ATI RN MEDICAL SURGICAL EXAM 2024 ACTUAL EXAM COMPLETE 270 QUESTIONS WITH
DETAILED VERIFIED ANSWERS (100% CORRECT ANSWERS) /ALREADY GRADED A+
1. Exam Section 1: Item 2 of 50 National, Board of Medical Examiners
Comprehensive Basic Science Self-Assessment
2. Free purine and pyrimidine bases are reutilized in normal metabolism. In
children with Lesch-Nyhan syndrome who have intellectual disability, poor
muscle coordination, and self-mutilation tendencies, there is a defect in
the salvage of which of the following
pairs of bases?
A) Adenine and thymine
B) Guanine and hypoxanthine
C) Guanine and uric acid
D) Uracil and cytosine
E) Xanthine and hypoxanthine: B.
Lesch-Nyhan syndrome presents with intellectual disability, aggressive
behavior, self-mutilation, gout, and dystonia. The disorder is due to
inactivating mutations of hypoxanthine-guanine
phosphoribosyltransferase (HGPRT), a key enzyme in the purine
salvage
pathway, and is inherited in an X-linked recessive fashion. HGPRT
catalyzes the conversion of guanine to guanosine monophosphate and
hypoxanthine to inosine monophosphate. Patients with deficient activity
of HGPRT are unable to salvage guanine and
hypoxanthine and develop resultant increased levels of xanthine and uri
To get this or any other Exam contact ()
, acid. Hyperuricemia in Lesch-Nyhan syndrome is treated with xanthine
oxidase inhibitors, such as allopurinol or febuxostat, in order to reduce
the synthesis of uric acid.
Incorrect Answers: A, C, D and E.
Adenine and thymine (Choice A) are purine and pyrimidine bases,
respectively. Purine and pyrimidine salvage are handled through two
distinct pathways that are not commonly involved in a single disease
process.
Guanine and uric acid (Choice C) accumulation may occur as part of
Lesch-Nyhan syndrome, however, the accumulation of uric acid is also
secondary to accumulation of hypoxanthine. Choice B more accurately
describes defective salvage of guanine and
hypoxanthine as the fundamental effect of HGPRT dysfunction. The
accumulation of uric acid is secondary.
Uracil and cytosine (Choice D) are pyrimidine nucleotides. Pyrimidine
salvage is not affected by mutations of HGPRT.
Defects of xanthine and hypoxanthine (Choice E) metabolism may resu
from
To get this or any other Exam contact ()
, defects in HGPRT. However, HGPRT dysfunction results in impaired
hypoxanthine salvage with resultant excessive production of xanthine,
rather than impaired xan- thine salvage.
Educational Objective: Lesch-Nyhan syndrome presents with
intellectual disability, aggressive behavior, self-mutilation, gout, and
dyst
2. 2
----------
Exam Section 1: Item 3 of 50
National Board of Medical
Examiners
Comprehensive Basic Science Self-Assessment
3. A 42-year-old man is struck by a motor vehicle. His only injury is a closed
fracture of the proximal tibia. Initial neurovascular examination shows no
deficits. Twenty-four hours later, he has increased leg pain and
paresthesias in the dorsal space between his
first and second toes. The patient begins to pass dark red urine and become
oliguric. Urinalysis is positive for blood but no erythrocytes are seen on
microscopic examination. Which of the following acute disorders is the most
likely cause of the renal
failure?
A) Glomerulonephritis
B) Hemolytic-uremic syndrome
C) Interstitial nephritis
To get this or any other Exam contact ()
, D) Nephrotic syndrome
E) Tubular necrosis: E.
Tibial fractures present a high risk for compartment syndrome. The
fracture results in blood vessel injury and muscle injury, inflammation,
and edema. Because the fascia containing the anterior compartment of
the leg does not stretch, bleeding and swelling can
cause increased pressure in the compartment. This increased pressure in
turn inhibits venous drainage, further increasing pressure in the
compartment. Eventually the nerve supply and associated arteries are
compromised, leading to the classic signs and
symptoms of compartment syndrome. Signs and symptoms of
compartment syn- drome include pain out of proportion to examination
findings, pain with passive movement of the muscles, paresthesia, pallor
pulselessness, and paralysis. Com- promised blood supply
deprives muscle and tissue of oxygen and glucose, leading to tissue
ischemia and necrosis. Muscle necrosis leads to rhabdomyolysis,
myoglobinuria, and acute renal failure. Evaluation of rhabdomyolysis
reveals red or brown urine and urinalysis is
To get this or any other Exam contact ()
DETAILED VERIFIED ANSWERS (100% CORRECT ANSWERS) /ALREADY GRADED A+
1. Exam Section 1: Item 2 of 50 National, Board of Medical Examiners
Comprehensive Basic Science Self-Assessment
2. Free purine and pyrimidine bases are reutilized in normal metabolism. In
children with Lesch-Nyhan syndrome who have intellectual disability, poor
muscle coordination, and self-mutilation tendencies, there is a defect in
the salvage of which of the following
pairs of bases?
A) Adenine and thymine
B) Guanine and hypoxanthine
C) Guanine and uric acid
D) Uracil and cytosine
E) Xanthine and hypoxanthine: B.
Lesch-Nyhan syndrome presents with intellectual disability, aggressive
behavior, self-mutilation, gout, and dystonia. The disorder is due to
inactivating mutations of hypoxanthine-guanine
phosphoribosyltransferase (HGPRT), a key enzyme in the purine
salvage
pathway, and is inherited in an X-linked recessive fashion. HGPRT
catalyzes the conversion of guanine to guanosine monophosphate and
hypoxanthine to inosine monophosphate. Patients with deficient activity
of HGPRT are unable to salvage guanine and
hypoxanthine and develop resultant increased levels of xanthine and uri
To get this or any other Exam contact ()
, acid. Hyperuricemia in Lesch-Nyhan syndrome is treated with xanthine
oxidase inhibitors, such as allopurinol or febuxostat, in order to reduce
the synthesis of uric acid.
Incorrect Answers: A, C, D and E.
Adenine and thymine (Choice A) are purine and pyrimidine bases,
respectively. Purine and pyrimidine salvage are handled through two
distinct pathways that are not commonly involved in a single disease
process.
Guanine and uric acid (Choice C) accumulation may occur as part of
Lesch-Nyhan syndrome, however, the accumulation of uric acid is also
secondary to accumulation of hypoxanthine. Choice B more accurately
describes defective salvage of guanine and
hypoxanthine as the fundamental effect of HGPRT dysfunction. The
accumulation of uric acid is secondary.
Uracil and cytosine (Choice D) are pyrimidine nucleotides. Pyrimidine
salvage is not affected by mutations of HGPRT.
Defects of xanthine and hypoxanthine (Choice E) metabolism may resu
from
To get this or any other Exam contact ()
, defects in HGPRT. However, HGPRT dysfunction results in impaired
hypoxanthine salvage with resultant excessive production of xanthine,
rather than impaired xan- thine salvage.
Educational Objective: Lesch-Nyhan syndrome presents with
intellectual disability, aggressive behavior, self-mutilation, gout, and
dyst
2. 2
----------
Exam Section 1: Item 3 of 50
National Board of Medical
Examiners
Comprehensive Basic Science Self-Assessment
3. A 42-year-old man is struck by a motor vehicle. His only injury is a closed
fracture of the proximal tibia. Initial neurovascular examination shows no
deficits. Twenty-four hours later, he has increased leg pain and
paresthesias in the dorsal space between his
first and second toes. The patient begins to pass dark red urine and become
oliguric. Urinalysis is positive for blood but no erythrocytes are seen on
microscopic examination. Which of the following acute disorders is the most
likely cause of the renal
failure?
A) Glomerulonephritis
B) Hemolytic-uremic syndrome
C) Interstitial nephritis
To get this or any other Exam contact ()
, D) Nephrotic syndrome
E) Tubular necrosis: E.
Tibial fractures present a high risk for compartment syndrome. The
fracture results in blood vessel injury and muscle injury, inflammation,
and edema. Because the fascia containing the anterior compartment of
the leg does not stretch, bleeding and swelling can
cause increased pressure in the compartment. This increased pressure in
turn inhibits venous drainage, further increasing pressure in the
compartment. Eventually the nerve supply and associated arteries are
compromised, leading to the classic signs and
symptoms of compartment syndrome. Signs and symptoms of
compartment syn- drome include pain out of proportion to examination
findings, pain with passive movement of the muscles, paresthesia, pallor
pulselessness, and paralysis. Com- promised blood supply
deprives muscle and tissue of oxygen and glucose, leading to tissue
ischemia and necrosis. Muscle necrosis leads to rhabdomyolysis,
myoglobinuria, and acute renal failure. Evaluation of rhabdomyolysis
reveals red or brown urine and urinalysis is
To get this or any other Exam contact ()
