DOD ANNUAL SECURITY AWARENESS
REFRESHER COMPREHENSIVE TEST 2026 FULL
QUESTIONS WITH ANSWERS
▶ Insulin resistance in HTN. Answer: -associated with endothelial injury
and affects renal function, causing renal salt and water retention
-Insulin resistance is associated with overactivity of the SNS and the
RAAS.
-BP will decrease when people are given meds to increase insulin
sensitivity
▶ SNS and HTN. Answer: Overactivity of the SNS leads to increased
production of catecholamines (epi/norepi) or from increased receptor
reactivity.
- Increase SNS = inc HR, systemic vasoconstriction (inc BP), renin release,
inc tubular sodium reabsorption, dec renal blood flow.
-vascular remodeling, insulin resistance, inc renin and angiotensin levels,
procoagulant effect.
- Tx: beta blockers
▶ Sustained HTN effects. Answer: - Inc. workload of myocardium, dec
blood flow through coronaries (LV hypertrophy, heart failure)
- Accelerated atherosclerosis (CAD) (ischemia, infarction, death)
- RAAS/SNS stimulation, inflammation (Glomerulosclerosis, dec GFR,
ESRD)
- dec. brain blood flow/o2, weak vessel walls (TIAs, CVA, thrombosis,
aneurysm, hemorrhage)
- hypertensive retinopathy, retinal exudates, hemorrhage
-dissecting aortic aneurysm
- intermittent claudication, gangrene
▶ 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)
REFRESHER COMPREHENSIVE TEST 2026 FULL
QUESTIONS WITH ANSWERS
▶ Insulin resistance in HTN. Answer: -associated with endothelial injury
and affects renal function, causing renal salt and water retention
-Insulin resistance is associated with overactivity of the SNS and the
RAAS.
-BP will decrease when people are given meds to increase insulin
sensitivity
▶ SNS and HTN. Answer: Overactivity of the SNS leads to increased
production of catecholamines (epi/norepi) or from increased receptor
reactivity.
- Increase SNS = inc HR, systemic vasoconstriction (inc BP), renin release,
inc tubular sodium reabsorption, dec renal blood flow.
-vascular remodeling, insulin resistance, inc renin and angiotensin levels,
procoagulant effect.
- Tx: beta blockers
▶ Sustained HTN effects. Answer: - Inc. workload of myocardium, dec
blood flow through coronaries (LV hypertrophy, heart failure)
- Accelerated atherosclerosis (CAD) (ischemia, infarction, death)
- RAAS/SNS stimulation, inflammation (Glomerulosclerosis, dec GFR,
ESRD)
- dec. brain blood flow/o2, weak vessel walls (TIAs, CVA, thrombosis,
aneurysm, hemorrhage)
- hypertensive retinopathy, retinal exudates, hemorrhage
-dissecting aortic aneurysm
- intermittent claudication, gangrene
▶ 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)
