Chapter 15: Infection (pp. 249-262)
1. COVID-19 (SARS-CoV-2)
● Pathophysiology: An RNA virus with a protein envelope featuring "spikes" that bind to
ACE2 receptors in the host (primarily in the upper respiratory tract). It triggers a
significant inflammatory cascade that can lead to acute respiratory distress syndrome
(ARDS) and multiorgan dysfunction (MODS).
● Clinical Manifestations: Ranges from asymptomatic to critical illness.
○ Common: Fever, cough, loss of taste/smell, dyspnea, fatigue.
○ Severe: Hypoxia, lung infiltrates, ARDS, septic shock.
○ Postacute COVID-19 Syndrome ("Long haulers"): Symptoms persisting >4 weeks
(fatigue, brain fog, dyspnea).
● Diagnostics: RT-PCR (NAAT) is the gold standard. Labs often show lymphopenia,
elevated liver enzymes, and high inflammatory markers (CRP, ferritin, D-dimer).
● Management: * Therapies: Monoclonal antibodies (for mild-to-moderate high-risk
patients), antivirals (remdesivir, Paxlovid), and corticosteroids (dexamethasone for
patients needing O2).
○ Prevention: mRNA vaccines (instruct cells to make spike proteins to build
antibodies) and viral vector vaccines.
2. Human Immunodeficiency Virus (HIV) Infection
● Transmission: Contact with infected blood, semen, vaginal secretions, or breast milk.
Note: U=U (Undetectable = Untransmittable) means a person with an undetectable viral
load cannot transmit the virus sexually.
● Pathophysiology: A retrovirus that binds to and destroys CD4+ T cells.
○ It uses reverse transcriptase (RNA to DNA), integrase (integrates into host DNA),
and protease (cleaves new virions).
○ Normal CD4 count is 800-1200 cells/μL. Immune problems start at <500; severe
problems at <200.
● Clinical Progression:
○ Acute Infection (2-4 weeks): Mononucleosis-like symptoms (fever, swollen
lymph nodes, sore throat). High viral load; highly infectious.
○ Chronic Asymptomatic: Lasts ~10 years untreated. Vague or no symptoms.
○ Chronic Symptomatic: CD4 drops closer to 200. Persistent fevers, night
sweats, oral thrush (Candidiasis), shingles, oral hairy leukoplakia.
○ AIDS: Diagnosed when CD4 < 200 cells/μL, OR an opportunistic infection
develops (e.g., Pneumocystis jiroveci pneumonia [PCP], Toxoplasmosis, CMV),
OR an opportunistic cancer develops (e.g., Kaposi Sarcoma), OR wasting
syndrome occurs.
● Diagnostic Studies: HIV antibody/antigen testing (beware of the 3-week "window
period" where false negatives occur). Progression is monitored via CD4 cell count
(immune function) and Viral Load (disease activity).
● Interprofessional Care & ART:
○ Antiretroviral Therapy (ART): Uses a combination of 3+ drugs from different
classes to prevent resistance. Strict adherence is vital to prevent viral mutation.
, ○ Prevention: PrEP (Preexposure prophylaxis like Truvada/Descovy for high-risk
individuals) and nPEP (post-exposure prophylaxis within 72 hours of exposure).
Chapter 34: Hematologic Problems
1. Anemia (pp. 716-723)
● Definition: A deficiency in the number of erythrocytes (RBCs), the quantity/quality of
hemoglobin, and/or volume of packed RBCs (hematocrit). It is a clinical sign, not a
specific disease.
● Clinical Manifestations: Tissue hypoxia leads to fatigue, pallor (decreased blood flow
to skin), jaundice (increased hemolysis of RBCs), pruritus, tachycardia, and dyspnea.
● Types of Decreased Erythrocyte Production:
○ Iron-Deficiency Anemia: Most common. Microcytic, hypochromic RBCs.
Manifestations include glossitis (inflamed tongue) and cheilitis (inflamed lips).
Treated with iron replacement (best absorbed in an acidic environment; take with
orange juice, causes black/green stools).
○ Megaloblastic Anemias: Large, fragile RBCs.
■ Cobalamin (B12) Deficiency: Often caused by pernicious anemia (lack of
intrinsic factor). Characterized by neurologic symptoms (paresthesias,
confusion) alongside anemia.
■ Folic Acid Deficiency: Similar to B12 deficiency but lacks neurologic
involvement.
○ Aplastic Anemia: Pancytopenia (decrease in all blood cell types—RBCs, WBCs,
platelets) due to bone marrow failure. High risk for infection and bleeding.
2. Sickle Cell Disease (SCD) (pp. 729-730)
● Pathophysiology: Autosomal recessive genetic disorder characterized by the presence
of an abnormal form of hemoglobin (Hgb S). Erythrocytes stiffen and elongate into a
sickle shape in response to low oxygen levels.
● Sickling Episodes & Crisis: Triggered by hypoxia, infection, stress, or dehydration.
Sickled cells occlude capillaries, causing severe local tissue hypoxia, ischemia, and
excruciating pain (Sickle Cell Crisis).
● Nursing Management: * O2 therapy for hypoxia and to control sickling.
○ Aggressive hydration (IV fluids) to reduce blood viscosity.
○ Pain management: Often requires continuous opioid analgesia (e.g., morphine,
hydromorphone).
○ Hydroxyurea is the only disease-modifying drug (increases fetal hemoglobin).
3. Thrombocytopenia (pp. 731-741)
● Definition: Platelet count below 150,000/μL, resulting in abnormal hemostasis and
prolonged bleeding.
● Major Types:
1. COVID-19 (SARS-CoV-2)
● Pathophysiology: An RNA virus with a protein envelope featuring "spikes" that bind to
ACE2 receptors in the host (primarily in the upper respiratory tract). It triggers a
significant inflammatory cascade that can lead to acute respiratory distress syndrome
(ARDS) and multiorgan dysfunction (MODS).
● Clinical Manifestations: Ranges from asymptomatic to critical illness.
○ Common: Fever, cough, loss of taste/smell, dyspnea, fatigue.
○ Severe: Hypoxia, lung infiltrates, ARDS, septic shock.
○ Postacute COVID-19 Syndrome ("Long haulers"): Symptoms persisting >4 weeks
(fatigue, brain fog, dyspnea).
● Diagnostics: RT-PCR (NAAT) is the gold standard. Labs often show lymphopenia,
elevated liver enzymes, and high inflammatory markers (CRP, ferritin, D-dimer).
● Management: * Therapies: Monoclonal antibodies (for mild-to-moderate high-risk
patients), antivirals (remdesivir, Paxlovid), and corticosteroids (dexamethasone for
patients needing O2).
○ Prevention: mRNA vaccines (instruct cells to make spike proteins to build
antibodies) and viral vector vaccines.
2. Human Immunodeficiency Virus (HIV) Infection
● Transmission: Contact with infected blood, semen, vaginal secretions, or breast milk.
Note: U=U (Undetectable = Untransmittable) means a person with an undetectable viral
load cannot transmit the virus sexually.
● Pathophysiology: A retrovirus that binds to and destroys CD4+ T cells.
○ It uses reverse transcriptase (RNA to DNA), integrase (integrates into host DNA),
and protease (cleaves new virions).
○ Normal CD4 count is 800-1200 cells/μL. Immune problems start at <500; severe
problems at <200.
● Clinical Progression:
○ Acute Infection (2-4 weeks): Mononucleosis-like symptoms (fever, swollen
lymph nodes, sore throat). High viral load; highly infectious.
○ Chronic Asymptomatic: Lasts ~10 years untreated. Vague or no symptoms.
○ Chronic Symptomatic: CD4 drops closer to 200. Persistent fevers, night
sweats, oral thrush (Candidiasis), shingles, oral hairy leukoplakia.
○ AIDS: Diagnosed when CD4 < 200 cells/μL, OR an opportunistic infection
develops (e.g., Pneumocystis jiroveci pneumonia [PCP], Toxoplasmosis, CMV),
OR an opportunistic cancer develops (e.g., Kaposi Sarcoma), OR wasting
syndrome occurs.
● Diagnostic Studies: HIV antibody/antigen testing (beware of the 3-week "window
period" where false negatives occur). Progression is monitored via CD4 cell count
(immune function) and Viral Load (disease activity).
● Interprofessional Care & ART:
○ Antiretroviral Therapy (ART): Uses a combination of 3+ drugs from different
classes to prevent resistance. Strict adherence is vital to prevent viral mutation.
, ○ Prevention: PrEP (Preexposure prophylaxis like Truvada/Descovy for high-risk
individuals) and nPEP (post-exposure prophylaxis within 72 hours of exposure).
Chapter 34: Hematologic Problems
1. Anemia (pp. 716-723)
● Definition: A deficiency in the number of erythrocytes (RBCs), the quantity/quality of
hemoglobin, and/or volume of packed RBCs (hematocrit). It is a clinical sign, not a
specific disease.
● Clinical Manifestations: Tissue hypoxia leads to fatigue, pallor (decreased blood flow
to skin), jaundice (increased hemolysis of RBCs), pruritus, tachycardia, and dyspnea.
● Types of Decreased Erythrocyte Production:
○ Iron-Deficiency Anemia: Most common. Microcytic, hypochromic RBCs.
Manifestations include glossitis (inflamed tongue) and cheilitis (inflamed lips).
Treated with iron replacement (best absorbed in an acidic environment; take with
orange juice, causes black/green stools).
○ Megaloblastic Anemias: Large, fragile RBCs.
■ Cobalamin (B12) Deficiency: Often caused by pernicious anemia (lack of
intrinsic factor). Characterized by neurologic symptoms (paresthesias,
confusion) alongside anemia.
■ Folic Acid Deficiency: Similar to B12 deficiency but lacks neurologic
involvement.
○ Aplastic Anemia: Pancytopenia (decrease in all blood cell types—RBCs, WBCs,
platelets) due to bone marrow failure. High risk for infection and bleeding.
2. Sickle Cell Disease (SCD) (pp. 729-730)
● Pathophysiology: Autosomal recessive genetic disorder characterized by the presence
of an abnormal form of hemoglobin (Hgb S). Erythrocytes stiffen and elongate into a
sickle shape in response to low oxygen levels.
● Sickling Episodes & Crisis: Triggered by hypoxia, infection, stress, or dehydration.
Sickled cells occlude capillaries, causing severe local tissue hypoxia, ischemia, and
excruciating pain (Sickle Cell Crisis).
● Nursing Management: * O2 therapy for hypoxia and to control sickling.
○ Aggressive hydration (IV fluids) to reduce blood viscosity.
○ Pain management: Often requires continuous opioid analgesia (e.g., morphine,
hydromorphone).
○ Hydroxyurea is the only disease-modifying drug (increases fetal hemoglobin).
3. Thrombocytopenia (pp. 731-741)
● Definition: Platelet count below 150,000/μL, resulting in abnormal hemostasis and
prolonged bleeding.
● Major Types:
