DOD ANNUAL SECURITY AWARENESS
REFRESHER ACTUAL TEST 2026 FULL SOLUTION
VIEW AND ANSWERS
▶ Unstable coronary artery plaque. Answer: -Lipid rich core and thin
fibrous cap
- breaks off by shear force, inflammation, apoptosis, macrophage-derived
degradative enzymes
- causes inflammation, release of multiple cytokines, platelet activation and
adherence, production of thrombin and vasoconstriction, thrombus
formation over lesion
▶ Atherosclerosis. Answer: cause: smoking, HTN, DM, aging
-injury to endothelial cells that line artery wall (inflammation and cannot
make normal amt of antithrombotic and vasodilating cytokines)
-LDL penetrates into subintima of arterial wall, and is trapped by
proteoglycans.
-inflammation, oxidized LDL cause endothelial cells to express adhesion
molecules that bind monocytes and immune cells.
-monocytes penetrate vessel vall and become macrophages.
-fatty streak- NTF, interferons, interleukins and CRP injure vessel wall.
-release of growth factors, collagen, migrate over fatty streak and form
fibrous plaque.
-plaque may calcify and cover vessel lumen
▶ Symptoms of inc LAP and Pulm Ven Press in heart failure. Answer: -
Pulmonary edema made worse with tachycardia (exercise)
-dyspnea and fatigue
▶ R Heart Failure. Answer: -caused by severe L heart failure, RV MI,
cardiomyopathies, and pulmonic valvular disease, PH, COPD, Cystic
fibrosis
-Sx: RV hypertrophy, JVD, peripheral edema, progressive diastolic and
systolic deterioration, hepatosplenomegaly
,▶ L vs R heart failure. Answer: L: Blood backs up into pulmonary
(inadequate systemic circulation)
Sx:pulmonary edema, waking in the middle of the night, SOB, fatigue
R: Blood backs up in the body (inadequate pulmonary circulation)
Sx:Peripheral edema, HTN, JVD, Dep. edema, hepatosplenomegaly
▶ infective endocarditis. Answer: -Infection and inflammation of the
endocardium (esp valves).
- Most common cause: Staphylococcus aureus.
- Risk fx: prosthetic valve, congenital lesions associated with highly
turbulent flow, IV drug use, long-term IV catheter, Pacemaker, heart
transplant with defective valve, dental procedures with manipulation of
gingiva,
- Endocardial damage, Bacterial adherence, and formation of vegetations
- Sx: fever, cardiac murmur, petechial lesions of the skin conjunctiva and
oral mucosa, night sweats, weight loss, back pain, heart failure, Osler
nodes (erythematous nodules on the pads of fingers or toes)
▶ Patho of DVT. Answer: Accumulation of clotting factors leads to
thrombus formation (often near a valve). Inflammation leads to further
platelet aggregation. Thrombus grows proximally
▶ Virchow's Triad. Answer: 1) Venous stasis (associated with immobility,
obesity, age, CHF)
2) Venous intimal damage (related to trauma, venipuncture, IV meds)
3) Hypercoagulable state ( from inherited disorders, smoking, liver disease,
pregnancy, oral contraceptives, hormone replacement, malignancy)
▶ Physiologic response to anemia. Answer: - Compensation for reduced
blood volume causes interstitial fluid to move intravascularly (inc. plasma
volume, dec. viscosity) causing hyperdynamic circulatory state (inc
SV/HR/cardiac dilation and heart valve insufficiency).
-Inc rate and depth of breathing, dizziness, fatigue, heart failure,
▶ Folate Deficiency Anemia. Answer: People at risk: Pregnant/ lactating,
alcoholics, chronic malnourishment,
▶ Labs for Iron def. anemia. Answer: - Low- HGB/Hct/ mcv/plasma
iron/ferritin, transferrin
, - High- Total iron binding capacity/free erythrocyte protoporphyrin
-Normal- reticulocyte count/B12, Folate, Bili
▶ sickle cell anemia. Answer: a genetic disorder that causes abnormal
hemoglobin, resulting in some red blood cells assuming an abnormal sickle
shape
-Chronic hemolysis, microvascular occlusions, and tissue damage, vaso
occlusive crisis
-abnormal or absent splenic function
▶ Cause of aplastic anemia. Answer: Failure of bone marrow to produce
mature cells causing pancytopenia (reduction of all 3 blood cell types)
- Idiopathic, acquired stem cell defects, immune mediated
- whole-body irradiation, viral infections, hepatitis, CMV, epstein-barr virus,
herpes zoster, inherited
-Chemica: alkylating agents, antimetabolites, benzene, chloramphenicol,
arsenicals, carbamazepine, gold salts
▶ Autoimmune Hemolytic Anemia. Answer: 1) Warm reactive antibody
type- IgG binds optimally to erythrocytes at a normal body temperature.
2) Cold agglutinin type- IgM antibodies optimally bind to erythrocytes at
colder temps (lower than 31 deg. Celsius). Recognized by phagocytes in
the liver and spleen. Fingers, toes, ears, may have obstructed blood flow
3) Cold hemolysin type- Hemoglobinuria
Acquired disorders caused by autoantibodies or complement or both, on
RBCs against antigens normally on the surface of erythrocytes.
▶ Secondary Polycythemia. Answer: -physiologic response from increased
erythropoietin secretion in response to chronic hypoxia.
-Noted in people living in high altitudes, smokers, COPD, CHF
-Abnormal hgb
▶ Anemia of chronic renal failure. Answer: - Kidney damage affects
secretion of erythropoietin, diminishes bone marrow erythropoiesis.
- Uremic toxins that increase in the blood d/t renal failure may suppress
bone marrow function and damage erythrocytes
- Platelet dysfunction (bleeding)
- loss of erythrocytes
REFRESHER ACTUAL TEST 2026 FULL SOLUTION
VIEW AND ANSWERS
▶ Unstable coronary artery plaque. Answer: -Lipid rich core and thin
fibrous cap
- breaks off by shear force, inflammation, apoptosis, macrophage-derived
degradative enzymes
- causes inflammation, release of multiple cytokines, platelet activation and
adherence, production of thrombin and vasoconstriction, thrombus
formation over lesion
▶ Atherosclerosis. Answer: cause: smoking, HTN, DM, aging
-injury to endothelial cells that line artery wall (inflammation and cannot
make normal amt of antithrombotic and vasodilating cytokines)
-LDL penetrates into subintima of arterial wall, and is trapped by
proteoglycans.
-inflammation, oxidized LDL cause endothelial cells to express adhesion
molecules that bind monocytes and immune cells.
-monocytes penetrate vessel vall and become macrophages.
-fatty streak- NTF, interferons, interleukins and CRP injure vessel wall.
-release of growth factors, collagen, migrate over fatty streak and form
fibrous plaque.
-plaque may calcify and cover vessel lumen
▶ Symptoms of inc LAP and Pulm Ven Press in heart failure. Answer: -
Pulmonary edema made worse with tachycardia (exercise)
-dyspnea and fatigue
▶ R Heart Failure. Answer: -caused by severe L heart failure, RV MI,
cardiomyopathies, and pulmonic valvular disease, PH, COPD, Cystic
fibrosis
-Sx: RV hypertrophy, JVD, peripheral edema, progressive diastolic and
systolic deterioration, hepatosplenomegaly
,▶ L vs R heart failure. Answer: L: Blood backs up into pulmonary
(inadequate systemic circulation)
Sx:pulmonary edema, waking in the middle of the night, SOB, fatigue
R: Blood backs up in the body (inadequate pulmonary circulation)
Sx:Peripheral edema, HTN, JVD, Dep. edema, hepatosplenomegaly
▶ infective endocarditis. Answer: -Infection and inflammation of the
endocardium (esp valves).
- Most common cause: Staphylococcus aureus.
- Risk fx: prosthetic valve, congenital lesions associated with highly
turbulent flow, IV drug use, long-term IV catheter, Pacemaker, heart
transplant with defective valve, dental procedures with manipulation of
gingiva,
- Endocardial damage, Bacterial adherence, and formation of vegetations
- Sx: fever, cardiac murmur, petechial lesions of the skin conjunctiva and
oral mucosa, night sweats, weight loss, back pain, heart failure, Osler
nodes (erythematous nodules on the pads of fingers or toes)
▶ Patho of DVT. Answer: Accumulation of clotting factors leads to
thrombus formation (often near a valve). Inflammation leads to further
platelet aggregation. Thrombus grows proximally
▶ Virchow's Triad. Answer: 1) Venous stasis (associated with immobility,
obesity, age, CHF)
2) Venous intimal damage (related to trauma, venipuncture, IV meds)
3) Hypercoagulable state ( from inherited disorders, smoking, liver disease,
pregnancy, oral contraceptives, hormone replacement, malignancy)
▶ Physiologic response to anemia. Answer: - Compensation for reduced
blood volume causes interstitial fluid to move intravascularly (inc. plasma
volume, dec. viscosity) causing hyperdynamic circulatory state (inc
SV/HR/cardiac dilation and heart valve insufficiency).
-Inc rate and depth of breathing, dizziness, fatigue, heart failure,
▶ Folate Deficiency Anemia. Answer: People at risk: Pregnant/ lactating,
alcoholics, chronic malnourishment,
▶ Labs for Iron def. anemia. Answer: - Low- HGB/Hct/ mcv/plasma
iron/ferritin, transferrin
, - High- Total iron binding capacity/free erythrocyte protoporphyrin
-Normal- reticulocyte count/B12, Folate, Bili
▶ sickle cell anemia. Answer: a genetic disorder that causes abnormal
hemoglobin, resulting in some red blood cells assuming an abnormal sickle
shape
-Chronic hemolysis, microvascular occlusions, and tissue damage, vaso
occlusive crisis
-abnormal or absent splenic function
▶ Cause of aplastic anemia. Answer: Failure of bone marrow to produce
mature cells causing pancytopenia (reduction of all 3 blood cell types)
- Idiopathic, acquired stem cell defects, immune mediated
- whole-body irradiation, viral infections, hepatitis, CMV, epstein-barr virus,
herpes zoster, inherited
-Chemica: alkylating agents, antimetabolites, benzene, chloramphenicol,
arsenicals, carbamazepine, gold salts
▶ Autoimmune Hemolytic Anemia. Answer: 1) Warm reactive antibody
type- IgG binds optimally to erythrocytes at a normal body temperature.
2) Cold agglutinin type- IgM antibodies optimally bind to erythrocytes at
colder temps (lower than 31 deg. Celsius). Recognized by phagocytes in
the liver and spleen. Fingers, toes, ears, may have obstructed blood flow
3) Cold hemolysin type- Hemoglobinuria
Acquired disorders caused by autoantibodies or complement or both, on
RBCs against antigens normally on the surface of erythrocytes.
▶ Secondary Polycythemia. Answer: -physiologic response from increased
erythropoietin secretion in response to chronic hypoxia.
-Noted in people living in high altitudes, smokers, COPD, CHF
-Abnormal hgb
▶ Anemia of chronic renal failure. Answer: - Kidney damage affects
secretion of erythropoietin, diminishes bone marrow erythropoiesis.
- Uremic toxins that increase in the blood d/t renal failure may suppress
bone marrow function and damage erythrocytes
- Platelet dysfunction (bleeding)
- loss of erythrocytes
