Pathophysiology — Renal, Endocrine, Neuro, GI and More flashcards
10 of 80 cards free to study here · 11 topics · the whole deck is built into Willys
Mechanism-first cards on AKI and CKD, glomerular disease, diabetes, DKA and HHS, thyroid and adrenal disorders, stroke and ICP, seizures, neurodegeneration, peptic ulcer, IBD, cirrhosis, pancreatitis, anemia, and bone and joint disease.
Learn deck · part of Pathophysiology · written against: Standard nursing/allied-health pathophysiology course; no dosing. Updated 2026-10-10.
Study the free sample
10 cards from the deck as they are. Flip, rate yourself, filter by topic; your progress stays in this browser.
Tap the card or press Space to flip
The 10 sample cards as a list
-
Why does prerenal acute kidney injury produce concentrated urine that contains very little sodium?The tubules are still healthy, and low renal perfusion switches on the renin–angiotensin–aldosterone system and ADH, so they reabsorb sodium and water avidly. The urine is concentrated and its sodium, and fractional excretion of sodium, are low.Acute Kidney Injury
Watch out: a recent diuretic raises urine sodium and can hide this pattern. -
Why does chronic kidney disease tend to keep progressing even after the original cause is controlled?As nephrons are lost, the survivors hyperfilter under raised glomerular pressure, which damages them in turn (glomerulosclerosis). Leaking protein injures the tubules, and angiotensin II promotes scarring.Chronic Kidney Disease
Why: this is why drugs that lower glomerular pressure, such as ACE inhibitors and ARBs, slow progression. -
How does damage to the glomerular filtration barrier produce the features of nephrotic syndrome?Injury to the podocytes and basement membrane lets large amounts of protein, mainly albumin, leak into the urine. Low plasma albumin lowers oncotic pressure, causing edema, and the liver responds by making more lipoproteins, causing hyperlipidemia and fat in the urine.Glomerular Disease
-
How does type 1 diabetes destroy insulin production, and why can symptoms seem to appear suddenly?Autoimmune T cells gradually destroy the pancreatic beta cells, and autoantibodies (such as anti-GAD) mark the process. Destruction may take months to years, but symptoms appear only once the remaining beta cells can no longer meet demand, often unmasked by an illness that raises insulin needs.Diabetes Mellitus
-
How do the antibodies of Graves disease cause both hyperthyroidism and a diffuse goiter?TSH-receptor-stimulating antibodies mimic TSH, driving the follicular cells both to make hormone and to grow. The rising thyroid hormone suppresses the pituitary, so the patient's own TSH is low.Thyroid and Adrenal Disorders
-
What is the basic neuronal mechanism of a seizure?A seizure is a sudden, excessive, synchronized discharge of a population of cortical neurons, arising when excitation (largely glutamate-driven) overwhelms inhibition (largely GABA-driven). The symptoms depend on which brain regions the discharge involves.Seizures and Neurodegenerative Disease
-
Which balance determines whether a peptic ulcer forms?The balance between aggressive factors (acid, pepsin, H. pylori, NSAIDs, bile) and mucosal defenses (the mucus–bicarbonate layer, prostaglandins, mucosal blood flow and rapid epithelial renewal). An ulcer forms when aggression outweighs defense, even if acid output is normal.Peptic Ulcer and Inflammatory Bowel Disease
-
How does chronic liver injury progress to cirrhosis?Repeated hepatocyte injury (from alcohol, viral hepatitis or fatty liver disease) activates hepatic stellate cells, which lay down collagen. Bands of fibrosis link the portal tracts and surround regenerative nodules, destroying the normal architecture and blood flow of the liver.Liver and Pancreas
-
Into which three mechanistic groups can anemias be divided?Decreased production (iron, B12 or folate deficiency, marrow failure, low erythropoietin in kidney disease), increased destruction (hemolysis) and blood loss. Sorting a new anemia into one of these groups guides every later test.Anemia
-
Why does bone mass fall rapidly after menopause?Estrogen normally restrains osteoclast formation and activity. When it falls, resorption outpaces formation, and the high-turnover trabecular bone of the vertebrae and wrist is lost fastest, which is where osteoporotic fractures often appear first.Bone and Joint Disorders
Unlock the whole deck
You are studying a free 10-card sample. All 80 cards of Pathophysiology — Renal, Endocrine, Neuro, GI and More, the other 2 Pathophysiology decks, and spaced-repetition scheduling are built into Willys. 14-day free trial, then $14.99 a year.
In Willys, tap Exam Library at the top of your Decks (or Browse Exam Library… under the + button), find the exam on its shelf or by search, tick it and tap Add.
More Pathophysiology decks
← All Pathophysiology decks, with the study guide and topic outline.
About these cards
Review status: Second-reader reviewed, with corrections applied.
Checked against:
- OpenStax Anatomy and Physiology 2e, consulted as a reference where applicable; no text copied.
These are independent study notes written for Willys. They are not official exam material, may contain mistakes, and are no substitute for your course, your teacher or the exam owner's own publications. Found an error? Tell us — corrections ship as a new version of the deck.
Not clinical guidance. These cards prepare you for an exam. Never use them to make decisions about a patient's care: follow current guidelines, prescribing information and your institution's policies. The decks contain no doses.
Use of these pages is covered by our Terms of Use.