NIGHTINGALE COLLEGE PATHOPHYSIOLOGY
MIDTERM UPDATED QUESTIONS AND ANSWERS
SURE A+
✔✔Impact of alcohol use during pregnancy - ✔✔Culturing neural stem cells in the
presence of ethanol leads to dense methylation and inactivation of loci typically active in
neurons. Alters fetal expression of the DNA methyltransferases (DNMTs).
✔✔Signs of the intentional and unintentional injuries, including asphyxiation and the
injuries described in Table 4.8 - ✔✔
✔✔Asphyxiation - ✔✔Caused by the failure of cells to receive or use oxygen.
Deprivation of oxygen may be partial (hypoxia) or total (anoxia)
✔✔Asphyxial Injury: Suffocation - ✔✔The process of dying as a result of lack of oxygen,
can result from either a lack of oxygen in the environment or from a blockage of the
respiratory airways
✔✔Asphyxial Injury: Strangulation - ✔✔Caused by compression of the blood vessels
and air passages resulting from external pressure on the neck. The compression
causes hypoxia from impaired blood flow to the brain.
, ✔✔Asphyxial Injury: Chemical Asphyxiants - ✔✔Chemicals that prevent the delivery of
oxygen to the tissues or block oxygen utilization (CO2, cyanide, hydrogen sulfide, and
methane)
✔✔Asphyxial Injury: Drowning - ✔✔Death from inhalation of and suffocation by a liquid,
usually water.
✔✔Pathophysiology, clinical manifestations of alterations in water movement -
✔✔Edema caused by: (1) increased capillary hydrostatic pressure, (2) decreased
plasma oncotic pressure, (3) increased capillary membrane permeability, and (4)
lymphatic channel obstruction.
✔✔Compensatory mechanisms for metabolic acidosis - ✔✔Respiratory C02 elimination
(hyperventilation)
✔✔Compensatory mechanisms for metabolic alkalosis - ✔✔Respiratory C02 retention
(hypoventilation)
✔✔Compensatory mechanisms for respiratory acidosis - ✔✔Renal bicarbonate
retention and hydrogen elimination
✔✔Compensatory mechanisms for respiratory alkalosis - ✔✔Renal bicarbonate
elimination and hydrogen retention
✔✔Major components of the innate response - ✔✔Natural barriers and inflammation
✔✔Role of histamine and proinflammatory cytokines - ✔✔Histamine: induces
vasodilation and increased capillary permeability
Proinflammatory cytokines: have a key role in the destruction of many pathogenic
microorganisms
✔✔Systemic manifestations of acute inflammation - ✔✔Fever, leukocytosis, increased
plasma protein synthesis
✔✔Describe the phases of wound healing - ensure that you understand the primary
cells involved in each phase. - ✔✔Phases of wound healing:
1. Hemostasis (coagulation) - Platelet activation & fibrin clot
2. Inflammation - Macrophages, cytokines, neutrophils, & lymphocytes
3. Proliferation/tissue formation - Angiogenesis, fibroblast activation, granulation tissue
formation, and cytokines & growth factors
MIDTERM UPDATED QUESTIONS AND ANSWERS
SURE A+
✔✔Impact of alcohol use during pregnancy - ✔✔Culturing neural stem cells in the
presence of ethanol leads to dense methylation and inactivation of loci typically active in
neurons. Alters fetal expression of the DNA methyltransferases (DNMTs).
✔✔Signs of the intentional and unintentional injuries, including asphyxiation and the
injuries described in Table 4.8 - ✔✔
✔✔Asphyxiation - ✔✔Caused by the failure of cells to receive or use oxygen.
Deprivation of oxygen may be partial (hypoxia) or total (anoxia)
✔✔Asphyxial Injury: Suffocation - ✔✔The process of dying as a result of lack of oxygen,
can result from either a lack of oxygen in the environment or from a blockage of the
respiratory airways
✔✔Asphyxial Injury: Strangulation - ✔✔Caused by compression of the blood vessels
and air passages resulting from external pressure on the neck. The compression
causes hypoxia from impaired blood flow to the brain.
, ✔✔Asphyxial Injury: Chemical Asphyxiants - ✔✔Chemicals that prevent the delivery of
oxygen to the tissues or block oxygen utilization (CO2, cyanide, hydrogen sulfide, and
methane)
✔✔Asphyxial Injury: Drowning - ✔✔Death from inhalation of and suffocation by a liquid,
usually water.
✔✔Pathophysiology, clinical manifestations of alterations in water movement -
✔✔Edema caused by: (1) increased capillary hydrostatic pressure, (2) decreased
plasma oncotic pressure, (3) increased capillary membrane permeability, and (4)
lymphatic channel obstruction.
✔✔Compensatory mechanisms for metabolic acidosis - ✔✔Respiratory C02 elimination
(hyperventilation)
✔✔Compensatory mechanisms for metabolic alkalosis - ✔✔Respiratory C02 retention
(hypoventilation)
✔✔Compensatory mechanisms for respiratory acidosis - ✔✔Renal bicarbonate
retention and hydrogen elimination
✔✔Compensatory mechanisms for respiratory alkalosis - ✔✔Renal bicarbonate
elimination and hydrogen retention
✔✔Major components of the innate response - ✔✔Natural barriers and inflammation
✔✔Role of histamine and proinflammatory cytokines - ✔✔Histamine: induces
vasodilation and increased capillary permeability
Proinflammatory cytokines: have a key role in the destruction of many pathogenic
microorganisms
✔✔Systemic manifestations of acute inflammation - ✔✔Fever, leukocytosis, increased
plasma protein synthesis
✔✔Describe the phases of wound healing - ensure that you understand the primary
cells involved in each phase. - ✔✔Phases of wound healing:
1. Hemostasis (coagulation) - Platelet activation & fibrin clot
2. Inflammation - Macrophages, cytokines, neutrophils, & lymphocytes
3. Proliferation/tissue formation - Angiogenesis, fibroblast activation, granulation tissue
formation, and cytokines & growth factors
