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NR507 Week 1 Advanced Pathophysiology 2026/2027 | Study Guide, Practice Questions & Exam Review

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Review foundational NR507 Week 1 Advanced Pathophysiology concepts with a focused study resource designed to support early-course learning, exam preparation, and understanding of core disease mechanisms.

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NR507 WEEK 1
NR507 WEEK 1
Study online at https://quizlet.com/_ei3l95

1. Neutrophils first responders

2. Type 1 hypersensi- -IgE mediated
tivity REACTION
-Ex: Asthma, allergic rhinitis, atopic dermatitis, anaphylactic shock, urticaria,
angioedema

LOCAL OR SYSTEMIC

3. Type 2 (Cytotoxic) IgG or IgM.
hypersensitivity re-
actions are mediat-
ed by

4. Sensitization Developing a sensitivity to a substance that initially caused no allergic reac-
tion.
After the allergen is cleared, the remaining IgE molecules will be bound
by mast cells, basophils, and eosinophils that contain receptors for the IgE
molecules.

5. Immediate degran- causes the release of inflammatory mediators such as histamine,
ulation leukotrienes, and prostaglandins that results in vasodilation, bronchial
smooth muscle contraction, and mucus production

6. Systemic reactions involve basophil degranulation; they occur throughout the body, can lead to
anaphylactic shock, and can be life-threatening EX. ALLERGIC ASTHMA

7. Type II hypersensi- -Cytotoxic
tivity reaction -Antibody attacks the antigen leading to lysis (complement mediated)
-IgG & IgM are the principal antibodies involved
-Examples: hemolytic anemia, thrombocytopenia

8. Hapten


1

, NR507 WEEK 1
NR507 WEEK 1
Study online at https://quizlet.com/_ei3l95

small molecule that has to bind to a larger molecule to form an antigen

CAN CAUSE AN IMMUNE RESPONSE WHEN IT ATTACHES TO A PROTEIN.

9. MACROPHAGES primary effector cells of Type II responses
ROLE IN TYPE 11
HYPERSENSITIVITY

10. Examples of Type II drug allergies, hemolytic anemia, blood transfusion mismatch with resulting
reactions transfusion reaction and Rh hemolytic disease.

11. Type II respons- The cell surface and cause:
es (antibody binds The cell to be destroyed by the antibody
to antigen where? Cell destruction through phagocytosis by macrophages
What happens?) Damage to the cell by neutrophils triggering phagocytosis
Natural killer cells to release toxic substances that destroy the target cell
Malfunction of the cell without destruction

12. Type III hypersensi- antibody binds to the antigen in the blood or body fluids and then circulates
tivity reaction binds to the tissue.
where?

13. WHAT Reactions are Type III
not organ specific
and use neutrophils
as the primary effec-
tor cell

14. What is a complica- increase accumulation of immune-complex deposition (ICD) causes autoim-
tion of type III hy- mune diseases, the mononuclear phagocytes, erythrocytes, and complement
persensitivity? system fail to remove immune complexes from the blood....inflammation
occurs. ex. serum sickness

15. serum sickness fever, joint pain, non-blanchable rash, swelling to fingers, knees and feet

2

, NR507 WEEK 1
NR507 WEEK 1
Study online at https://quizlet.com/_ei3l95


16. type IV hypersensi- cell-mediated responses
tivity reactions lymphocytes and macrophages are primary mediators
mediated by T-lymphocytes & MACROPHAGES, DONT use antibodies
EX. contact dermatitis
epidermal reactions characterized by erythema, cellular infiltration and vesi-
cles

17. humoral immunity a type of immune response that depends on antibodies (TYPE 1-3 HYPER-
SENSITIVITY RX)

18. Type 1 pathophysi- Mast cell degranulation results in an inflammatory response
ology

19. Type II pathophysi- 1-Complement damages RBC membrane and cells lyse
ology 5-Autoantibodies specific for thyroid tissue impair receptor for TSH

20. Type III - Pathophys- Complex deposited in small peripheral vessels in cool temperatures leading
iology to vasoconstriction and blocked circulation

21. TYPE IV PATHO- T cells attack tissue directly (no antibody)
PHYSIOLOGY

22. TYPE II EXAMPLES 1-ABO incompatibility
5-Graves' disease

23. TYPE I EXAMPLES hay fever and asthma

24. TYPE III EXAMPLES Raynaud's phenomenon

25. TYPE II MECHANISM Tissue-specific destruction or impairment because of:
OF ACTION Antibody binding followed by lysis via complement,
macrophage phagocytosis, neutrophil destruction, Antibody-dependent cell



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