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Study from your own notes.

Paste in PDFs, slides, even photos of handwriting. MySummaries organises them into boards — then makes the flashcards, the written papers, the audio lectures and a spoken examiner from what you wrote.

Free to start. Web and iOS.

Physiology The cardiovascular system
Part III — Circulation The cardiovascular system 17 sections · 4 columns
Vessels compared
Vessel Wall Pressure Job
Artery Thick, elastic High Smooths the pulse into steady flow
Arteriole Muscular Falls steeply Resistance — TPR is set here
Capillary One cell thick Low The exchange surface
Vein Thin, distensible Low Capacitance — holds two-thirds of the blood
The cardiac cycle 4 due
  • Systole — isovolumetric contraction, then ejection; the AV valves shut at S1
  • Diastole — relaxation, then filling; the semilunar valves shut at S2
  • Atrial kick — tops up the last fifth of ventricular filling
Preload and afterload
  • Preload — the end-diastolic stretch; venous return sets it
  • Afterload — the pressure the ventricle has to open the aortic valve against
Cardiac output

At rest about 5 L/min; hard exercise takes it past 25.

Starling's law

More stretch, stronger contraction — venous return sets preload, and preload sets stroke volume, up to a limit.

Baroreflex

Stretch means slow down — the carotid sinus and aortic arch report pressure; a rise adds vagal tone and cuts sympathetic outflow within a beat or two.

Murmurs
Lesion Timing
Aortic stenosis Ejection systolic
Mitral regurgitation Pansystolic
Aortic regurgitation Early diastolic
The double circulation
Conduction system

The SA node sets the pace — 60–100 a minute. The AV node delays about 0.1 s so the atria finish; His–Purkinje fires the ventricles from the apex up.

Capillary exchange

Hydrostatic out, oncotic in — filtration wins at the arteriolar end and reabsorption at the venular end; the lymphatics carry off the difference.

Coronary flow

The left coronary fills in diastole — systolic compression all but stops it, so a tachycardia starves the myocardium by shortening the phase that feeds it.

ECG

P — atrial depolarisation; QRS — the ventricles depolarising, hiding atrial repolarisation; T — ventricular repolarisation.

Blood pressure Clear

MAP sits a third of the way up the pulse pressure — 120/80 gives about 93 mmHg.

Normal pressures
Site mmHg
Aorta 120/80
Left ventricle 120/10
Right ventricle 25/5
Pulmonary artery 25/10
Shock at a glance
Type Output TPR
Hypovolaemic Low High
Cardiogenic Low High
Septic High Low
Autoregulation

Brain, heart and kidney hold their own flow across a wide pressure range; skin and gut are handed to the sympathetic supply instead.

Section tools Edit mode
Heart sounds

s1 av valves closing loudest at apex,, s2 = semilunar. s2 splits on inspiration - normal??

  • S1 — the AV valves closing; loudest at the apex
  • S2 — the semilunar valves; splits on inspiration (normal)
Cards — The cardiovascular system 3 of 14

Which valves close at S1 — and where is it loudest?

The AV valves; at the apex.

Paper marked — 82%

Two lost marks became cards. They're waiting in your tray.

Lecture — The cardiac cycle 12 min

…filling is passive until the atrial kick tops up the ventricle…

Oral exam Recording
Examiner

Talk me through why S2 splits on inspiration.

Platform

One board per topic. You build it from your own material, and every card, paper and lecture is written from it.

Built from your material. PDFs, slides, photos of handwriting, voice notes — you review every line the AI proposes. Then the finished board teaches it back.

Edit mode — building the board

Pick the pages.

Drop a PDF and tick the pages that matter. The rest never reaches the board.

cell-cycle.pdf 4 of 12 pages
Add 4 pages

Tools on every section.

Ask a section to check itself, tighten up, or restructure — in place.

Review the merge.

Additions in green, edits in amber, a tick on every line. Nothing lands until you approve it.

Cell biology The cell cycle Merge review
Review changes — Lecture slides

Two sections change. Nothing lands until you approve it, line by line.

Edit Cyclins & CDKs The slides add how cyclin B is switched off. Apply

Cyclin levels rise and fall through the cycle; the CDKs are constant

Cyclin B is degraded at mitotic exit

+Cyclin B is ubiquitinated by the APC/C, then degraded — CDK1 switches off

New section Checkpoints Nothing on the board covers them yet. Apply

+The spindle checkpoint holds anaphase until every kinetochore is attached

+DNA damage arrests the cycle at G1/S — p53 stands guard

4 changes selected

Discard Apply 4 changes
Study mode — studying from it

Must not miss core.

The points you cannot afford to miss, written from your notes — the thing to read first.

Must not miss core The cell cycle
Cyclins rise and fall; the CDKs are constant — the pair is the engine
Anaphase begins only when every kinetochore is attached
p53 guards G1/S — lose it and damaged DNA replicates

The board, seen another way.

Mind map, algorithm, timeline or comparison table — drawn from the same sections, on demand.

Highlight it. Ask what it means.

Four pens on a read-only board — a click takes the sentence, a drag takes the phrase. Explain answers under the tray in two or three sentences, from a model fast enough that it reads as a look-up.

Cell biology The cell cycle Study
The spindle checkpoint

Anaphase waits for every kinetochore — one unattached kinetochore keeps the APC/C switched off, so the sister chromatids stay held together.

Explained in your language.

The notes can be in one language and the explanation in another. Pick it once in the pen tray; read-aloud follows.

Focus in blocks.

25 and 5, 50 and 10, or your own minutes. It keeps counting on every page and in the tab title, and the durations sync to the phone.

Written from your sections. Scheduled by FSRS — every grade books a date, and what's fading comes back first.

Reviews land just before you'd forget.

Each recall pushes the next one further out — so the gaps grow, and a card you know stops taking up your day.

The better you know it, the longer it waits.

The same card's buttons after three straight Goods. Every grade prints the date it books before you press it.

Drill what's due.

Cards written from your own sections. Grade what you remembered and the next date is booked — only Again puts the card back in today's queue.

Cards — The cell cycle 5 due

From what you missed

What triggers the start of anaphase?

The APC/C — securin is degraded, separase cleaves cohesin.

The due queue.

One queue per board, per subject, or everything at once — the board shows what's due where.

Due today
The cell cycle 14 due
Enzyme kinetics 6 due
Membrane transport Clear

Misses become cards.

Lose a mark twice, or keep failing a card, and a new card is written for exactly that. One tap files it.

Remediation tray

You lost this mark twice: what triggers the start of anaphase?

Add card Dismiss

Sit the exam before the exam. Papers set from your own notes and sat under the clock, then marked against them — question by question, with the marker's reasoning.

Multiple choice marks itself.

Single-best-answer questions are marked in the browser the moment you answer — instantly, and free.

Question 7 1 mark

Which complex triggers the start of anaphase?

Cyclin B–CDK1
The APC/C your answer
The mitotic checkpoint complex
Separase

The APC/C destroys securin; separase is only then freed to cleave cohesin.

Where marks keep going missing.

Every marked paper adds to it — worst section first, each row a door back to the notes it came from.

Where marks go missing
41% Checkpoints
63% Cyclins & CDKs
88% Mitosis

Marked against your own notes.

Not a score out of ten. Every question comes back with what you earned, what the marker thought, and the exact point you left out.

Paper — The cell cycle 18:42
82% The cell cycle — marked 27/33 marks · 18:42 taken

Explain why CDK activity falls at mitotic exit.

3/4

Cyclin B is tagged by the APC/C and destroyed, so CDK1 loses its activating partner.

The APC/C link is there. But losing the cyclin only stops new phosphorylation — it does not undo the old.

Missed

The phosphorylations CDK1 already made have to be reversed

Model answer The APC/C ubiquitinates cyclin B, and PP2A and Cdc14 then strip CDK1's marks off its substrates.

Resit what you lost.

A fresh paper of only the questions that cost you marks. Same questions, clean answers — and no charge, because nothing has to be written.

After marking
Resit the 3 you lost marks on Re-mark this paper

Under the clock.

Papers are timed the way the real one is. The clock turns at five minutes, and hands the paper in for you when it runs out.

Exam conditions
05:12 11/15 answered Submit for marking

Lectures that teach it back. Pick the sections and say how long you have. Your own notes come back as a spoken lecture — for the walk, the drive, the ten minutes before you sit down.

Aimed at what you keep getting wrong.

Pick the sections yourself, or let the board pick: the cards you keep failing and the marks you dropped on your last paper both show up hot, with a lecture on that section one tap away.

New lecture
How long have you got? 5 min 10 min 15 min 20 min
Checkpoints Cyclins & CDKs Mitosis

Checkpoints · Struggling — getting 4 of 9 cards wrong, scored 41% when last examined

Suggest lectures

It plans the set, you pick one.

Four or five ways through the same material, each with one line on what it does that the others don't — and only as many as your notes can honestly fill.

10-minute ideas from 3 sections
The checkpoint, end to end Follows one unattached kinetochore from the signal it makes to the moment anaphase starts. ~10 min
Cyclins as the clock Reads the cycle as one rising and falling concentration rather than four separate stages. ~10 min
Where it fails The same machinery read backwards, from the things that go wrong when a control is lost. ~10 min

Ten minutes, in the examiner's voice.

The voice that marks your vivas reads the lecture back — your own sections, in the order they make sense in.

Lecture — The cell cycle 10 min
The checkpoint, end to end Follows one unattached kinetochore from the signal it makes to the moment anaphase starts.
04:3210:04
Speed 1.25×1.5×

Transcript · tap any word to jump there

So the checkpoint is not a timer. It is a signal that has to be switched off, and until it is, the cell simply waits.

A single kinetochore with no microtubule on it keeps making the mitotic checkpoint complex, and that complex sits on the APC/C and holds it shut. One chromosome out of place is enough.

Answer it out loud. Stations written from the board's own sections. You record one spoken answer, and it comes back marked against that station's criteria — the marker's reasoning, the wording that cost you, and the sections to reread.

An examiner that fits your exam.

Say the exam and the examiner is shaped to it — its emphases, its manner, counting down to your date.

Every attempt, scored.

Best and average side by side, and whether you are talking to time — the station carries its own target.

Station Attempts Best Avg
The spindle checkpoint Talk me through what stops a cell entering anaphase early… 4 82 74
Viva Best: Strong 04:41 on target · target 05:00

One answer, marked like an examiner marks.

Not a score out of ten. Every criterion comes back with what you earned, why, and the one thing that would have earned the rest.

Oral — The spindle checkpoint Recording Marked

Examiner

Talk me through what stops a cell entering anaphase with one chromosome still unattached.

02:143:00 Mark answer
78% The spindle checkpoint — marked 78/100 · Competitive · 2:14 spoken of 3:00
Knowledge and reasoning 21/25

You named the complex and what it holds shut, and you got there in the right order.

Improve Say what switches the signal off once the last kinetochore attaches — that is where the last marks were.

Structure and prioritisation 10/15

The answer arrived, but the headline came last. Lead with it, then explain.

It marks what you actually said.

Your answer comes back as a transcript with the wording that cost you marked in place — what was wrong with each phrase, and the words to use instead.

Transcript

The spindle checkpoint. An unattached kinetochore keeps making the complex, and that stops it going ahead.

not enough detail
that stops it going ahead

Which complex, and what it holds shut, is where the mark is.

Say: the MCC binds the APC/C and keeps it inactive.

The debrief is spoken back.

Read or listen — the marker's feedback is narrated in the examiner's own voice, word by word.

Spoken feedback

You named the complex and what it inhibits, which is the mark most candidates lose. Reread Checkpoints for how the signal is switched off.

Why it works

Made from your notes.

Every card, paper, lecture and viva question is generated from your own board — and marked against it. What you study is what you wrote.

Your words, not a bank.

Nothing comes from a generic question bank. The material is yours.

An examiner that fits.

Say what you're studying, and it marks the way that exam marks.

Misses come back.

Lost marks and failed cards turn into new cards, automatically.

Web and iOS.

Build on the web; drill, sit and listen anywhere from your phone.

Boards you can share.

Invite someone into a subject to read it, or to build it with you.

iOS app

The boards, in your pocket.

Drill the cards that are due, sit papers, play lectures on a commute, and take the oral examiner anywhere you can speak. Everything syncs with the web workspace.

  • Everything syncs both ways, as it happens
  • Share anything into the scratchpad straight from other apps
  • A note to yourself lands beside the exact card or question that prompted it

Currently in early access on TestFlight.

Today

The cell cycle 14 due
Enzyme kinetics 6 due
Lecture — The cardiac cycle 12 min
Oral — Checkpoints Resume

Start with one subject.

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