What is the difference between DIC and TTP?

DIC consumes clotting factors, so fibrinogen is low, D-dimer is high, and PT and PTT are prolonged. TTP leaves coagulation normal: low platelets and schistocytes appear with normal PT, PTT, fibrinogen, and D-dimer.

How do you tell primary from secondary hemostasis bleeding?

Primary hemostasis bleeding is mucocutaneous: petechiae, purpura, gum bleeding, and heavy menses from a platelet or von Willebrand problem. Secondary hemostasis bleeding is deep and delayed: hemarthrosis and muscle hematomas from a clotting factor problem.

What lab pattern suggests vitamin K deficiency?

PT prolongs first because factor VII has the shortest half-life, then PTT follows as factors IX and X fall. Platelets, fibrinogen, and D-dimer stay normal, which separates vitamin K deficiency from DIC.

How do you separate hemophilia from von Willebrand disease?

Both can prolong PTT. Hemophilia gives deep joint and muscle bleeding with a normal platelet count and a normal bleeding time. Von Willebrand disease gives mucosal bleeding with a prolonged bleeding time and low von Willebrand factor, and it is the most common inherited bleeding disorder.

Heme deep dive

Bleeding Disorder Decoder

A bleeding patient is a panel waiting to be read. Set platelets, PT, PTT, fibrinogen, D-dimer, and the smear, and the diagnosis falls out. The board move is to read the surface and the consumption trio before you panic about the name.

The surface Petechiae, purpura, and mucosal bleeding point to platelets. Hemarthrosis and deep muscle bleeds point to clotting factors.

The consumption trio Low fibrinogen plus high D-dimer plus long PT and PTT means factors are being eaten. That is DIC.

The clean coags fork Low platelets with schistocytes but normal coags is TTP. Isolated long PTT is hemophilia or von Willebrand.

Signal	Board meaning
Low fibrinogen and high D-dimer	Consumption is happening. Think DIC.
Schistocytes with normal coags	Microangiopathy without consumption. Think TTP.
PT prolongs before PTT	Factor VII falls first. Think vitamin K.

Read the panel

Toggle the labs. Watch the diagnosis resolve.

This is the move the board rewards: stop guessing the disease and start reading the panel. Set each value, and the decoder names the disorder and tells you which clue clinched it. Try the sepsis preset first.

Platelets 150000 to 400000

PT extrinsic and common

PTT intrinsic and common

Fibrinogen clotting substrate

D-dimer fibrin breakdown

Smear red cells and platelets

The framework

Two doors: platelet plug or fibrin clot.

Every bleeding disorder enters through one of two doors. Primary hemostasis is the platelet plug at the mucosa and skin. Secondary hemostasis is the fibrin clot that holds in deep tissue. The bleeding surface tells you which door before any lab returns.

Primary hemostasis: the platelet plug

Platelets and von Willebrand factor seal small surface breaks fast. When that fails, bleeding is mucocutaneous and immediate: petechiae, purpura, gum bleeding, epistaxis, and heavy menses. Split it into quantity and quality. Quantity problems are ITP, TTP, and DIC. Quality problems are von Willebrand disease, Bernard-Soulier, and Glanzmann.

Pinpoint petechiae on skin — Tap to enlarge. Petechiae and purpura are primary hemostasis surfaces.

Purpura on skin from small vessel bleeding — Tap to enlarge. Purpura over the legs is a mucocutaneous clue.

Secondary hemostasis: the fibrin clot

Clotting factors weave fibrin so the plug holds under pressure. When a factor is missing, the first plug forms then fails, so bleeding is deep and delayed: hemarthrosis, muscle hematomas, and rebleeding hours after a procedure. Hemophilia A is factor VIII, hemophilia B is factor IX, and vitamin K deficiency starves factors II, VII, IX, and X.

Swollen knee from joint bleeding — Tap to enlarge. Hemarthrosis is a secondary hemostasis surface.

Sort the surface

Which hemostasis is broken?

For each finding, call the door before you reveal the reason. Mucocutaneous and immediate is primary. Deep and delayed is secondary.

Mechanism first

DIC eats the clotting system alive.

This is the case that scares students into the wrong answer. A septic patient bleeds and clots at the same time. Watch the consumption happen: a trigger fires tissue factor everywhere, microthrombi consume platelets and fibrinogen, red cells shear into schistocytes, and the leftover system has nothing left to stop bleeding while fibrinolysis floods the blood with D-dimer.

Trigger: sepsis, trauma, obstetric disaster, or cancer activates tissue factor across the whole vasculature.

Platelets Normal

Fibrinogen Normal

D-dimer Normal

The same shear shows on the smear

Red cells forced through the fibrin mesh get sliced into fragments called schistocytes. That is microangiopathic hemolysis. Both DIC and TTP produce it, so the smear alone does not separate them. The coags do.

Peripheral blood smear with schistocytes — Tap to enlarge. Schistocytes appear in both DIC and TTP.

Side by side

Six patterns, one panel each.

Each disorder has a panel fingerprint. Read them across the same six values so the differences jump out. Then challenge yourself on the two forks students miss most.

DIC: consumption coagulopathy

Platelets	Low
PT and PTT	Both prolonged
Fibrinogen	Low (consumed)
D-dimer	High (fibrinolysis)
Smear	Schistocytes
Bleeding pattern	Diffuse oozing and clotting at once, often very sick
The lock	Low fibrinogen and high D-dimer with long PT and PTT. Sepsis is the classic trigger.

TTP: microangiopathy with clean coags

Platelets	Low
PT and PTT	Normal
Fibrinogen	Normal
D-dimer	Normal
Smear	Schistocytes
Bleeding pattern	The pentad: low platelets, hemolytic anemia, neurologic signs, kidney injury, and fever
The lock	Schistocytes with normal coags and normal fibrinogen. ADAMTS13 is deficient, so do not give platelets.

ITP: isolated low platelets

Platelets	Low, often very low
PT and PTT	Normal
Fibrinogen	Normal
D-dimer	Normal
Smear	Few platelets, sometimes large young platelets, otherwise normal
Bleeding pattern	Mucocutaneous: petechiae and purpura, often a child after a virus or a young adult
The lock	Everything normal except a low platelet count. Antibodies coat platelets and the spleen clears them.

von Willebrand disease: the common one

Platelets	Normal count
PT	Normal
PTT	Normal or mildly long (carries factor VIII)
Bleeding time and platelet function	Prolonged
Smear	Normal
Bleeding pattern	Mucocutaneous: epistaxis, gum bleeding, and lifelong heavy menses
The lock	The most common inherited bleeding disorder. Normal platelet count with a long bleeding time and low von Willebrand factor.

Hemophilia A and B: the deep bleeders

Platelets	Normal count
PT	Normal
PTT	Prolonged, corrects on mixing study
Fibrinogen and D-dimer	Normal
Smear	Normal
Bleeding pattern	Deep and delayed: hemarthrosis and muscle hematomas, X linked in boys
The lock	Isolated long PTT that corrects on mixing. Factor VIII low is A, factor IX low is B.

Vitamin K deficiency: the PT-first bleed

Platelets	Normal
PT	Prolonged first
PTT	Prolonged later
Fibrinogen and D-dimer	Normal
Smear	Normal
Bleeding pattern	Newborn without prophylaxis, malabsorption, prolonged antibiotics, or warfarin effect
The lock	Factors II, VII, IX, and X cannot be activated. Factor VII has the shortest half-life so PT rises first.

Low platelets and schistocytes. PT, PTT, fibrinogen, and D-dimer are all normal. Which fits?

Correct. Schistocytes with clean coags means microangiopathy without consumption. Normal fibrinogen and normal D-dimer rule out DIC. This is TTP from ADAMTS13 deficiency, so plasma exchange, not platelets.

Look again at the coags. DIC consumes fibrinogen and spikes D-dimer and prolongs PT and PTT. This stem keeps all of those normal, so the consumption that defines DIC is not happening. This is TTP.

An adult on warfarin-style physiology bleeds. PT is long, PTT is mildly long, platelets normal, fibrinogen normal, D-dimer normal. Which fits?

Correct. Normal platelets, fibrinogen, and D-dimer mean nothing is being consumed. PT prolonging before PTT points to vitamin K dependent factors, and factor VII falls first because it has the shortest half-life.

DIC would drop the platelets and fibrinogen and raise the D-dimer. This panel keeps that trio normal. A normal consumption trio with PT leading is vitamin K deficiency or warfarin effect, not DIC.

Lifelong nosebleeds and heavy menses. PTT is long, PT normal, platelet count normal, bleeding time long. Which fits?

Correct. The mucosal surface plus a long bleeding time plus a normal platelet count is von Willebrand disease. Low von Willebrand factor lowers factor VIII too, which is why the PTT can stretch.

Hemophilia gives deep bleeding such as hemarthrosis with a normal bleeding time, and it is X linked in boys. This stem is mucosal with a long bleeding time, which is von Willebrand disease.

Board walkthrough

Read the panel, then commit.

One vignette appears at a time. Right-click or long-press to cross out an option. Double-click or double-tap to highlight an option. Answer choices are shuffled each round.

Vignette 1 of 6 Never-repeat tracking ready

Exam tools: right-click or long-press to cross out. Double-click or double-tap to highlight. A tool gesture will not submit the answer.

Final locks

Compress it into three reads.

If the stem gets noisy, run these three reads in order and most board traps collapse.

Read the surface

Mucocutaneous bleeding, that is petechiae, purpura, gums, and menses, is primary hemostasis. Deep and delayed bleeding, that is hemarthrosis and muscle hematomas, is secondary hemostasis.

Read the consumption trio

Low fibrinogen plus high D-dimer plus long PT and PTT is DIC. Schistocytes with a normal trio is TTP. Both shear red cells, only DIC eats the factors.

Split the times

PT leading with a normal trio is vitamin K. Isolated long PTT is hemophilia or von Willebrand. Mixing study corrects means a missing factor, not an inhibitor.

Keep studying heme

Use this decoder before you reach for a name on any bleeding stem. When you are ready, push deeper into the platelet, factor, and joint mechanisms.

Platelet disorders Coagulation cascade Hemophilic arthropathy