The 20 Highest-Yield Facts

If you only have an hour left, these 20 facts are the ones to hold onto — each one below, in order, with the reasoning behind it spelled out.

1. Type II hypersensitivity happens when antibodies attack an antigen that's sitting directly ON a cell — the cell itself is the target. Type III is different: antibodies and antigens link up into immune complexes out in the blood first, and those complexes deposit into tissue afterward, causing damage wherever they land.
2. For SLE, ANA is the screening test — it raises suspicion but isn't specific enough on its own. Anti-dsDNA and anti-Sm are what confirm it. And because the complement system is being consumed fighting the immune complexes, complement comes back LOW.
3. Iron deficiency anemia has a distinctive signature: ferritin (iron storage) is LOW because the stores are truly depleted, while TIBC (the blood's iron-carrying capacity) is HIGH because the body is straining to grab whatever iron it can find. No other anemia pairs low ferritin with high TIBC — that combination is unique to iron deficiency. — ⚠️ The TIBC half is slide-only — your chapter does not corroborate it. check the card
4. Both B12 and folate deficiency cause large red blood cells, so cell size alone can't tell them apart. The tiebreaker is neuropathy — numbness, tingling, nerve damage — which shows up with B12 deficiency because B12 is also needed for nerve health, but does not show up with folate deficiency.
5. The kidneys produce EPO, the hormone that tells the bone marrow to make red blood cells. In CKD, failing kidneys make less EPO, so fewer red cells get produced — but the ones that are made are normal-sized, which is why CKD causes a normocytic anemia rather than one where the cells themselves look abnormal.
6. When the LEFT side of the heart fails, blood backs up behind it — into the lungs — causing breathlessness and crackles. When the RIGHT side fails, blood backs up behind it instead — into the rest of the body — causing leg swelling, JVD, and ascites. Which side failed tells you where the congestion shows up.
7. An S3 gallop points to systolic heart failure, where the ventricle has stretched out (dilated) and can't squeeze effectively. An S4 gallop points to diastolic heart failure, where the ventricle has thickened and stiffened (hypertrophied) and can't relax and fill properly.
8. ACC/AHA stages (A–D) track structural heart disease, and once you've reached a stage you don't move back — the structural damage doesn't reverse. NYHA class tracks how symptomatic someone is day to day, so a patient can move both up and down between classes as symptoms improve or worsen.
9. When a heart failure patient is symptomatic and fluid-overloaded (congested), the first move is a diuretic like furosemide, to get the excess fluid off. Beta blockers, though a mainstay of long-term management, are actually contraindicated in acute decompensation — they blunt the heart's ability to compensate while it's already struggling.
10. Aortic stenosis classically presents with three exertional symptoms: chest pain (angina), fainting (syncope), and shortness of breath (dyspnea) — all brought on by activity, because the narrowed valve can't increase output to meet demand. Of the three, syncope is the worst sign — it means the heart is dangerously failing to keep up during exertion.
11. An FEV1/FVC ratio below 70% defines an obstructive pattern — air isn't flowing out fast enough. A total lung capacity (TLC) below 80% defines a restrictive pattern — the lungs simply can't hold as much volume as they should.
12. For someone with COPD, the oxygen target is 88–92% — lower than you would aim for in a healthy patient. Your book gives the reason plainly: oxygen is titrated with care in a person who retains CO2. — ⚠️ The old wording here said higher oxygen "suppresses the hypoxic drive". That mechanism is in nothing your course gave you, and current teaching treats it as overstated — so it has been removed. The 88-92% target itself is solid. check the card
13. Early in an asthma attack, rapid breathing blows off extra CO2, producing respiratory ALKALOSIS. As the attack worsens and the patient tires, they can no longer breathe fast enough to clear CO2, and it flips to respiratory ACIDOSIS — a sign of impending respiratory failure, and a true emergency. Absent breath sounds are even more ominous — so little air is moving you can't even hear a wheeze, signaling the patient may be close to death.
14. Interstitial lung disease (ILD) presents with a dry cough, clubbed fingers, fine crackles at both lung bases, and a reduced DLCO (scarred tissue can't transfer gas as well). The underlying process is scarring, and that scarring is irreversible.
15. On a urine dipstick, nitrites and leukocyte esterase point to a UTI. If the urine also shows WBC casts, the infection has reached the kidney — pyelonephritis, not just a bladder infection. When a kidney stone is suspected, a non-contrast CT is the gold-standard test to confirm it.
16. Acute renal failure moves through phases with opposite lab pictures. In the oliguric phase, output drops below 400 mL/day and potassium rises (HYPERkalemia) because the kidneys aren't clearing it. In the diuretic phase, as the kidneys recover, output can climb as high as 4,000 mL/day, and potassium falls (HYPOkalemia) because so much is being flushed out.
17. CKD is defined as a GFR below 60 sustained for 3 months or longer. Within that, Stage 2 is 60–89, Stage 3 covers 30–59, and Stage 5 is below 15. — ⚠️ Stage 2 is 60-89, not the 60-88 on week 4 slide 54 — that would leave a GFR of 89 in no stage at all. check the card
18. When someone actually starts dialysis is decided more by how sick they are — the symptoms — than by hitting a particular GFR number.
19. Anaphylaxis is treated with epinephrine given intramuscularly into the anterolateral thigh. The dose depends on weight: 0.3 mg for anyone above 25 kg, and 0.15 mg for someone 5–25 kg. If symptoms persist, the dose can be repeated every 5–15 minutes. The patient should be positioned supine with legs elevated to help maintain blood pressure. — ⚠️ The dose and route come from her eDapt Week 1 module, which we do not hold. Ch. 48 states neither. check the card
20. This course has two classifications worth calling out because they might look off at first glance: it classifies a LATEX rash as Type IV (not the Type I you might expect for an immediate allergic reaction), and RAYNAUD phenomenon as Type III. Both come straight from the textbook’s own table, so they are the right answer, not a quirk.