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NRMS 5190 Advanced Pathophysiology Final Exam Study Guide 2026 | SUNY Downstate | Comprehensive Review.

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NRMS 5190 Advanced Pathophysiology Final Exam Study Guide 2026 | SUNY Downstate | Comprehensive Review.

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NRMS 5190 Advanced Pathophysiology Final Exam Study Guide 2026 | SUNY Downstate |
Comprehensive Review.

I cross-checked your uploaded Patho Final Review, the NRMS 5190 materials currently
indexed for SUNY Downstate on Studocu and Course Hero, SUNY Downstate's official course
description, and current clinical references. SUNY describes NRMS 5190 Advanced
Pathophysiology as a 3-credit course built around mechanisms of cellular injury, pathologic
processes by body system, and especially the etiology, epidemiology, pathogenesis, and
manifestations of disease across the lifespan. (Downstate Medical Center) The current Studocu
NRMS 5190 page specifically lists a 2025/2026 “Patho Final Exam Study Guide: Disorders
of Hemostasis and Blood Cells” as well as a highly rated neuro/psych final-exam guide.
(Studocu)

I would not treat every bullet in older student notes as equally authoritative. Where the material
conflicts with current clinical standards, I flag the distinction below rather than blindly
reproducing it.

The uploaded final review is especially useful because it identifies what receives emphasis and
what apparently does not. It specifically calls out osteoporosis risk factors, cerebral-lobe injuries,
HIV/AIDS, Gram-positive vs. Gram-negative bacteria, visceral vs. deep somatic pain, cystic
kidney disease causes, kidney stones, and AKI. It also specifically says to distinguish prerenal,
intrarenal, and postrenal AKI and emphasizes breast-cancer risks, bladder-cancer manifestations,
and HPV.

Most importantly for efficient studying, this review says no headaches, no stroke questions, no
spinal-cord-injury questions, no photosensitivity questions, and no testing of GFR rate
categories; pressure-injury staging is considered baseline nursing knowledge rather than a
specific focus.




FINAL EXAM PRIORITY MAP
I would study the course in roughly this order:

1. Hemostasis, thrombosis, DIC, platelet abnormalities, hemophilia, anemia,
Hodgkin/NHL
2. Renal/urinary disorders — especially AKI, stones, bladder dysfunction and cancer
3. Neuro/psych — MS, Parkinson disease, seizures, cerebral lobes, dementia,
schizophrenia, trigeminal neuralgia
4. HIV/AIDS and infectious disease
5. STIs and reproductive disorders
6. Inflammation, SIRS, wound healing, burns and major skin disorders
7. Musculoskeletal disease — osteoporosis, injuries, scoliosis, osteomyelitis
8. Breast cancer risk factors

,That weighting follows the repeated “please know/definitely know” statements in the final
review, especially its hematology section. The review explicitly identifies thromboembolism
risk, DIC, hemophilia-factor deficiencies, platelet abnormalities, Hodgkin/NHL, MS,
Parkinson disease, seizures, cerebral-lobe injury, dementia, and schizophrenia as exam
material.




PART I — HEMOSTASIS AND BLOOD
DISORDERS
★ Extremely high yield
1. Normal hemostasis

Hemostasis is the physiologic process that prevents excessive blood loss after vascular injury.

Know the sequence:

Vascular injury → vasoconstriction → platelet adhesion/activation/aggregation →
coagulation → fibrin stabilization → later fibrinolysis

Vessel spasm

Damage to a vessel stimulates transient vasoconstriction.

Purpose:

 reduce local blood flow
 limit blood loss
 facilitate platelet and coagulation activity

Primary hemostasis: platelet plug

After endothelial injury, normally hidden subendothelial collagen becomes exposed.

von Willebrand factor (vWF) binds exposed collagen and platelet receptors, allowing platelet
adhesion.

Activated platelets:

 change shape
 release mediators such as ADP

,  produce thromboxane A₂
 recruit additional platelets
 aggregate into a temporary platelet plug

Secondary hemostasis: fibrin formation

The coagulation cascade produces thrombin.

Thrombin converts:

fibrinogen → fibrin

Fibrin forms a strong mesh around the platelet plug.

Fibrinolysis

After repair begins:

plasminogen → plasmin

Plasmin breaks down fibrin.

The uploaded final review specifically says students should know the core sequence—vessel
spasm, platelet plug formation and fibrin-producing coagulation—but do not need to
memorize its timeline.




2. Thrombosis
Thrombosis = inappropriate formation of a blood clot within an intact vascular system.

Virchow triad

Always associate thrombosis with:

1. Endothelial injury
2. Abnormal blood flow — especially stasis
3. Hypercoagulability

Major risk patients

Think:

 prolonged immobility

,  recent surgery
 trauma
 malignancy
 pregnancy/postpartum
 estrogen-containing therapy
 heart failure
 prior VTE
 inherited thrombophilia
 obesity
 smoking
 increasing age

Arterial versus venous thrombosis

Arterial thrombus

 strongly associated with endothelial injury and turbulent flow
 platelet rich
 atherosclerotic disease is important
 can cause MI or ischemic stroke

Venous thrombus

 strongly associated with blood stasis
 fibrin and RBC rich
 commonly forms in deep lower-extremity veins
 may embolize to lungs → pulmonary embolism

The final review specifically instructs students to know venous thrombi and what kinds of
patients are at risk for thromboembolism.




3. Platelet disorders
Thrombocytopenia

A low platelet count impairs primary hemostasis.

Expect:

 petechiae
 purpura
 easy bruising
 epistaxis

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