Principles of Diagnostic Medicine I Exam 2 · Class of 2028

Principles of Diagnostic Medicine I Exam 2 Cram Sheet

Lectures 7, 8, 9 and 10. Electrocardiography — the action potential, the conduction system, paper, leads, rate and the normal intervals. Cardiac imaging — the chest radiograph, echocardiography, stress testing, nuclear, computed tomography, magnetic resonance, angiography and vascular ultrasound. Cardiac biomarkers and lipid testing. Coagulation and hemostasis testing — the three phases, the platelet, PT, INR, aPTT, thrombin time, fibrinogen and D-dimer tests, and how to read the patterns. Opens with how the exam is written.

How to use this: this is a condensed, night-before-the-exam reference, not a replacement for the full study guide — it assumes you've already learned the material and just need the highest-yield facts at a glance. If a term feels unfamiliar, go back to the full guide for the explanation.

How This Exam Is Written

Term	What you need to know
Reference ranges are GIVEN	“I'm not going to just throw a random number at you” — a troponin, triglyceride or C-reactive protein in a stem comes with the limit that reads it. Learn what a value MEANS.
Name the rhythm	Electrocardiography is the one place where naming the finding is fair game. Lecture 7 is the toolkit: paper, leads, rate, intervals.
Next-best-test	“What would be the next test that you would order?” Know what each imaging study can and cannot show, and what to do when one is equivocal.
★ Two calculations ARE examinable	Friedewald LDL-C and non-HDL-C, worked in class on the Lecture 9 practice slide: “two calculations, and then we have to interpret.” The newer LDL equations are calculator-only.
Not examined (said out loud)	Ion-channel subtypes (but which ion moves in each phase IS). Bazett's formula (“I will never ask you about the formula”). The bifascicular-block aside. The order of the exercise-endpoint chart and the treadmill protocol tables.

Action Potential & Refractory Periods

Term	What you need to know
Four cell properties	AUTOMATICITY (makes its own impulse) · EXCITABILITY (responds to one) · CONTRACTILITY · CONDUCTIVITY (passes it on).
Phase order	4 → 0 → 1 → 2 → 3. “You need to know what happens in each phase.”
Phase 4 / 0	4 = rest (diastole), −90 mV, potassium inside. 0 = upstroke: FAST SODIUM CHANNELS open, sodium rushes in.
Phase 1 / 2 / 3	1 = early repolarization (sodium closes). 2 = PLATEAU: CALCIUM IN causes contraction, balanced by potassium OUT. 3 = rapid repolarization: calcium closes, potassium out, back to −90 mV. (Slide text says potassium “in”; its own figure shows efflux.)
Depolarization vs repolarization	Depolarization = membrane LESS negative, ACTIVATION, PRECEDES contraction. Repolarization = return toward rest, RECOVERY.
Absolute refractory	Will NOT respond. Phase 0 to MID phase 3, about 180 ms.
Relative refractory	WILL respond but fragile. Mid phase 3 to END of phase 3. The T-WAVE PEAK divides the two. Basis of R on T, P on T and the danger of a long QTc.

Conduction System

Term	What you need to know
Sinoatrial node	Main pacemaker, upper right atrium below the vena cava. 60–100 per minute. Three internodal tracts; most people use the superior anterior (FAST) tract.
Atrioventricular node	Near the coronary sinus. PAUSES and AMPLIFIES the signal; back-up pacemaker. 40–60 per minute.
Bundle of His	The ONLY electrical path from atria to ventricles in a normal heart, through the nonconductive atrioventricular septum.
Bundle branches	Left splits into THREE fascicles (posterior, septal, anterior). Right is MUCH LONGER than the left. Bifascicular block is NOT a left bundle branch block.
Purkinje network	Third pacemaker, 20–40 per minute; fastest conduction of all.
Cardiac vector	Direction and strength of current; true pathway is LEFT AND DOWN toward the anterior chest.

Paper, Leads & Rate

Term	What you need to know
Time	Small box 0.04 s · large box 0.2 s · 5 large boxes = 1 s. Strips are 3 or 6 seconds.
Voltage	Small box 1 mm = 0.1 mV; 10 mm (two large boxes) = 1 mV.
Bipolar vs unipolar	BIPOLAR = two electrodes: I, II, III (Einthoven's triangle). UNIPOLAR = one electrode: aVR, aVL, aVF (augmented) and V1–V6.
10 wires, 12 leads	Four limb electrodes make SIX hexaxial leads (I, II, III, aVR, aVL, aVF, used for axis); plus six chest leads. Placement must be MEMORIZED.
Lead II	Best view of the heart's vector, so it is the RHYTHM lead.
Which leads look where	Inferior II, III, aVF · septum V1–V2 · anterior V3–V4 · lateral I, aVL, V5–V6. Anteroseptal infarction shows in V1–V4 (both supplied by the left anterior descending artery).
Cannot tell you	Hemodynamic status, cardiac output, or WHETHER THERE IS A PULSE.
Rate methods	REGULAR rhythms only. 6-second: QRS count × 10 (P count × 10 for atrial). 300 method: heavy lines count 300, 150, 100, 75, 60, 50.

Waves & Intervals

Term	What you need to know
P wave	Atrial depolarization; under 0.12 s; upright in lead II.
PR interval	0.12–0.20 s (3–5 small boxes): atria, atrioventricular node delay, His-Purkinje.
QRS	Ventricular depolarization; under 0.12 s, narrow and sharp. Q = septum, R = anterior left ventricle, S = lateral left ventricle.
J point & ST	J point = end of QRS, start of ST; at baseline (1 mm variance). “Very important that you know how to identify the J point.” ST = ventricles holding contraction; at baseline.
T wave	Ventricular repolarization, 0.16–0.25 s.
QT / QTc	Start of QRS to end of T. 350–450 ms males, 360–460 ms females. QTc = rate-corrected; above 450 (460) to 500 = borderline; ABOVE 500 ms = HIGH-RISK.
U wave & TP	U: after T, same direction, best V2–V3; prominent in hypokalemia, hypercalcemia, long QT, post-infarction. TP segment = best place to judge the isoelectric line.
The system	Rhythm → rate → P waves → P for every QRS → QRS width → PR → ST → T → QTc → extra waves or beats → voltage.

Chest Radiograph & Cardiothoracic Ratio

Term	What you need to know
Its standing	NOT the primary modality for function or detailed anatomy, but gives clues when obtained: silhouette, great vessels, pulmonary vasculature, lungs and pleura.
Right border	Superior vena cava → right atrium.
Left border	Aortic knuckle → main pulmonary artery → left atrial appendage → left ventricle (forms the apex).
Cardiac findings	Pulmonary edema · pleural effusion · cardiomegaly · CEPHALIZATION · great vessel, valve or pericardial calcification · tension physiology.
Cephalization	Upper-lobe vessels bigger than lower. Heart failure or pulmonary hypertension.
Cardiothoracic ratio	Widest heart ÷ widest INTERNAL thorax. Normal 0.42–0.5; ABOVE 0.5 on a PROPER POSTEROANTERIOR film suggests cardiomegaly.

Echocardiography & Stress Testing

Term	What you need to know
Echo shows	STRUCTURE AND FUNCTION: chambers, walls, ejection fraction, Doppler flow, valves, shunts, pressures.
TTE (transthoracic echocardiogram)	Most common, bedside, noninvasive. Poor for the POSTERIOR heart.
TEE (transesophageal echocardiogram)	Probe in the esophagus. Aorta and great vessels, myxoma, prosthetic valves, VEGETATIONS, cerebral ischemia, LEFT ATRIAL APPENDAGE THROMBUS.
TEE contraindications	Anything the probe can injure or an airway you cannot protect: esophageal stricture, malignancy, bleeding varices; dysphagia; ZENKER'S DIVERTICULUM; cervical arthritis; sleep apnea; uncooperative patient.
Valid exercise test	At least 85% of predicted maximum; predicted maximum = 220 − AGE. Under 85% cannot exclude ischemia.
Exercise test reads	Ischemia indirectly: ST DEPRESSION or new premature ventricular contractions. Bruce protocol; bicycle preferred.
Echo stress	Can exercise but baseline ST-T changes. Look for NEW WALL-MOTION abnormality right after exercise.
Pharmacologic stress	Cannot exercise. ADENOSINE or DIPYRIDAMOLE vasodilate; DOBUTAMINE raises workload.

Nuclear, CT (Computed Tomography) & MRI (Magnetic Resonance Imaging)

Term	What you need to know
Nuclear perfusion	Tracer at rest and after stress. Less uptake after stress = ischemia; NO uptake = dead tissue (VIABILITY). More accurate than standard or echo stress.
Coronary CT angiography	Presence and distribution of coronary disease; detect or exclude stenosis or plaque; EQUIVOCAL OR NON-DIAGNOSTIC STRESS TEST → next best step.
Cardiac CT	Non-contrast = CALCIUM SCORING. Metoprolol slows the heart, nitroglycerin dilates, electrocardiogram gating.
CT limits	ANATOMY ONLY, NOT FUNCTION. Radiation, contrast, rate dependent, BLOOMING artifact overstates calcium.
Cardiac magnetic resonance	Anatomy, function, viability, perfusion, INFLAMMATION — no ionizing radiation or iodinated contrast. ECHO FIRST. Aorta, congenital disease, cardiomyopathies, myocarditis, sarcoid.
Magnetic resonance limits	Implants (aneurysm clips, some pacemakers), long acquisition, claustrophobia. Titanium is acceptable.

Angiography, Catheterization & Vascular Ultrasound

Term	What you need to know
GOLD STANDARD	Coronary angiography for coronary disease — “a high-miss last year.” Can treat in the same sitting (balloon, stent).
Why go to the catheter	Noninvasive tests say IF disease is there; angiography says HOW MUCH, and intervention is by percentage. Positive CT angiogram with left anterior descending disease → catheter.
Left vs right heart cath	LEFT (artery) = CORONARY ARTERIES. RIGHT (vein) = PULMONARY HYPERTENSION.
Complications	Access-site HEMATOMA and PSEUDOANEURYSM (pulsatile, communicates with the artery). Always check the site.
Electrophysiology testing	Catheters via a vein into the right heart provoke and locate an arrhythmia; ablation can treat it.
Vascular ultrasound	Veins COLLAPSE, arteries PULSATE on compression. Deep vein thrombosis, carotid, peripheral arterial disease, aneurysm, venous insufficiency. No radiation; HIGHLY OPERATOR DEPENDENT.

The Four Cardiac Biomarkers

Term	What you need to know
★ One word each	CRP = INFLAMMATION · BNP = STRETCH, so volume · troponin = INJURY (“troponin is your friend”). “If you have troponin, don't even waste your time ordering a CK.”
The frame	Biomarkers: “is there ACUTE cardiac injury or stress?” Lipids: “what is the LONG-TERM atherosclerotic risk?”
Troponin	Myocyte INJURY. Marker of choice. Infarction = above the 99th PERCENTILE upper reference limit + ischemic symptoms. Sex-specific limits.
Troponin subunits	I = CARDIAC SPECIFIC. T = mostly cardiac, trace skeletal. C = NOT useful.
High-sensitivity troponin	The ASSAY, not a subunit. Draw at 0 and 1–2 HOURS; up to 90 minutes earlier. Pitfall: measurable in healthy people.
Injury vs infarction	Injury = any elevation. Infarction = injury + ISCHEMIA + RISING/FALLING pattern. Chronically raised in kidney disease, heart failure, structural disease — never read one value alone.
Creatine kinase	Skeletal muscle: RHABDOMYOLYSIS, STATIN MYOPATHY. Low cardiac specificity. Creatine kinase-MB, myoglobin, lactate dehydrogenase are RETIRED for infarction.
BNP (B-type natriuretic peptide)	STRETCH, not injury. Rule-out of new heart failure; monitor, guide, prognosis. Rises with age, female sex, kidney disease; FALSELY LOW IN OBESITY. Not stand-alone.
hs-CRP (high-sensitivity C-reactive protein)	Inflammation; a RISK ENHANCER, never an acute test. Non-specific. Highest in bacterial infection. Lowered by statins, NSAIDs (nonsteroidal anti-inflammatory drugs), GLP-1 (glucagon-like peptide-1) agonists, lifestyle. In the Reynolds Risk Score.

When to Order Which

Term	What you need to know
★ Acute chest pain, in full	Troponin + EKG as soon as possible, plus a metabolic panel for KIDNEY FUNCTION (to read the troponin, for cath-lab contrast, for diabetes and hypertension). hs-CRP is “an office visit type lab”, never the chest-pain answer.
Chest pain	SERIAL HIGH-SENSITIVITY TROPONIN, first-line; first value is also prognostic.
Dyspnea / heart failure	BNP (B-type natriuretic peptide) or NT-proBNP (N-terminal pro B-type natriuretic peptide); also prognostic after acute coronary syndrome.
Muscle pain on a statin	CREATINE KINASE, not troponin.
Risk refinement	hs-CRP (high-sensitivity C-reactive protein) in select primary prevention.
Do NOT order	Routine natriuretic peptides in healthy people; creatine kinase-MB or myoglobin for infarction.
Troponin, other uses	Unstable angina (normal = no injury) · reinfarction · infarct size (late 4-week value INVERSELY related to ejection fraction) · procedural: type 4a more than 5×, type 5 (bypass) more than 10× the 99th percentile limit.

Lipoproteins & Apolipoproteins

Term	What you need to know
Why particles	Cholesterol and triglycerides are INSOLUBLE. Lipoprotein = lipid core + phospholipid shell + apolipoproteins.
One apoB particle	Liver VLDL (very low-density lipoprotein) → lipoprotein lipase strips triglyceride → remnant → LDL (low-density lipoprotein). Under ~70 nm can be TRAPPED in the artery wall.
ApoB-48 / ApoB-100	B-48 = intestine, CHYLOMICRONS. B-100 = liver: very low-, intermediate-, low-density lipoprotein and lipoprotein(a). NOT in HDL (high-density lipoprotein).
ApoA-I / ApoE	A-I = ALL HDL (high-density lipoprotein). E = triglyceride CLEARANCE. C-III and A-V regulate triglyceride metabolism.
LDL vs HDL	LDL (low-density lipoprotein) = PRINCIPAL DRIVER, log-linear with risk. HDL = REVERSE CHOLESTEROL TRANSPORT. Remnants carry RESIDUAL risk.
Lipoprotein(a)	LDL-like + apo(a) on apoB-100. Over 90% GENETIC, stable, NO FASTING, measure ONCE in all adults; repeat after menopause if borderline; CASCADE test families. STATINS DO NOT LOWER IT. About 20% of people elevated.

Ordering & Reading a Lipid Panel

Term	What you need to know
★ LDL-C goal, both ends	No single normal, so know the ends: average risk UNDER 100 · highest risk UNDER 55 (middle tier under 70). “LDL is the big one.” Golf, not bowling.
★ Well patient + family history	SCREENING, not diagnostic (the slide's asterisk): fasting lipid panel, A1C, lipoprotein(a) if never measured.
Measured	Total cholesterol, HDL-C (high-density lipoprotein cholesterol), triglycerides.
Calculated	LDL-C (low-density lipoprotein cholesterol) — an ESTIMATE — and non-HDL-C = total cholesterol − HDL-C.
Friedewald	LDL-C = total − HDL-C − triglycerides ÷ 5. INVALID when triglycerides are 400 mg/dL or above; Martin/Hopkins or Sampson/NIH (National Institutes of Health) preferred.
Non-HDL-C	Every atherogenic apoB lipoprotein, NO added cost, BETTER predictor than LDL-C.
No single normal	LDL-C and non-HDL-C goals depend on RISK TIER; triglyceride, apoB and lipoprotein(a) thresholds are fixed. HDL-C is a MARKER, not a target.
Triglycerides	150+ = risk enhancer · 500+ = SEVERE, PANCREATITIS risk · 1000+ = extreme.
ApoB	Modifiable, repeated to monitor therapy; use with triglycerides 150+, diabetes or low LDL-C to find residual risk.
Fasting?	NONFASTING for most. Fasting with triglycerides 400+, a triglyceride disorder, or FAMILY HISTORY OF PREMATURE DISEASE or genetic dyslipidemia.
Screening	Children 9–11 (from age 2 with family history or familial hypercholesterolemia) · again at 19 · adults about EVERY 5 YEARS · on therapy recheck 4–12 WEEKS, then every 6–12 months.

Risk Assessment

Term	What you need to know
PREVENT (Predicting Risk of cardiovascular disease EVENTs)	Lipids feed a 10-YEAR risk estimate, which sets treatment intensity.
Calculate → Personalize → Reclassify	Low under 3% · borderline 3 to under 5% (add RISK ENHANCERS) · intermediate 5 to under 10% · high 10% or above.
Uncertain?	At borderline or intermediate risk, a CORONARY ARTERY CALCIUM SCORE reclassifies.
LDL-C goals	Under 100 if risk under 10% · under 70 if 10%+, familial hypercholesterolemia, diabetes with risk factors, or calcium 100+ · under 55 for very-high-risk clinical disease. 190+ = statin regardless of risk.
Elevated lipoprotein(a)	Earlier, more intensive control of EVERY OTHER risk factor.

Hemostasis: The Terms & Three Phases

Term	What you need to know
★ The frame (three phases)	Hemostasis = the BALANCE between clot formation and clot breakdown. EACH TEST evaluates ONE PART of that balance.
Hemostasis	Arrest of bleeding from an injured vessel, while preventing pathologic thrombosis.
Primary hemostasis	Formation of a PLATELET PLUG at the site of injury. von Willebrand factor tethers platelets to collagen; they aggregate through glycoprotein IIb/IIIa.
Secondary hemostasis	Insoluble, cross-linked FIBRIN from activated coagulation factors, specifically THROMBIN (the cascade).
Thrombus	A clot formed IN SITU within the vascular system that impedes flow.
Fibrinolysis	Enzymatic breakdown of fibrin: tissue plasminogen activator makes PLASMIN, which degrades fibrin.
Fibrin degradation products	Fragments after PLASMIN degrades fibrinogen or fibrin; markedly raised in disseminated intravascular coagulation.
D-dimer	A cross-linked fibrin degradation product from THREE enzymes: thrombin, activated factor XIII, plasmin.
Pathway map	Extrinsic = tissue factor + factor VII. Intrinsic = XII, XI, IX, VIII. Both feed factor X; common = X, V, II, I, XIII. Thrombin activates VIII, V and XIII. Vitamin K deficiency hits II, VII, IX, X.

Primary Hemostasis Tests (Platelets)

Term	What you need to know
Platelet count	Adults 140,000–400,000 per microliter. The deck calls thrombocytopenia below 100,000 and thrombocytosis above 350,000.
Mean platelet volume	UNIFORMITY OF PLATELET SIZE; used in the differential diagnosis of thrombocytopenia. Normal 7.4–10.4 femtoliters.
Smear	Platelet MORPHOLOGY: macrothrombocytopenia, gray platelets, neutrophil inclusions, clumps.
★ von Willebrand studies	von Willebrand factor ANTIGEN and ACTIVITY plus a factor VIII level. von Willebrand disease = MOST COMMON inherited bleeding disorder.
Platelet function tests	Light transmission aggregometry, lumiaggregometry, platelet function analyzer (PFA-100), flow cytometry.
Bleeding time	Minutes for a standard skin puncture to stop bleeding (3–10). ONLY USEFUL if the platelet count is ABOVE 100,000, because thrombocytopenia itself lengthens it. Largely replaced in practice.
False low count	Low count? CONFIRM in a citrated or heparinized tube: EDTA (ethylenediaminetetraacetic acid) can make platelets CLUMP (pseudothrombocytopenia). The smear shows clumps and satellitism.

Secondary Hemostasis Tests

Term	What you need to know
PT (prothrombin time)	Clot time after TISSUE FACTOR is added: EXTRINSIC + common. Liver-made, VITAMIN K dependent. Reference 11–13 seconds. Prolonged: factor VII, liver disease, vitamin K deficiency, warfarin.
★ INR (international normalized ratio)	PT STANDARDIZED across laboratories. Reference 0.8–1.2; on anticoagulation the goal is typically 2.0–3.0. On warfarin LOW = CLOT risk, HIGH = BLEEDING risk.
aPTT (activated partial thromboplastin time)	Clot time after a PHOSPHOLIPID ACTIVATOR: INTRINSIC + common. Reference 21–35 seconds; above 70 seconds signifies spontaneous bleeding. Prolonged: VIII, IX, XI, heparin, inhibitor, lupus anticoagulant, XII.
Thrombin time	Raised by HEPARIN and DABIGATRAN; normal in a simple factor deficiency.
Fibrinogen	CLAUSS assay preferred. Reference 2.0–4.0 g/L. LOW = BLEED (below 0.5 g/L: hemorrhage after traumatic surgery). HIGH = CLOT (above 7.0 g/L: coronary and cerebrovascular risk). Raised in tissue damage or inflammation.
Mixing study	Mix with normal plasma. CORRECTS = factor DEFICIENCY. Does NOT correct = INHIBITOR.
Factor assays	CONFIRM a deficiency; inherited or acquired; acquired can raise or lower levels.
Caveats	Normal PT/INR does NOT rule out coagulopathy. Low-molecular-weight heparin and most direct oral anticoagulants may not derange PT/aPTT yet raise bleeding risk; no routine monitoring. PREGNANCY: PT, aPTT, thrombin time shorten; fibrinogen and D-dimer RISE. Mild PT/aPTT prolongation does not predict bleeding.

D-dimer & Fibrinolysis Tests

Term	What you need to know
D-dimer	Normal below 250 micrograms per liter. Produced ONLY by plasmin on cross-linked fibrin: confirms BOTH thrombin and plasmin were generated. NONSPECIFIC.
★ D-dimer: best use	High NEGATIVE predictive value: a NORMAL result helps EXCLUDE thrombosis. Raised in acute thrombosis, DIC (disseminated intravascular coagulation), pregnancy and many acute illnesses.
Fibrin monomers	POSITIVE = thrombin activity, consistent with intravascular coagulation. NEGATIVE does NOT exclude it. Also positive in some severe liver disease and inflammatory disorders.
Clot vs breakdown	Thrombin = clot generation; plasmin = clot breakdown.
Other fibrinolysis tests	Euglobulin clot lysis time; alpha-2 antiplasmin and plasminogen activator inhibitor 1 assays.

Memory Aid: The Wall-Building Crew

Term	What you need to know
A story, not a fact	The lecturer's own picture: platelets are the BRICKS, clotting factors the MORTAR. A vessel is a flood wall; bleeding is a breach; hemostasis is a repair crew against a demolition crew. Full story in guide 10.0, with where it breaks.
Bricks (primary hemostasis)	Platelets = bricks. von Willebrand factor = scaffolding hooks that bolt bricks to the bare wall. Glycoprotein IIb/IIIa and fibrinogen = clips between bricks. Prostacyclin = non-stick coating on healthy wall. Too few bricks = bleeding tiers.
Mortar crew (secondary hemostasis)	Factors make the mortar: the workers that mix it (prothrombin comes from the liver); vitamin K licenses II, VII, IX, X (warfarin revokes it). Tissue factor + VII = outside alarm (PT). XII, XI, IX, VIII = inside chain (aPTT). X with V = shared foreman. Thrombin = master mixer; fibrinogen = powder; fibrin = wet mortar; XIII = hardener.
Brakes and saboteurs	Antithrombin III, protein C, protein S = safety inspectors (deficient = clots; low in DIC). Heparin and dabigatran = saboteurs at the mixers (aPTT and thrombin time up). Mixing study: spare crew corrects = a worker is missing; no correction = a saboteur.
Demolition crew (fibrinolysis)	Plasminogen waits, tissue plasminogen activator calls it out, plasmin tears down hardened mortar. FIBRIN DEGRADATION PRODUCTS = rubble. D-DIMER = rubble from HARDENED mortar only (thrombin + XIII + plasmin): it proves a wall was built and torn down, never WHICH wall, so a normal one helps exclude thrombosis.
Disseminated intravascular coagulation	Both crews run wild everywhere: bricks used up (platelets down), powder used up (fibrinogen down), mortar slow (PT and aPTT up), rubble everywhere (D-dimer up). Nothing is normal.

Reading the Patterns

Term	What you need to know
Start here	Bleeding workup: blood count with smear, PT/INR, aPTT, fibrinogen. INTERPRET BY THE PT/aPTT PATTERN FIRST.
★ Where to begin	An abnormal PTT means CLOTTING FACTORS (secondary hemostasis), never platelets. Normal PT and aPTT with bleeding means think PLATELETS (function, von Willebrand). Bleeding and clotting use the SAME tests; the INR places a patient on the clot-to-bleed spectrum.
PT up, aPTT normal	Factor VII, early vitamin K deficiency, liver disease, warfarin (or oral factor Xa inhibitor).
PT normal, aPTT up	Intrinsic: VIII, IX, XI; von Willebrand disease; heparin or dabigatran (thrombin time up too); inhibitor; LUPUS ANTICOAGULANT or FACTOR XII (no bleeding history).
PT up AND aPTT up	Common pathway or combined deficiency, DIC, liver disease, severe vitamin K deficiency. Normal thrombin time = X, V, II; prolonged = fibrinogen problem.
★ Normal PT AND aPTT, yet bleeding	Platelet disorder, mild von Willebrand disease, factor XIII or alpha-2 antiplasmin deficiency, impaired fibrinolysis.
★ DIC pattern	PT up, aPTT up, fibrinogen DOWN, D-dimer UP, platelets DOWN. Protease inhibitors (protein C, antithrombin, protein S) DOWN. Every abnormality has other causes; the PATTERN matters.
Acute thrombosis pattern	ONLY the D-dimer is up (nonspecific); PT, aPTT, fibrinogen, platelets normal.
Factor XII	Prolongs the aPTT but does NOT cause bleeding.
★ Isolated long aPTT	Rule out HEPARIN first, then fibrinogen. Corrects on mixing = factor deficiency: low VIII, then von Willebrand studies (abnormal = von Willebrand disease, normal = HEMOPHILIA). Does not correct = inhibitor: phospholipid-dependent = LUPUS ANTICOAGULANT (dilute Russell viper venom time).
Reptilase time	Normal with heparin; assesses FIBRINOGEN function.

Platelet Abnormalities

Term	What you need to know
★ Bleeding tiers	Below 50,000: bruises easily, bleeds with trauma or mucosal surgery. Below 20,000: SPONTANEOUS bleeding, PETECHIAE. Below 10,000: spontaneous INTRACRANIAL bleeding.
Quantitative	Thrombocytopenia AND extreme thrombocythemia (above 1,000 × 10⁹ per liter) can BOTH bleed.
Morphology	Gray platelets = gray platelet syndrome; neutrophil inclusions = May-Hegglin; clumps = spurious low count; fragmented red cells (schistocytes) = thrombotic thrombocytopenic purpura.
★ Qualitative	Normal PT and aPTT WITH bleeding = platelet dysfunction: von Willebrand types 2 and 3, uremia, drugs (aspirin).
Low count, normal clotting times	Immune thrombocytopenia, thrombotic thrombocytopenic purpura, hemolytic uremic syndrome, heparin-induced thrombocytopenia (normal PT, aPTT, platelet function analysis).
Platelet function analysis abnormal	von Willebrand disease, DIC, uremia, aspirin and other nonsteroidal anti-inflammatory drugs, late liver failure. NORMAL in hemophilia A or B.
Low count: causes	Impaired production · increased destruction (immune, microangiopathy, CONSUMPTION in DIC) · dilution (massive transfusion) · SEQUESTRATION (hypersplenism).

Indications & the Two Workups

Term	What you need to know
Indications	Symptomatic bleeding; preprocedural risk (but mild prolongation does not predict bleeding); WARFARIN monitoring; DIC, liver disease, vitamin K deficiency; suspected thrombosis (D-dimer to rule OUT).
Five screening tests	Platelet count/size/shape, bleeding time, aPTT, PT, fibrinogen. Then factor assays and fibrinolysis tests.
Bleeding workup	Blood count with smear, PT/INR, aPTT, fibrinogen: the FACTOR AND PLATELET screens.
Thrombotic workup	PT, aPTT, D-DIMER (thrombin-generation markers); most abnormal in DIC. PT and D-dimer are independent risk factors for arterial thrombosis.
Hypercoagulable testing	Primary causes: antithrombin III, protein C, protein S (the slide also lists factor XII, which is not an established thrombophilia); fibrinolytic mechanisms. Tests: anticoagulant factors (incl. LUPUS ANTICOAGULANT), fibrinogen, PT, aPTT, thrombin time.
Inherited bleeding, screens normal	Skin bruising, petechiae, mucosal = platelet disorder or mild vWD · hemarthroses/deep hematoma = fibrinolytic inhibitor deficiency (euglobulin clot lysis time) · umbilical stump bleeding = FACTOR XIII.
Inherited bleeding, screens prolonged	PT only = VII. aPTT only = VIII (hemophilia A), IX (hemophilia B), XI, severe von Willebrand disease. Both = X, V, II (normal thrombin time) or fibrinogen (prolonged thrombin time). Bleeding into joints and muscles = factor deficiency.