Test Bank Complete_
Robbins And Kumar Basic Pathology| Robbins Pathology| 11th Edition, (2022)
By Vinay Kumar, Abul K. Abbas, Jon C. Aster & Andrea T Deyrup
All Chapters 1-22| Latest Version With Well Explained Answers| Verified| grade A+
,CHAPTER 1. CELL INJURY, CELL DEATH, AND ADAPTATIONS ___________________________ 3
CHAPTER 2. INFLAMMATION AND REPAIR ________________________________________ 15
CHAPTER 3. HEMODYNAMIC DISORDERS, THROMBOEMBOLISM, AND SHOCK ___________ 25
CHAPTER 4. GENETIC AND PEDIATRIC DISEASES ____________________________________ 34
CHAPTER 5. DISEASES OF THE IMMUNE SYSTEM ___________________________________ 44
CHAPTER 6. NEOPLASIA _______________________________________________________ 53
CHAPTER 7. ENVIRONMENTAL AND NUTRITIONAL DISEASES _________________________ 63
CHAPTER 8. BLOOD VESSELS ___________________________________________________ 72
CHAPTER 9. HEART ___________________________________________________________ 83
CHAPTER 10. HEMATOPOIETIC AND LYMPHOID SYSTEMS ____________________________ 92
CHAPTER 11. LUNG __________________________________________________________ 103
CHAPTER 12. KIDNEY AND ITS COLLECTING SYSTEM _______________________________ 112
CHAPTER 13. ORAL CAVITIES AND GASTROINTESTINAL TRACT _______________________ 120
CHAPTER 14. LIVER AND GALLBLADDER _________________________________________ 129
CHAPTER 15. PANCREAS AND BILIARY SYSTEM ___________________________________ 138
CHAPTER 16. MALE GENITAL SYSTEM AND LOWER URINARY TRACT __________________ 148
CHAPTER 17. FEMALE GENITAL SYSTEM AND BREAST ______________________________ 158
CHAPTER 18. ENDOCRINE SYSTEM _____________________________________________ 168
CHAPTER 19. BONES, JOINTS, AND SOFT TISSUE TUMORS ___________________________ 177
CHAPTER 20. PERIPHERAL NERVES AND MUSCLES _________________________________ 186
CHAPTER 21. CENTRAL NERVOUS SYSTEM _______________________________________ 197
CHAPTER 22. SKIN___________________________________________________________ 207
,CHAPTER 1. CELL INJURY, CELL DEATH, AND ADAPTATIONS
Vinay Kumar: Robbins & Kumar Basic Pathology (Robbins Pathology) 11th Edition, (2022)
MULTIPLE CHOICE
1. WHICH OF THE FOLLOWING STATEMENTS IS TRUE? CELL DEATH BY APOPTOSIS:
A. MAY BE REGULATED OR INDUCED BY WITHDRAWAL OF GROWTH FACTORS
B. IS A PASSIVE PROCESS, NOT REQUIRING ENERGY
C. AFFECTS LARGE NUMBERS OF NEIGHBORING CELLS
D. IS USUALLY CAUSED BY EXPOSURE TO SEVERE PATHOLOGICAL INJURY
E. IS THE SAME AS THE PROCESS OF NECROSIS
ANS: A)
EXPLANATION:
APOPTOSIS, ALSO KNOWN AS PROGRAMMED CELL DEATH, IS A TIGHTLY REGULATED PROCESS
THAT CAN BE TRIGGERED BY SEVERAL FACTORS, INCLUDING THE WITHDRAWAL OF GROWTH
FACTORS, DNA DAMAGE, OR CELLULAR STRESS. UNLIKE NECROSIS, WHICH IS A FORM OF
UNCONTROLLED CELL DEATH TYPICALLY TRIGGERED BY SEVERE INJURY OR TRAUMA, APOPTOSIS
IS AN ENERGY-DEPENDENT AND REGULATED PROCESS THAT OFTEN INVOLVES SIGNALING
PATHWAYS AND MOLECULAR MECHANISMS LIKE THE ACTIVATION OF CASPASES. IT IS A
CONTROLLED PROCESS THAT ELIMINATES DAMAGED OR UNNECESSARY CELLS WITHOUT CAUSING
INFLAMMATION.
2. ED HAS A BLOCKED CORONARY ARTERY (SUPPLYING HIS HEART) AND SUFFERS FROM A
MYOCARDIAL INFARCTION AND PERMANENT DAMAGE AND DEATH OF SOME OF HIS HEART
MUSCLE. WHICH OF THE FOLLOWING STATEMENTS IS NOT TRUE?
A. HE HAS SOME NECROSIS OF THE CARDIAC MUSCLE
B. THERE HAS PROBABLY BEEN ISCHEMIA AND HYPOXIA OF SOME OF THE HEART MUSCLE
C. HYPOXIA RESULTS IN A DECREASE OF ATP PRODUCTION
,D. SOME DAMAGE TO THE HEART MUSCLE MAY HAVE ARISEN FROM INJURY DUE TO PRODUCTION
OF EXCESS FREE RADICALS FOLLOWING THE RESTORATION OF BLOOD FLOW TO HIS HEART
E. THE HEART MUSCLE WILL BE RESTORED TO NORMAL AS THERE WAS REVERSIBLE DAMAGE
ANS: E)
EXPLANATION:
A MYOCARDIAL INFARCTION (MI) OCCURS WHEN A CORONARY ARTERY BECOMES BLOCKED,
LEADING TO ISCHEMIA (LACK OF BLOOD FLOW) AND HYPOXIA (LACK OF OXYGEN) IN THE HEART
MUSCLE. THIS CAUSES CELL INJURY AND, IF PROLONGED, RESULTS IN NECROSIS (PERMANENT
DEATH OF THE HEART MUSCLE CELLS). IN THIS CASE, THE DAMAGE IS PERMANENT, AND THE
HEART MUSCLE WILL NOT BE FULLY RESTORED TO NORMAL.
3. ISCHEMIA AND OTHER TOXIC INJURIES INCREASE THE ACCUMULATION OF
INTRACELLULAR CALCIUM AS A RESULT OF:
A) RELEASE OF STORED CALCIUM FROM THE MITOCHONDRIA.
B) IMPROVED INTRACELLULAR VOLUME REGULATION.
C) DECREASED INFLUX ACROSS THE CELL MEMBRANE.
D) ATTRACTION OF CALCIUM TO FATTY INFILTRATES.
ANS: A)
EXPLANATION:
ISCHEMIA AND TOXIC INJURIES DISRUPT THE NORMAL FUNCTIONING OF THE CELL, LEADING TO
THE RELEASE OF STORED CALCIUM FROM INTRACELLULAR COMPARTMENTS LIKE THE
MITOCHONDRIA. THE INCREASED CALCIUM CONCENTRATION INSIDE THE CELL CAN ACTIVATE
HARMFUL ENZYMES THAT DAMAGE CELL STRUCTURES.
4. THE NURSE IN AN INFECTIOUS-DISEASE CLINIC WILL PRIMARILY TREAT INJURIES TO
TISSUES AND CELLS CAUSED BY:
A) CHEMICAL AGENTS.
,B) BIOLOGIC AGENTS.
C) CALCIFICATION.
D) ONCOGENIC AGENTS.
ANS: B)
EXPLANATION:
INJURY FROM BIOLOGIC AGENTS DERIVES FROM BACTERIAL AND VIRAL INFECTIONS. THE
INJURIES DIFFER FROM THE OTHER FORMS BECAUSE THEY ARE ABLE TO REPLICATE AND CAN
CONTINUE TO PRODUCE THEIR INJURIOUS EFFECTS. THE ETIOLOGY OF INFECTIONS DOES NOT
NORMALLY INCLUDE ONCOGENIC AGENTS, CHEMICAL AGENTS, OR CALCIFICATIONS
5. THE PATIENT IS FOUND TO HAVE LIVER DISEASE, RESULTING IN THE REMOVAL OF A LOBE
OF HIS LIVER. ADAPTATION TO THE REDUCED SIZE OF THE LIVER LEADS TO __________ OF THE
REMAINING LIVER CELLS.
A) METAPLASIA
B) ORGAN ATROPHY
C) COMPENSATORY HYPERPLASIA
D) PHYSIOLOGIC HYPERTROPHY
ANS: C)
EXPLANATION:
COMPENSATORY HYPERPLASIA IS A PROCESS WHERE CELLS INCREASE IN NUMBER TO
COMPENSATE FOR THE LOSS OF TISSUE OR ORGAN FUNCTION. IN THIS CASE, THE REMAINING
LIVER CELLS UNDERGO HYPERPLASIA TO MAKE UP FOR THE LOST LOBE.
6. A PERSON EATING PEANUTS STARTS CHOKING AND COLLAPSES. HIS AIRWAY OBSTRUCTION
IS PARTIALLY CLEARED, BUT HE REMAINS HYPOXIC UNTIL HE REACHES THE HOSPITAL. THE
PROLONGED CELL HYPOXIA CAUSED A CEREBRAL INFARCTION AND RESULTING __________ IN
THE BRAIN.
, A) CASPASE ACTIVATION
B) COAGULATION NECROSIS
C) RAPID PHAGOCYTOSIS
D) PROTEIN P53 DEFICIENCY
ANS: B)
EXPLANATION:
PROLONGED HYPOXIA CAUSES IRREVERSIBLE DAMAGE TO CELLS, LEADING TO COAGULATION
NECROSIS. IN THIS CASE, A LACK OF OXYGEN LEADS TO CELL DEATH IN THE BRAIN,
CHARACTERIZED BY COAGULATIVE NECROSIS WHERE THE TISSUE STRUCTURE REMAINS
RELATIVELY INTACT FOR SOME TIME.
7. A PREGNANT CLIENT IS ATTENDING A NUTRITION CLASS FOR FIRST-TIME MOMS. DURING
THE CLASS, THE INSTRUCTOR STRESSED THAT THEY SHOULD AVOID CONSUMPTION OF
WHICH FOOD THAT MAY CAUSE BRAIN DAMAGE FROM METHYL MERCURY EXPOSURE?
A) RAW HAMBURGER
B) BEETS
C) TUNA
D) FRESH MILK
ANS: C)
EXPLANATION:
THE MAIN SOURCE OF METHYL MERCURY EXPOSURE IS FROM CONSUMPTION OF LONG-LIVED FISH,
SUCH AS TUNA AND SWORDFISH. FISH CONCENTRATE MERCURY FROM SEDIMENT IN THE WATER.
BECAUSE THE DEVELOPING BRAIN IS MORE SUSCEPTIBLE TO MERCURY-INDUCED DAMAGE, IT IS
RECOMMENDED THAT YOUNG CHILDREN AND PREGNANT AND NURSING WOMEN SHOULD AVOID
CONSUMPTION OF FISH KNOWN TO CONTAIN HIGH MERCURY CONTENT. NONE OF THE OTHER
FOODS LISTED POSE A THREAT OF MERCURY TOXICITY
Robbins And Kumar Basic Pathology| Robbins Pathology| 11th Edition, (2022)
By Vinay Kumar, Abul K. Abbas, Jon C. Aster & Andrea T Deyrup
All Chapters 1-22| Latest Version With Well Explained Answers| Verified| grade A+
,CHAPTER 1. CELL INJURY, CELL DEATH, AND ADAPTATIONS ___________________________ 3
CHAPTER 2. INFLAMMATION AND REPAIR ________________________________________ 15
CHAPTER 3. HEMODYNAMIC DISORDERS, THROMBOEMBOLISM, AND SHOCK ___________ 25
CHAPTER 4. GENETIC AND PEDIATRIC DISEASES ____________________________________ 34
CHAPTER 5. DISEASES OF THE IMMUNE SYSTEM ___________________________________ 44
CHAPTER 6. NEOPLASIA _______________________________________________________ 53
CHAPTER 7. ENVIRONMENTAL AND NUTRITIONAL DISEASES _________________________ 63
CHAPTER 8. BLOOD VESSELS ___________________________________________________ 72
CHAPTER 9. HEART ___________________________________________________________ 83
CHAPTER 10. HEMATOPOIETIC AND LYMPHOID SYSTEMS ____________________________ 92
CHAPTER 11. LUNG __________________________________________________________ 103
CHAPTER 12. KIDNEY AND ITS COLLECTING SYSTEM _______________________________ 112
CHAPTER 13. ORAL CAVITIES AND GASTROINTESTINAL TRACT _______________________ 120
CHAPTER 14. LIVER AND GALLBLADDER _________________________________________ 129
CHAPTER 15. PANCREAS AND BILIARY SYSTEM ___________________________________ 138
CHAPTER 16. MALE GENITAL SYSTEM AND LOWER URINARY TRACT __________________ 148
CHAPTER 17. FEMALE GENITAL SYSTEM AND BREAST ______________________________ 158
CHAPTER 18. ENDOCRINE SYSTEM _____________________________________________ 168
CHAPTER 19. BONES, JOINTS, AND SOFT TISSUE TUMORS ___________________________ 177
CHAPTER 20. PERIPHERAL NERVES AND MUSCLES _________________________________ 186
CHAPTER 21. CENTRAL NERVOUS SYSTEM _______________________________________ 197
CHAPTER 22. SKIN___________________________________________________________ 207
,CHAPTER 1. CELL INJURY, CELL DEATH, AND ADAPTATIONS
Vinay Kumar: Robbins & Kumar Basic Pathology (Robbins Pathology) 11th Edition, (2022)
MULTIPLE CHOICE
1. WHICH OF THE FOLLOWING STATEMENTS IS TRUE? CELL DEATH BY APOPTOSIS:
A. MAY BE REGULATED OR INDUCED BY WITHDRAWAL OF GROWTH FACTORS
B. IS A PASSIVE PROCESS, NOT REQUIRING ENERGY
C. AFFECTS LARGE NUMBERS OF NEIGHBORING CELLS
D. IS USUALLY CAUSED BY EXPOSURE TO SEVERE PATHOLOGICAL INJURY
E. IS THE SAME AS THE PROCESS OF NECROSIS
ANS: A)
EXPLANATION:
APOPTOSIS, ALSO KNOWN AS PROGRAMMED CELL DEATH, IS A TIGHTLY REGULATED PROCESS
THAT CAN BE TRIGGERED BY SEVERAL FACTORS, INCLUDING THE WITHDRAWAL OF GROWTH
FACTORS, DNA DAMAGE, OR CELLULAR STRESS. UNLIKE NECROSIS, WHICH IS A FORM OF
UNCONTROLLED CELL DEATH TYPICALLY TRIGGERED BY SEVERE INJURY OR TRAUMA, APOPTOSIS
IS AN ENERGY-DEPENDENT AND REGULATED PROCESS THAT OFTEN INVOLVES SIGNALING
PATHWAYS AND MOLECULAR MECHANISMS LIKE THE ACTIVATION OF CASPASES. IT IS A
CONTROLLED PROCESS THAT ELIMINATES DAMAGED OR UNNECESSARY CELLS WITHOUT CAUSING
INFLAMMATION.
2. ED HAS A BLOCKED CORONARY ARTERY (SUPPLYING HIS HEART) AND SUFFERS FROM A
MYOCARDIAL INFARCTION AND PERMANENT DAMAGE AND DEATH OF SOME OF HIS HEART
MUSCLE. WHICH OF THE FOLLOWING STATEMENTS IS NOT TRUE?
A. HE HAS SOME NECROSIS OF THE CARDIAC MUSCLE
B. THERE HAS PROBABLY BEEN ISCHEMIA AND HYPOXIA OF SOME OF THE HEART MUSCLE
C. HYPOXIA RESULTS IN A DECREASE OF ATP PRODUCTION
,D. SOME DAMAGE TO THE HEART MUSCLE MAY HAVE ARISEN FROM INJURY DUE TO PRODUCTION
OF EXCESS FREE RADICALS FOLLOWING THE RESTORATION OF BLOOD FLOW TO HIS HEART
E. THE HEART MUSCLE WILL BE RESTORED TO NORMAL AS THERE WAS REVERSIBLE DAMAGE
ANS: E)
EXPLANATION:
A MYOCARDIAL INFARCTION (MI) OCCURS WHEN A CORONARY ARTERY BECOMES BLOCKED,
LEADING TO ISCHEMIA (LACK OF BLOOD FLOW) AND HYPOXIA (LACK OF OXYGEN) IN THE HEART
MUSCLE. THIS CAUSES CELL INJURY AND, IF PROLONGED, RESULTS IN NECROSIS (PERMANENT
DEATH OF THE HEART MUSCLE CELLS). IN THIS CASE, THE DAMAGE IS PERMANENT, AND THE
HEART MUSCLE WILL NOT BE FULLY RESTORED TO NORMAL.
3. ISCHEMIA AND OTHER TOXIC INJURIES INCREASE THE ACCUMULATION OF
INTRACELLULAR CALCIUM AS A RESULT OF:
A) RELEASE OF STORED CALCIUM FROM THE MITOCHONDRIA.
B) IMPROVED INTRACELLULAR VOLUME REGULATION.
C) DECREASED INFLUX ACROSS THE CELL MEMBRANE.
D) ATTRACTION OF CALCIUM TO FATTY INFILTRATES.
ANS: A)
EXPLANATION:
ISCHEMIA AND TOXIC INJURIES DISRUPT THE NORMAL FUNCTIONING OF THE CELL, LEADING TO
THE RELEASE OF STORED CALCIUM FROM INTRACELLULAR COMPARTMENTS LIKE THE
MITOCHONDRIA. THE INCREASED CALCIUM CONCENTRATION INSIDE THE CELL CAN ACTIVATE
HARMFUL ENZYMES THAT DAMAGE CELL STRUCTURES.
4. THE NURSE IN AN INFECTIOUS-DISEASE CLINIC WILL PRIMARILY TREAT INJURIES TO
TISSUES AND CELLS CAUSED BY:
A) CHEMICAL AGENTS.
,B) BIOLOGIC AGENTS.
C) CALCIFICATION.
D) ONCOGENIC AGENTS.
ANS: B)
EXPLANATION:
INJURY FROM BIOLOGIC AGENTS DERIVES FROM BACTERIAL AND VIRAL INFECTIONS. THE
INJURIES DIFFER FROM THE OTHER FORMS BECAUSE THEY ARE ABLE TO REPLICATE AND CAN
CONTINUE TO PRODUCE THEIR INJURIOUS EFFECTS. THE ETIOLOGY OF INFECTIONS DOES NOT
NORMALLY INCLUDE ONCOGENIC AGENTS, CHEMICAL AGENTS, OR CALCIFICATIONS
5. THE PATIENT IS FOUND TO HAVE LIVER DISEASE, RESULTING IN THE REMOVAL OF A LOBE
OF HIS LIVER. ADAPTATION TO THE REDUCED SIZE OF THE LIVER LEADS TO __________ OF THE
REMAINING LIVER CELLS.
A) METAPLASIA
B) ORGAN ATROPHY
C) COMPENSATORY HYPERPLASIA
D) PHYSIOLOGIC HYPERTROPHY
ANS: C)
EXPLANATION:
COMPENSATORY HYPERPLASIA IS A PROCESS WHERE CELLS INCREASE IN NUMBER TO
COMPENSATE FOR THE LOSS OF TISSUE OR ORGAN FUNCTION. IN THIS CASE, THE REMAINING
LIVER CELLS UNDERGO HYPERPLASIA TO MAKE UP FOR THE LOST LOBE.
6. A PERSON EATING PEANUTS STARTS CHOKING AND COLLAPSES. HIS AIRWAY OBSTRUCTION
IS PARTIALLY CLEARED, BUT HE REMAINS HYPOXIC UNTIL HE REACHES THE HOSPITAL. THE
PROLONGED CELL HYPOXIA CAUSED A CEREBRAL INFARCTION AND RESULTING __________ IN
THE BRAIN.
, A) CASPASE ACTIVATION
B) COAGULATION NECROSIS
C) RAPID PHAGOCYTOSIS
D) PROTEIN P53 DEFICIENCY
ANS: B)
EXPLANATION:
PROLONGED HYPOXIA CAUSES IRREVERSIBLE DAMAGE TO CELLS, LEADING TO COAGULATION
NECROSIS. IN THIS CASE, A LACK OF OXYGEN LEADS TO CELL DEATH IN THE BRAIN,
CHARACTERIZED BY COAGULATIVE NECROSIS WHERE THE TISSUE STRUCTURE REMAINS
RELATIVELY INTACT FOR SOME TIME.
7. A PREGNANT CLIENT IS ATTENDING A NUTRITION CLASS FOR FIRST-TIME MOMS. DURING
THE CLASS, THE INSTRUCTOR STRESSED THAT THEY SHOULD AVOID CONSUMPTION OF
WHICH FOOD THAT MAY CAUSE BRAIN DAMAGE FROM METHYL MERCURY EXPOSURE?
A) RAW HAMBURGER
B) BEETS
C) TUNA
D) FRESH MILK
ANS: C)
EXPLANATION:
THE MAIN SOURCE OF METHYL MERCURY EXPOSURE IS FROM CONSUMPTION OF LONG-LIVED FISH,
SUCH AS TUNA AND SWORDFISH. FISH CONCENTRATE MERCURY FROM SEDIMENT IN THE WATER.
BECAUSE THE DEVELOPING BRAIN IS MORE SUSCEPTIBLE TO MERCURY-INDUCED DAMAGE, IT IS
RECOMMENDED THAT YOUNG CHILDREN AND PREGNANT AND NURSING WOMEN SHOULD AVOID
CONSUMPTION OF FISH KNOWN TO CONTAIN HIGH MERCURY CONTENT. NONE OF THE OTHER
FOODS LISTED POSE A THREAT OF MERCURY TOXICITY
