GNRS 588 EXAM 5 EXAM QUESTIONS
WITH 100% CORRECT ANSWERS |
LATEST VERSION 2025/2026.
Disseminated Intravascular Coagulation (DIC) - ANS A condition involving systemic activation
of blood clotting, leading to clot formation, depletion of clotting factors, and bleeding.
Key signs of DIC - ANS Bleeding, bruising, petechiae, oozing from IV sites, and organ
dysfunction due to microclots.
Heparin-Induced Thrombocytopenia (HIT) - ANS An immune-mediated reaction to heparin
causing a severe drop in platelets and increased clotting risk.
Type 1 and Type 2 HIT - ANS Type 1 is non-immune and mild; Type 2 is immune-mediated,
serious, and can cause thrombosis.
HIT appearance after heparin therapy starts - ANS Usually 5-14 days after initiation; faster if
patient was previously exposed to heparin.
Sickle Cell Anemia - ANS A genetic disorder causing abnormal hemoglobin that leads to
misshapen RBCs and blockages in small vessels.
Complications of sickle cell anemia - ANS Vaso-occlusive crises, stroke, acute chest
syndrome, infection risk, and organ damage.
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, Tumor Lysis Syndrome (TLS) - ANS A life-threatening condition where cancer treatment
causes rapid tumor breakdown, leading to electrolyte imbalances.
Lab findings in TLS - ANS Hyperkalemia, hyperuricemia, hyperphosphatemia, hypocalcemia.
Signs of TLS - ANS Muscle cramps, seizures, tetany (positive Chvostek/Trousseau), ECG
changes, renal failure.
Anemia of Critical Illness - ANS A common, multifactorial anemia in ICU patients due to
inflammation, poor RBC production, and blood loss.
Pathophysiology of HIT - ANS Heparin binds to platelet factor 4 → new antigen forms → IgG
antibody binds → immune complex triggers platelet activation → thrombosis.
Hallmark lab finding of HIT - ANS Sudden drop in platelet count (usually >50% from baseline),
especially during or after heparin use.
First step in treating HIT - ANS Immediately stop all forms of heparin and initiate a non-
heparin anticoagulant (like argatroban).
Cause of hyperuricemia in Tumor Lysis Syndrome - ANS Massive cell lysis releases nucleic
acids, which are metabolized to uric acid.
Why TLS causes hypocalcemia - ANS Released phosphate binds calcium, forming calcium
phosphate crystals and lowering serum calcium levels.
ECG changes seen in TLS - ANS Peaked T waves (hyperkalemia), prolonged QT
(hypocalcemia), widened QRS.
Treatment for TLS - ANS Aggressive hydration, allopurinol or rasburicase, manage
electrolytes, and dialysis if needed.
2 | Page @COPYRIGHT 2025/2026 ALLRIGHTS RESERVED
WITH 100% CORRECT ANSWERS |
LATEST VERSION 2025/2026.
Disseminated Intravascular Coagulation (DIC) - ANS A condition involving systemic activation
of blood clotting, leading to clot formation, depletion of clotting factors, and bleeding.
Key signs of DIC - ANS Bleeding, bruising, petechiae, oozing from IV sites, and organ
dysfunction due to microclots.
Heparin-Induced Thrombocytopenia (HIT) - ANS An immune-mediated reaction to heparin
causing a severe drop in platelets and increased clotting risk.
Type 1 and Type 2 HIT - ANS Type 1 is non-immune and mild; Type 2 is immune-mediated,
serious, and can cause thrombosis.
HIT appearance after heparin therapy starts - ANS Usually 5-14 days after initiation; faster if
patient was previously exposed to heparin.
Sickle Cell Anemia - ANS A genetic disorder causing abnormal hemoglobin that leads to
misshapen RBCs and blockages in small vessels.
Complications of sickle cell anemia - ANS Vaso-occlusive crises, stroke, acute chest
syndrome, infection risk, and organ damage.
1 | Page @COPYRIGHT 2025/2026 ALLRIGHTS RESERVED
, Tumor Lysis Syndrome (TLS) - ANS A life-threatening condition where cancer treatment
causes rapid tumor breakdown, leading to electrolyte imbalances.
Lab findings in TLS - ANS Hyperkalemia, hyperuricemia, hyperphosphatemia, hypocalcemia.
Signs of TLS - ANS Muscle cramps, seizures, tetany (positive Chvostek/Trousseau), ECG
changes, renal failure.
Anemia of Critical Illness - ANS A common, multifactorial anemia in ICU patients due to
inflammation, poor RBC production, and blood loss.
Pathophysiology of HIT - ANS Heparin binds to platelet factor 4 → new antigen forms → IgG
antibody binds → immune complex triggers platelet activation → thrombosis.
Hallmark lab finding of HIT - ANS Sudden drop in platelet count (usually >50% from baseline),
especially during or after heparin use.
First step in treating HIT - ANS Immediately stop all forms of heparin and initiate a non-
heparin anticoagulant (like argatroban).
Cause of hyperuricemia in Tumor Lysis Syndrome - ANS Massive cell lysis releases nucleic
acids, which are metabolized to uric acid.
Why TLS causes hypocalcemia - ANS Released phosphate binds calcium, forming calcium
phosphate crystals and lowering serum calcium levels.
ECG changes seen in TLS - ANS Peaked T waves (hyperkalemia), prolonged QT
(hypocalcemia), widened QRS.
Treatment for TLS - ANS Aggressive hydration, allopurinol or rasburicase, manage
electrolytes, and dialysis if needed.
2 | Page @COPYRIGHT 2025/2026 ALLRIGHTS RESERVED
