NR283 PATHOPHYSIOLOGY
Enhanced Master Exam Study Guide • Exams 1–3 + Final Review
Purpose: Original expanded study material based on the publicly visible topic structure of the referenced Stuvia preview. It
does not reproduce the paid document or claim that any item is an actual/leaked exam question.
Coverage: integumentary/immune concepts, hematology, cardiovascular disease, shock, respiratory disease,
congenital/cardiac disorders, and integrated clinical reasoning.
Study method: Learn the mechanism → connect it to manifestations → identify diagnostics/complications → practice active
recall.
NR283 Pathophysiology • Original enhanced study guide Page 1
, 1. INTEGUMENTARY PATHOPHYSIOLOGY
Skin anatomy: the exam map
The epidermis is the outer epithelial barrier and is avascular; it receives nutrients by diffusion from underlying tissues. The
dermis contains blood vessels, nerves, glands, hair follicles, and connective tissue. The subcutaneous layer provides
insulation, energy storage, cushioning, and anchoring. A useful exam shortcut is: epidermis = barrier; dermis =
support/sensation; subcutaneous = insulation/storage.
Primary lesion vocabulary
A macule is a flat color change. A papule is a small solid raised lesion. A vesicle is a small, fluid-filled blister. A pustule
contains purulent material. A plaque is a broader elevated lesion, often formed by coalescing papules. Recognizing
morphology is often more useful than memorizing disease names in isolation.
Psoriasis
Psoriasis involves accelerated epidermal cell proliferation and abnormal shedding. Classic plaques are erythematous with
silvery scale. The key mechanism is immune-mediated inflammation with rapid keratinocyte turnover. Exam trap: do not
confuse psoriasis with a simple superficial infection; the visible scale reflects abnormal epidermal turnover.
Hypersensitivity and urticaria
Type I hypersensitivity is IgE-mediated and can produce mast-cell mediator release, vasodilation, increased vascular
permeability, pruritus, and bronchoconstriction. In the skin, urticaria (hives) is a classic manifestation. Severe systemic
reactions can progress to anaphylaxis and shock.
Bacterial, viral, fungal, and parasitic skin disease
Impetigo is highly contagious and classically produces crusted superficial lesions. Furuncles are deeper infections centered on
hair follicles and are commonly associated with Staphylococcus aureus. Tinea is fungal. Tinea capitis involves the scalp; tinea
corporis commonly produces an annular/ring-like lesion. Scabies is caused by mites burrowing into the epidermis, producing
intense pruritus. Pediculosis is suggested by lice or nits attached near hair shafts.
Herpes simplex
A recurrent HSV outbreak may be preceded by localized tingling or burning. Antiviral therapy suppresses replication and can
shorten the acute course and shedding; it does not eradicate latent virus. Memory cue: tingle → vesicles → crust →
latency.
Necrotizing fasciitis
This is a rapidly progressive, life-threatening soft-tissue infection with tissue necrosis and systemic toxicity. Pain may be severe
and out of proportion to visible skin findings. Rapid recognition and urgent treatment are critical. A major exam principle is that
delayed diagnosis increases morbidity and mortality.
Skin cancer and UV injury
Ultraviolet exposure is a major risk factor for actinic keratoses and nonmelanoma skin cancers. Melanoma arises from
melanocytes and is concerning when a lesion is asymmetric, has irregular borders, varied color, or changes over time. Think
ABCDE: asymmetry, border, color, diameter, evolving.
Scleroderma and connective-tissue disease
Scleroderma involves abnormal connective-tissue deposition and fibrosis and may affect skin and internal organs. The
exam-level distinction is that the pathology is dominated by excessive collagen/fibrosis rather than a simple infectious process.
NR283 Pathophysiology • Original enhanced study guide Page 2
, 2. HEMATOLOGY & IMMUNOHEMATOLOGY
Blood-cell logic
RBCs transport oxygen; WBCs participate in immune defense; platelets support primary hemostasis. Bone marrow is the major
site of blood-cell production. Erythropoietin stimulates erythrocyte production in response to reduced oxygen delivery. When a
question asks what happens after RBC loss, expect reduced hematocrit and impaired oxygen-carrying capacity.
Anemia: recognize the pattern
Anemia is a reduction in RBC mass or hemoglobin sufficient to impair oxygen delivery. Common manifestations include
fatigue, pallor, dyspnea, tachycardia, and reduced exercise tolerance. Severe or acute anemia can cause chest pain,
confusion, or ischemic symptoms because tissues are receiving inadequate oxygen.
Iron-deficiency anemia
Iron deficiency impairs hemoglobin synthesis and typically produces microcytic, hypochromic RBCs. Causes include chronic
blood loss, inadequate intake, or impaired absorption. In an exam stem, chronic menstrual or gastrointestinal blood loss is a
major clue. Memory: iron = small + pale cells.
Vitamin B12 deficiency / pernicious anemia
Vitamin B12 deficiency impairs DNA synthesis and produces megaloblastic, macrocytic anemia. Pernicious anemia results
from impaired absorption related to loss of intrinsic-factor function. Neurologic findings such as paresthesias are an important
discriminator from folate deficiency. Treatment may require parenteral B12 when absorption is severely impaired.
Aplastic anemia
Aplastic anemia reflects bone-marrow failure with reduced production of multiple cell lines. Therefore, pancytopenia can
occur: anemia, leukopenia/neutropenia, and thrombocytopenia. The clinical triad is fatigue from anemia, infection from low
WBCs, and bleeding from low platelets.
Hemolytic anemia and sickle cell disease
Hemolysis shortens RBC survival and can produce bilirubin elevation and jaundice. Sickle cell disease results from an inherited
hemoglobin abnormality; deoxygenation promotes HbS polymerization and RBC sickling. Sickled cells can obstruct
microcirculation, producing ischemia, pain crises, and organ injury. Core chain: deoxygenation → sickling → vaso-occlusion
→ ischemia/pain.
Thalassemia
Thalassemias result from reduced synthesis of alpha or beta globin chains. They are inherited disorders of hemoglobin
production rather than iron deficiency. This distinction matters because both can be microcytic, but the underlying mechanism
differs.
Polycythemia
Polycythemia increases RBC mass. In primary polycythemia, marrow overproduction occurs; secondary polycythemia can
arise from chronic hypoxia, such as chronic lung disease. Increased blood viscosity can raise vascular resistance and
thrombosis risk.
Hemostasis and coagulation
Platelets form the initial plug, while coagulation factors stabilize it with fibrin. Vitamin K is needed for hepatic synthesis of
several clotting factors. Heparin is an anticoagulant. Hemophilia A involves factor VIII deficiency/dysfunction and typically
causes deep bleeding such as hemarthroses; von Willebrand disease impairs platelet adhesion and can cause mucosal
bleeding.
NR283 Pathophysiology • Original enhanced study guide Page 3
Enhanced Master Exam Study Guide • Exams 1–3 + Final Review
Purpose: Original expanded study material based on the publicly visible topic structure of the referenced Stuvia preview. It
does not reproduce the paid document or claim that any item is an actual/leaked exam question.
Coverage: integumentary/immune concepts, hematology, cardiovascular disease, shock, respiratory disease,
congenital/cardiac disorders, and integrated clinical reasoning.
Study method: Learn the mechanism → connect it to manifestations → identify diagnostics/complications → practice active
recall.
NR283 Pathophysiology • Original enhanced study guide Page 1
, 1. INTEGUMENTARY PATHOPHYSIOLOGY
Skin anatomy: the exam map
The epidermis is the outer epithelial barrier and is avascular; it receives nutrients by diffusion from underlying tissues. The
dermis contains blood vessels, nerves, glands, hair follicles, and connective tissue. The subcutaneous layer provides
insulation, energy storage, cushioning, and anchoring. A useful exam shortcut is: epidermis = barrier; dermis =
support/sensation; subcutaneous = insulation/storage.
Primary lesion vocabulary
A macule is a flat color change. A papule is a small solid raised lesion. A vesicle is a small, fluid-filled blister. A pustule
contains purulent material. A plaque is a broader elevated lesion, often formed by coalescing papules. Recognizing
morphology is often more useful than memorizing disease names in isolation.
Psoriasis
Psoriasis involves accelerated epidermal cell proliferation and abnormal shedding. Classic plaques are erythematous with
silvery scale. The key mechanism is immune-mediated inflammation with rapid keratinocyte turnover. Exam trap: do not
confuse psoriasis with a simple superficial infection; the visible scale reflects abnormal epidermal turnover.
Hypersensitivity and urticaria
Type I hypersensitivity is IgE-mediated and can produce mast-cell mediator release, vasodilation, increased vascular
permeability, pruritus, and bronchoconstriction. In the skin, urticaria (hives) is a classic manifestation. Severe systemic
reactions can progress to anaphylaxis and shock.
Bacterial, viral, fungal, and parasitic skin disease
Impetigo is highly contagious and classically produces crusted superficial lesions. Furuncles are deeper infections centered on
hair follicles and are commonly associated with Staphylococcus aureus. Tinea is fungal. Tinea capitis involves the scalp; tinea
corporis commonly produces an annular/ring-like lesion. Scabies is caused by mites burrowing into the epidermis, producing
intense pruritus. Pediculosis is suggested by lice or nits attached near hair shafts.
Herpes simplex
A recurrent HSV outbreak may be preceded by localized tingling or burning. Antiviral therapy suppresses replication and can
shorten the acute course and shedding; it does not eradicate latent virus. Memory cue: tingle → vesicles → crust →
latency.
Necrotizing fasciitis
This is a rapidly progressive, life-threatening soft-tissue infection with tissue necrosis and systemic toxicity. Pain may be severe
and out of proportion to visible skin findings. Rapid recognition and urgent treatment are critical. A major exam principle is that
delayed diagnosis increases morbidity and mortality.
Skin cancer and UV injury
Ultraviolet exposure is a major risk factor for actinic keratoses and nonmelanoma skin cancers. Melanoma arises from
melanocytes and is concerning when a lesion is asymmetric, has irregular borders, varied color, or changes over time. Think
ABCDE: asymmetry, border, color, diameter, evolving.
Scleroderma and connective-tissue disease
Scleroderma involves abnormal connective-tissue deposition and fibrosis and may affect skin and internal organs. The
exam-level distinction is that the pathology is dominated by excessive collagen/fibrosis rather than a simple infectious process.
NR283 Pathophysiology • Original enhanced study guide Page 2
, 2. HEMATOLOGY & IMMUNOHEMATOLOGY
Blood-cell logic
RBCs transport oxygen; WBCs participate in immune defense; platelets support primary hemostasis. Bone marrow is the major
site of blood-cell production. Erythropoietin stimulates erythrocyte production in response to reduced oxygen delivery. When a
question asks what happens after RBC loss, expect reduced hematocrit and impaired oxygen-carrying capacity.
Anemia: recognize the pattern
Anemia is a reduction in RBC mass or hemoglobin sufficient to impair oxygen delivery. Common manifestations include
fatigue, pallor, dyspnea, tachycardia, and reduced exercise tolerance. Severe or acute anemia can cause chest pain,
confusion, or ischemic symptoms because tissues are receiving inadequate oxygen.
Iron-deficiency anemia
Iron deficiency impairs hemoglobin synthesis and typically produces microcytic, hypochromic RBCs. Causes include chronic
blood loss, inadequate intake, or impaired absorption. In an exam stem, chronic menstrual or gastrointestinal blood loss is a
major clue. Memory: iron = small + pale cells.
Vitamin B12 deficiency / pernicious anemia
Vitamin B12 deficiency impairs DNA synthesis and produces megaloblastic, macrocytic anemia. Pernicious anemia results
from impaired absorption related to loss of intrinsic-factor function. Neurologic findings such as paresthesias are an important
discriminator from folate deficiency. Treatment may require parenteral B12 when absorption is severely impaired.
Aplastic anemia
Aplastic anemia reflects bone-marrow failure with reduced production of multiple cell lines. Therefore, pancytopenia can
occur: anemia, leukopenia/neutropenia, and thrombocytopenia. The clinical triad is fatigue from anemia, infection from low
WBCs, and bleeding from low platelets.
Hemolytic anemia and sickle cell disease
Hemolysis shortens RBC survival and can produce bilirubin elevation and jaundice. Sickle cell disease results from an inherited
hemoglobin abnormality; deoxygenation promotes HbS polymerization and RBC sickling. Sickled cells can obstruct
microcirculation, producing ischemia, pain crises, and organ injury. Core chain: deoxygenation → sickling → vaso-occlusion
→ ischemia/pain.
Thalassemia
Thalassemias result from reduced synthesis of alpha or beta globin chains. They are inherited disorders of hemoglobin
production rather than iron deficiency. This distinction matters because both can be microcytic, but the underlying mechanism
differs.
Polycythemia
Polycythemia increases RBC mass. In primary polycythemia, marrow overproduction occurs; secondary polycythemia can
arise from chronic hypoxia, such as chronic lung disease. Increased blood viscosity can raise vascular resistance and
thrombosis risk.
Hemostasis and coagulation
Platelets form the initial plug, while coagulation factors stabilize it with fibrin. Vitamin K is needed for hepatic synthesis of
several clotting factors. Heparin is an anticoagulant. Hemophilia A involves factor VIII deficiency/dysfunction and typically
causes deep bleeding such as hemarthroses; von Willebrand disease impairs platelet adhesion and can cause mucosal
bleeding.
NR283 Pathophysiology • Original enhanced study guide Page 3
