StudyFix
the app surface, rebuilt on the locked design system

Every screen below is drawn by the app's real stylesheet, lifted straight out of apps/web/index.html, with the markup copied from app.js's own templates and the sentences generated by importing the real applogic.js. If the app is wrong, this page is wrong — it cannot flatter the redesign. The lecture content is invented for this page and no pipeline was run to make it. This page is responsive, so on a phone you are seeing the phone layout, not a shrunken desktop one.

01 Upload nothing chosen yet. One box on the screen, and it is not dashed.
Upload a lecture

Drop a lecture PDF

or click to choose — Gemini reads the actual slides, diagrams and all

runs locally on your machine
Look up a single concept instead
02 Mid-run the stage ladder as an instrument log — mono index, hairline between rows.
Working…
✓Handing your lecture in
✓Reading it, slide by slide
✓Writing it up as one story
✓Mapping how it all connects
→Making cards you'll remember
·Writing exam-style questions
·Adding OSCE & written questions
·Scripting your 60-second refresher
·Auditing every fact against the source
·Packing your Anki deck
03 Result · Master Doc the reference rail and the work column. This replaces seven stacked full-width bands.
story covers 17/17 facts · nothing dropped

Diabetic ketoacidosis

DKA is what happens when there is no insulin at all. It is not "high sugar, worse". The sugar is a symptom of the real problem, which is that the cell is starving while the bloodstream is full.

Why the glucose climbs

Insulin is the key that lets glucose into the cell. Take the key away and the glucose stays outside, so the serum level rises while the cell behaves as if it is in a famine.

What the body does next

A starving cell burns fat. Unopposed glucagon drives lipolysis, the liver oxidises the fatty acids, and the products are acetoacetate and beta-hydroxybutyrate — both strong acids. That is the whole mechanism: no insulin, so burn fat; burn fat, so make acid.

A normal glucose does not exclude DKA. Euglycaemic DKA is the trap.

The three numbers

ComponentThresholdWhy it is in the definition
Glucose> 11 mmol/LConfirms the insulin deficit — but see the trap above
Ketones> 3 mmol/LBeta-hydroxybutyrate, measured at the bedside
AcidosispH < 7.3 or bicarb < 15Proves the acid load has outrun the buffer
04 Result · Cards was ~40 bordered white cards on grey. Now a ruled list — that one change removes 40 boxes.
6 cards · Pass 2 · Encode · isolated 2-button burn-down — or download the .apkg
In DKA, why does the glucose climb even though the cells are starving?
Without insulin, cells cannot take up glucose — so serum glucose rises while the cell starves.
Where do the acids in ketoacidosis actually come from?
Unopposed glucagon drives lipolysis, and beta-oxidation yields acetoacetate and beta-hydroxybutyrate — both strong acids.
A registrar asks you for the three numbers that make the diagnosis. Give all three.
DKA = glucose >11 mmol/L + ketones >3 mmol/L + pH <7.3 or bicarbonate <15.
The patient is needle-phobic. Do you need an arterial gas?
No — a venous gas answers pH and bicarbonate; an arterial sample adds pain, not information.
The potassium reads 5.1 before you start. Is the patient potassium-replete?
No — total body potassium is depleted even when the serum level reads normal or high, because insulin drives potassium into cells.
Fluid or insulin first, and why?
Fluid first, always — volume replacement precedes and outlasts the insulin infusion.
05 Result · SBAs, one answered correct is ACHROMATIC and marked by weight and a mono word; only the wrong pick takes colour.

1 SBAs · click an option to check

1. A 19-year-old with type 1 diabetes is drowsy after two days of vomiting. Glucose 28 mmol/L, pH 7.14, bicarbonate 9, potassium 5.4. What is the FIRST step?
06 Result · Disease Index the second row in each bucket is shown highlighted — the student's own mark, an ink margin rule, never a yellow ground.
click any fact to highlight · ★ = high-yield
Diabetic ketoacidosis
Causes / RF
·Type 1 diabetes — most first presentations — DKA is the presenting event in roughly a quarter of new type 1 diagnoses.
·Missed or stopped insulin — The commonest precipitant in a known diabetic.
·Infection — the precipitant that hides — Sepsis raises counter-regulatory hormones; the source is often occult.
Mechanism
★No insulin → cells cannot take up glucose — Absolute insulin deficiency blocks cellular glucose uptake despite high serum glucose.
★The body burns fat instead — Unopposed glucagon drives lipolysis and hepatic fatty-acid oxidation.
★Fat breakdown makes ketoacids — Beta-oxidation yields acetoacetate and beta-hydroxybutyrate — both strong acids.
C/P
·pH < 7.3 with a raised anion gap — Ketoacids consume bicarbonate and widen the anion gap.
·Deep sighing breathing, ketotic breath — Kussmaul respiration is respiratory compensation for the metabolic acidosis.
·Osmotic diuresis → litres of deficit — Glycosuria drags water and electrolytes; a typical adult is 5-7 L down.
·Abdominal pain that mimics a surgical abdomen — Common in severe acidosis and resolves as the acidosis corrects.
Inves
·VBG first — it answers pH and bicarbonate in minutes — A venous gas is sufficient; an arterial sample adds pain, not information.
·Bedside beta-hydroxybutyrate, not urine dipstick — Urine ketones lag and measure the wrong ketone body.
Mng
·Fluid first, always — 0.9% saline — Volume replacement precedes and outlasts the insulin infusion.
·Fixed-rate insulin infusion 0.1 units/kg/h — Fixed rate, not sliding scale; continue the long-acting basal insulin alongside.
·Potassium falls as insulin drives it into cells — Total body potassium is depleted even when the serum level reads normal or high.
Criteria
★Glucose >11 · ketones >3 · pH <7.3 or bicarb <15 — All three are required; a normal glucose does not exclude it in euglycaemic DKA.
07 Result · map drill, the arc the four slot rows keep their region rule — as a margin rule on an unboxed row, not a tab on a card.
click a topic to reveal its arc, then a slot for its facts
›Diabetic ketoacidosis

Name what sits in each slot before you open it — the guess is the point.

08 Result · map drill, one slot open the atoms. `.md-atom.mech` used to carry a teal left stroke, which MANIFESTO §3.2 bans; mechanism is carried by weight now.
››Fault
No insulin → cells cannot take up glucose — Absolute insulin deficiency blocks cellular glucose uptake despite high serum glucose.
The body burns fat instead — Unopposed glucagon drives lipolysis and hepatic fatty-acid oxidation.
Fat breakdown makes ketoacids — Beta-oxidation yields acetoacetate and beta-hydroxybutyrate — both strong acids.
09 Result · PARTIAL run two artifacts did not come back. Amber margin rule + a mono state word; the tab says so from the other ten; the panel says which.
Everything is ready except the exam questions and the 60-second script. The lecture itself came through — this is one output missing, not a failed run.
This did not come back.

It is not that the lecture had none — the step failed, and everything else is unaffected.

10 Result · deck delivered the receipt. A hanging label column with leader dots — what was built, where it went, and what it EXCLUDES.

Your deck is in Downloads

Diabetic_ketoacidosis.apkg
Cards6
Facts carded14 of 17
Left out of the deck3 facts
6 cards · Pass 2 · Encode · isolated 2-button burn-down — or download the .apkg
In DKA, why does the glucose climb even though the cells are starving?
Without insulin, cells cannot take up glucose — so serum glucose rises while the cell starves.
Where do the acids in ketoacidosis actually come from?
Unopposed glucagon drives lipolysis, and beta-oxidation yields acetoacetate and beta-hydroxybutyrate — both strong acids.
A registrar asks you for the three numbers that make the diagnosis. Give all three.
DKA = glucose >11 mmol/L + ketones >3 mmol/L + pH <7.3 or bicarbonate <15.
The patient is needle-phobic. Do you need an arterial gas?
No — a venous gas answers pH and bicarbonate; an arterial sample adds pain, not information.
The potassium reads 5.1 before you start. Is the patient potassium-replete?
No — total body potassium is depleted even when the serum level reads normal or high, because insulin drives potassium into cells.
Fluid or insulin first, and why?
Fluid first, always — volume replacement precedes and outlasts the insulin infusion.
11 Result · Fidelity audit the moat, made visible. Four pill badges became four Martian Mono words; the hanging label column carries the claim/problem/source.
Fidelity audit

Two checks the extractor can't be trusted to do on itself — so one is deterministic Python, the other an independent pass.

Coverage — was anything dropped?
!Every fact carded14/17
✓Story covers every fact17/17

Checked by deterministic code, not the AI — every fact the model extracted is provably carried into a card and into the master doc. Flagged items above were not carried through.

Facts the source had that the extraction may have missed (1)
Slide 14 gives a cerebral-oedema warning for paediatric DKA that no node carries.
Mistakes — is anything wrong vs the source?

A second model re-read the source and compared it against the graph and the cards.

card likely error potassium
Card says Potassium replacement should begin once serum potassium is below 5.5 mmol/L.
Problem The card states a threshold the slide does not give, and it is one step short of the protocol.
Source says Slide 22: "Add potassium to the second bag once K+ is below 5.5, provided the patient is passing urine."
12 Review · front the ONE genuinely raised object in the app. LAW 4: no decisions in here.
Pass 2 · Encode · 18 left
A registrar asks you for the three numbers that make the diagnosis. Give all three.
DKA = [  …  ].
13 Review · back the answer is carried by weight and an ink underline, not by teal on mint.
Pass 2 · Encode · 18 left
A registrar asks you for the three numbers that make the diagnosis. Give all three.
DKA = glucose >11 mmol/L + ketones >3 mmol/L + pH <7.3 or bicarbonate <15.
14 Pass cleared · the compression readout LAW 13 made observable. Both states shown together — growth at a pass boundary is the design, and it must not read as a failure.
Pass 2 · Encode cleared.
Stop — sleep consolidates it. Come back for the next pass.
This pile was 41. It is 34 now.
7 cards have dropped out of rotation since your last session. That is the whole point — the load is meant to fall as the knowledge rises.
Pass 3 · Interleave cleared.
Pass 4 is the cram window — it appears when your exam is inside the final week.
This pile went from 12 to 30.
Pass 3 reopened cards you had already rested — that is the design, not a setback. The count falls again as you clear them.
15 Hard failure the run died. One headline, one fix, the stage ladder frozen where it stopped, and the raw exception behind a disclosure — never as the headline.
✓Handing your lecture in
✓Reading it, slide by slide
✓Writing it up as one story
✓Mapping how it all connects
✕Making cards you'll remember
·Writing exam-style questions
·Adding OSCE & written questions
·Scripting your 60-second refresher
·Auditing every fact against the source
·Packing your Anki deck
Gemini's daily limit is used up.

Nothing was lost. It resets at midnight Pacific, or top the key up to keep going.

Technical detailResourceExhausted: 429 Quota exceeded for quota metric 'Generate requests' and limit 'GenerateRequestsPerDayPerProjectPerModel'
16 Library · the deck tree indent carries the hierarchy, so the rows stay flat and scannable. The 44px stat number in a white box is now a 28px Besley figure under a rule.
Your library
47
for today · across 4 lectures
12 you marked weak · 9 never seen
118 due in total — capped at a day
ICC-2
4 lectures · 118 due · 47 today
Endocrine
2 lectures · 61 due · 22 today
Diabetic ketoacidosis
62 cards · 34 due · 18 today · Pass 2 Encode · exam in 34d (module)
Thyroid emergencies
31 cards · 27 due · 4 today · Pass 1 Orient · exam in 34d (module)
Acid–base for finals
25 cards · 25 due · 8 today · no exam set