childhood. ◉ pathologic atrophy. Answer: occurs as a result of decreases in workload, pressure, use, blood supply, nutrition, hormonal stimulation, and nervous stimulation ◉ hypertrophy. Answer: Increase in the size of the cells that increase the size of the affected organ. Heart and kidneys (responsive to enlargement) and skeletal muscle. ◉ physiologic hypertrophy. Answer: occurs with increased demand, stimulation of hormones, and growth factors. Ex. Pregnancy causes hormone induced hypertrophy of the uterus, in skeletal muscle occurs as a response to heavy workload. ◉ pathologic hypertrophy. Answer: results from chronic hemodynamic overload. Ex. Hypertension or heart valve dysfunction. Hypertrophic cells have increased accumulation of ER, plasma membrane, myofilaments, mitochondria (not cellular fluid). Nucleus is also hypertrophic with increased DNA synthesis. Triggers for cardiac hypertrophy include mechanical signals (stretch) and trophic signals (growth factors and vasoactive agents).

◉ Cause of metaplasia. Answer: develops from reprogramming of stem cells. Found in association with tissue damage, repair, and regeneration. ◉ pathophysiology of metaplasia. Answer: Adaptive replacement cell may be more suitable to the changed conditions in the surrounding environment. Ex. GERD damages squamous epithelium of the esophagus, cells are replaced by glandular epithelium which may tolerate the acid better. Not always beneficial. Ex. Smoking causes changes in bronchi cells, which don't have cilia or secrete mucus, causing loss of protective mechanism. ◉ What is the significance of metaplasia. Answer: Can be reversed if stimulus is removed. If continues, can cause malignant transformation. ◉ Dysplasia. Answer: abnormal changes in the size, shape, and organization of mature cells. mostly found in epithelia ◉ Significance of dysplasia. Answer: can be reversed if it does not involve the entire epithelium. When dysplastic changes penetrate the basement membrane it is considered a preinvasive neoplasm (carcinoma in situ) ◉ mechanisms of cell injury. Answer: ATP depletion, mitochondrial damage, accumulation of oxygen and oxygen-derived free radicals

membrane damage protein folding defects DNA damage defects calcium level alterations ◉ reperfusion injury. Answer: injury to tissue that occurs after blood flow is restored restoration of needed oxygen is accompanied by oxidative stress with the generation of toxic oxygen radicals which damage cellular membranes and mitochndria ◉ What helps reperfusion injury?. Answer: antioxidants and anti- inflammatory drugs ◉ examples of cell injury. Answer: ischemic and hypoxic injury ischemia-reperfusion injury oxidative stress or accumulation of oxygen-derived free radicals induced injury chemical injury ◉ Cell injury: ATP depletion. Answer: loss of mitochondrial ATP and decreased ATP synthesis results include:

  • failed NA+/K pump
  • Na, Ca enter cell, K leaves
  • organelle swelling
  • protein synthesis stops
  • ATP via oxidative phosphorylation declines, glycolysis increases
  • glycogen stores depleated
  • lactic acid produced
  • decrease in intracellular Ph declines
  • rupture of lysosomes
  • autodigestion of the cell contents and membrane ◉ Deleterious effects of free radicals on cells. Answer: - unstable compounds with an unpaired electron in outer ring
  • anxious to "mate" with other substances affinity for lipid substances (there is a phospholipid bilayer membrane around cell)
  • combine avidly with cell and organelle membranes
  • lipid peroxidation - dissolution of the membrane
  • "drills a hole" ◉ examples o diseases linked to oxygen-derived free radicals. Answer: aging

atherosclerosis brain disorders Cancer Cardiac myopathy Diabetes Eye disorders inflammatory disorders iron overload emphysema radiation injury reperfusion injury rheumatoid arthritis sleep apnea Burns ◉ Most types of cellular accumulations occur as a result of what 4 mechanisms. Answer: 1 - insufficient removal of normal substance because of altered packaging/transport 2 - abnormal substance (result of mutated gene) accumulated because of deficits in protein folding, transport, or abnormal degredation 3 - endogenous substance not effectively catabolized because of lack of vital lysosomal enzyme

  • Failure of metabolic process that converts fatty acids to phospholipids resulting in the preferential conversion of the fatty acids to triglycerides
  • increased synthesis of triglycerides from fatty acids
  • decreased synthesis of apoproteins (lipid acceptors)
  • failure of lipids to bind with apoproteins and form lipoproteins
  • failure of mechanisms that transport lipoproteins out of the cell
  • direct damage to the ER by free radicals released by alcohol's toxic effects ◉ pathogenesis of bilirubin. Answer: - released when RBCs break down
  • released into blood (unconjugated)
  • fat-soluble, cannot be elimintated through urine
  • unconjugated is taken up in the liver cells, bound to glucuronic acid, becomes conjugated bilirubin
  • can now be eliminated through the kidney
  • some becomes part of bile, some is eliminated in urine and feces giving yellow and brown color (bilirubin is a pigment) ◉ What is jaundice caused by. Answer: excess bilirubin ◉ what is excess bilirubin caused by. Answer: - diseases that cause destruction of RBC (hemolytic jaundice)
  • Diseases affecting the metabolism and excretion of bilirubin in the liver
  • diseases that can obstruct the common bile duct (gallstones/pancreatic tumors) ◉ Effects of free cytosolic calcium. Answer: - normally removed by ATP dependent calcium pumps
  • If abnormal permeability of calcium ion channels, direct damage to membranes, or depletion of ATP (i.e. hypoxic injury)
  • then calcium level increases
  • if not buffered or pumped out, uncontrolled enzyme activation takes place
  • leading to: phosphorylation of protein and chromatin fragmentation, membrane damage, cytoskeletal disassembly (damage), nucleus chromatin damage
  • often final pathway in many causes of cell death ◉ pyknosis. Answer: in some cells the nucleus shrinks and becomes a small dense (clumped together) mass of genetic material. The pyknotic nucleus eventually dissolves (by karyolysis) ◉ karyorrhexias. Answer: a degenerative cellular process involving fragmentation of the nucleus and the breakup of the chromatin into unstructured granules

◉ Fat necrosis. Answer: occurs in the breast, pancreas, and other abdominal structures cellular dissolution caused by powerful enzymes called lipases break down triglycerides releasing free fatty acids which combine with calcium, magnesium, and sodium ions, creating soaps necrotic tissue appears opaque and chalk white ◉ Gangrenous necrosis. Answer: refers to death of tissue and results from severe hypoxic injury commonly occurring becasuse of arteriosclerosis especially in lower leg with hypoxia and subsequent bacterial invasion, the tissues undergo necrosis ◉ dry gangrene. Answer: an area that is free of infection and in which the line of demarcation between live and dead tissue is apparent tissue becomes dry and shrunken - mummified ◉ wet gangrene. Answer: often malodorous and the line of demarcation between live and dead tissue is unclear until the infection is arrested

◉ gas gangrene. Answer: wet gangrene caused by clostridium perfringes, an organisms that produces gas within the destroyed tissue. This accumulation of gas produces a distinctive sound on palpation of the area called crepitus ◉ systemic manifestations of cellular injury. Answer: fever increased heart rate increase in number of leukocytes pain presence of cellular enzymes in extracellular fluid lactate dehydrogenase CK AST ALT ALP amylase aldolase tropinins ◉ cellular processes involved in necrosis. Answer: - caused by an injurious agent, or - cells are induced to commit suicide

  • a disorganized sequence of events that stimulates the inflammatory process

◉ what is the time course for apoptosis. Answer: 12 - 24 hours ◉ what is the time course for necrosis. Answer: 20 - 30 minutes ◉ cell characteristics of apoptosis. Answer: shrinkage of the cell condensation of the cytoplasm detachment of cell from ECM membrane budding phagocytosis by neighboring cells nuclear DNA fragmentation activation of capases and DNAses ◉ cell characteristics of necrosis. Answer: cell swelling and rupture of cell membrane clumping of nuclear chromatin swelling of intracellular organelles calcium and other electrolyte overload ◉ what are the three mechanisms of apoptosis. Answer: intrinsic or mitochondrial pathway extrinsic or death receptor pathway

apoptosis inducing factor ◉ Apoptosis - mitochondrial pathway. Answer: - healthy cell - protein Bcl-2 on surface - inhibits apoptosis

  • internal damage to cell
    • protein Bax migrates to the surface of the mitochondria where it inhibits protective effect of Bcl- 2
    • inserts self into outer mitochondrial membrane punching holes in it
    • cytochrome c leaks out
  • cytochrome c binds to the protein Apaf- 1
  • complexes aggregate to form apoptosomes
  • bind to and activate caspase- 9
  • cleaves and activates other caspases (executioner ones)
  • digestion of structural proteins in the cytoplasm
  • degradation of chromosomal DNA
  • phagocytosis of the cell ◉ Apoptosis death-receptor pathway. Answer: - Fas and TNF receptor are integral membrane proteins with their receptor domains exposed at the surface of the cell
  • binding of the complementary death activator (FasL and TNF) transmits a signal to the cytoplasm