This unit is about the blood and the heart. Module 9, Blood Disorders, covers the anemias, B12 and pernicious anemia, thalassemia, polycythemia vera, the bleeding and clotting disorders such as von Willebrand disease and DIC, and transfusion reactions. Module 10, Cardiovascular, covers coronary artery disease and heart attack, heart failure, high blood pressure, abnormal rhythms, inflamed and leaky heart valves, poor circulation in the limbs, and heart defects present at birth. The exam has 50 questions, both multiple choice and select-all-that-apply.
Anemia means the blood carries less oxygen, because the hemoglobin or the red cell count is low. Whatever the cause, the general signs are the same: tiredness, pale skin, a fast heart rate, shortness of breath with effort, dizziness, and feeling cold. All of them come from tissues going short on oxygen.
| Type | Patho and Cause | Telltale Clue |
|---|---|---|
| Iron-deficiency (microcytic) | Too little iron, so hemoglobin falls. It comes from blood loss, too little iron in food, or pregnancy | A low ferritin, spoon-shaped nails (koilonychia), and craving odd things to eat (pica) |
| Thalassemia (microcytic) | An inherited defect. The body makes less globin chain, so the red cells come out abnormal and fragile | Normal iron studies, target cells, and a family history |
| B12 / folate (macrocytic) | DNA cannot be built properly, so the red cells come out large and immature | B12 brings nerve signs, such as tingling and an unsteady walk. Folate does not |
| Sickle cell (normo, hemolytic) | A single point mutation. HbS sickles when oxygen runs low, which blocks vessels and breaks cells apart | Pain crises. The triggers are low oxygen, dehydration, infection, and cold |
| Aplastic (normo) | The bone marrow fails, so every blood line drops. Causes are drugs, radiation, or no known reason | All three lines are low, so you get anemia, infections, and bleeding. The reticulocyte count is low |
| Hemolytic (normo) | Red cells are destroyed faster than the body can make them | A high reticulocyte count, a high indirect bilirubin, a high LDH, and a low haptoglobin, plus jaundice |
Pernicious anemia is the classic cause of low B12. The immune system destroys intrinsic factor, which the stomach's parietal cells make, so B12 cannot be absorbed. The signs are a macrocytic anemia plus nerve symptoms, such as numbness, tingling, and poor balance, along with a sore tongue and tiredness.
Here is the other half of Module 9: too little clotting, which gives bleeding disorders. Too much clotting that uses everything up, which is DIC. Too many cells, which is polycythemia vera. And the dangerous transfusion reaction.
| Disorder | Patho |
|---|---|
| Von Willebrand disease | There is too little von Willebrand factor, or it does not work. Platelets cannot stick well, so you get bleeding from mucous membranes, such as nosebleeds, easy bruising, and heavy periods. The tests that confirm it are the vWF antigen level, vWF activity by the ristocetin cofactor assay, and a platelet function assay. The old bleeding time test was dropped years ago because it was unreliable, so do not name it. This is the most common inherited bleeding disorder. |
| Disseminated intravascular coagulation (DIC) | Clotting breaks out everywhere and uses up the platelets and clotting factors. After that comes heavy bleeding. It is set off by sepsis, trauma, problems in childbirth, or cancer. Labs show a long PT, a long aPTT, low platelets, low fibrinogen, and a very high D-dimer. |
| Polycythemia vera | A JAK2 mutation makes the marrow pour out too many red cells, and sometimes white cells and platelets too. The blood turns thick and syrupy. Signs are a red, ruddy face, headache, itching after a warm shower, high blood pressure, and a risk of clots. |
| Acute hemolytic transfusion reaction | The blood type does not match, so this is ABO incompatibility. The patient's own antibodies attack the donor red cells and break them apart inside the vessels within minutes. |
If the blood given does not match the ABO type, the patient's existing antibodies latch onto the donor red cells and destroy them. Within minutes you see fever, chills, flank or back pain, dark urine from hemoglobin, and a falling blood pressure. It can move on to shock, DIC, and kidney injury. The first thing you do: STOP the transfusion. Keep the IV line open with saline.
Atherosclerosis is fatty plaque building up inside artery walls. It is the root of coronary artery disease (CAD), heart attack, stroke, and poor circulation in the limbs.
| You Can Change These | You Cannot Change These |
|---|---|
| Smoking, high blood pressure, a high LDL or low HDL, diabetes, extra weight, sitting too much, a poor diet, and stress | Age, being male, and family history or genes |
When the heart muscle needs more oxygen than it gets, it goes short on blood. The range runs from angina all the way to a full heart attack.
| Condition | Patho | Main Features |
|---|---|---|
| Stable angina | A fixed narrowing. The muscle goes short on oxygen only when demand rises, as with effort | The pain is predictable and eases with rest or nitroglycerin. No cells die |
| Unstable angina | The plaque tears and a partial clot forms, so the muscle goes short on oxygen at rest | New or worsening pain at rest, with a normal troponin, since no muscle has died yet. Treat it as a warning |
| NSTEMI | The artery is partly blocked, so the infarct hits the inner layer of muscle | Troponin is up, with ST depression or T-wave changes, but no ST elevation |
| STEMI | The artery is completely blocked, so the infarct goes through the full thickness of muscle | Troponin is up AND the ST segment is elevated. This is a true emergency, so open the artery fast |
Troponin is a protein that leaks out when heart muscle is damaged. So it is high in a heart attack, both NSTEMI and STEMI, and in other heart muscle injury such as myocarditis. It is the lab that separates unstable angina, with a normal troponin, from an infarct, with a high troponin. The classic symptoms are crushing chest pain behind the breastbone, which may spread to the left arm or jaw, along with sweating, nausea, and shortness of breath. Women, older adults, and people with diabetes often have less typical symptoms.
The most common cause of sudden cardiac death is a deadly ventricular rhythm, usually ventricular fibrillation. It is almost always set off by coronary artery disease and a heart muscle short on blood.
Heart failure means the heart cannot pump enough to meet the body's needs. Split it two ways. Ask which side is failing, and ask whether the problem is squeezing or filling.
| Systolic HF (HFrEF) | Diastolic HF (HFpEF) | |
|---|---|---|
| The problem | A weak pump. The squeeze is weaker, so the ejection fraction drops below 40% | A stiff ventricle. It cannot relax and fill, but the ejection fraction stays above 50% |
| Causes | A heart attack, a stretched-out (dilated) heart muscle, long-term lack of blood flow, or a leaky valve | Years of high blood pressure that thickened the left ventricle, a thickened or stiff heart muscle, and aging |
| Left-sided HF | Right-sided HF | |
|---|---|---|
| Blood backs up into | the lungs | the veins and the rest of the body |
| Signs | Shortness of breath, trouble breathing when lying flat, crackles, pink frothy sputum, and fluid in the lungs | Bulging neck veins, swollen legs, a large liver, fluid in the belly, and weight gain |
| Common cause | High blood pressure, poor blood flow, or valve disease | Most often left-sided heart failure. Lung disease can also do it, which is called cor pulmonale |
Hypertension means the pressure in the arteries stays too high. It is usually quiet, with few symptoms, until it has damaged organs. That is why people call it the silent killer.
| Organ | Damage |
|---|---|
| Heart | The left ventricle thickens, which leads to heart failure. It also speeds up coronary artery disease and heart attack |
| Brain | Stroke, and aneurysm |
| Kidneys | Long-term kidney disease, because the small kidney vessels get damaged |
| Eyes / vessels | Damage to the retina, an aneurysm or a torn artery, and poor circulation in the limbs |
When the blood volume drops after bleeding, the body defends the blood pressure in a set order:
An arrhythmia is an abnormal heart rhythm, caused by disordered electrical activity. The exam favorite is atrial fibrillation.
It depends on the rate and rhythm. You may see less blood pumped, which brings dizziness, fainting, and low blood pressure. You may see a clot that travels and causes a stroke, as in AFib. You may see heart failure. And with the deadly ventricular rhythms, VT and VF, you can see sudden cardiac death.
Infection and inflammation can hit each layer of the heart, and the valves too. Match the layer to the disease.
| Condition | Patho and Signs |
|---|---|
| Pericarditis | Inflammation of the pericardium, the sac around the heart. It gives sharp chest pain that is worse with a breath and eases when you sit and lean forward. You hear a rubbing sound |
| Pericardial effusion | Fluid collects in the sac around the heart. It can muffle the heart sounds and cause shortness of breath |
| Cardiac tamponade | A large or fast-growing pocket of fluid squeezes the heart, so it cannot fill, and the output falls. Beck's triad is low blood pressure, bulging neck veins, and muffled heart sounds. It is an emergency, treated by draining the fluid |
| Myocarditis | Inflammation of the myocardium, the muscle itself, and it is often viral. The pump weakens, rhythms go off, and heart failure can follow. The troponin may rise |
| Infective endocarditis | Infection of the endocardium and the valves, which grows clumps called vegetations. Look for fever, a new murmur, Janeway lesions, Osler nodes, and splinter hemorrhages. The risk is higher with IV drug use and artificial valves |
| Rheumatic heart disease | An immune reaction after an untreated strep infection, which is rheumatic fever. Over time it scars the heart valves, and the mitral valve most of all |
These are vessel problems outside the heart. Blood may have trouble getting in through the arteries, trouble getting back through the veins, or the vessels may clamp down in spasms.
| Condition | Patho and Signs |
|---|---|
| Peripheral artery disease (PAD) | Atherosclerosis narrows the leg arteries, so blood has trouble getting in. Signs: cramping leg pain with walking, called claudication, plus cool, pale, hairless legs, weak pulses, pain that worsens when the leg is raised, and wounds that will not heal. The ulcers show up on the toes and feet |
| Claudication | This is the telltale sign of PAD: cramping pain in the leg or calf when you walk, which eases with rest. The muscle runs short on blood once it starts asking for more |
| Chronic venous insufficiency | The valves in the veins fail, so blood has trouble getting back and it pools in the legs. Signs: swelling, brown-stained skin, and ulcers on the inner ankle. Over time it brings lasting ulcers and a risk of deep vein clots |
| Raynaud's | The small arteries spasm shut, set off by cold or stress. The fingers or toes turn white, then blue, then red, with numbness, and then they warm back up |
Congenital heart defects are problems with the heart's structure that are there at birth. The key split is cyanotic vs non-cyanotic. It depends on one thing: does blood without oxygen reach the body?
| Non-cyanotic (acyanotic) | Cyanotic | |
|---|---|---|
| Which way blood crosses | Left to right. Blood that already has oxygen goes back through the lungs again | Right to left. Blood without oxygen goes out to the body |
| Cyanosis? | No. The blood going out still has oxygen | Yes. The skin turns bluish |
| Examples | VSD, ASD, PDA, and a narrowed aorta (coarctation) | Tetralogy of Fallot, and transposition of the great arteries |
There are four defects, and the memory aid is PROVe: Pulmonary stenosis, Right ventricular hypertrophy, Overriding aorta, and a Ventricular septal defect. The narrowed pulmonary valve plus the hole in the septum push blood without oxygen out to the body, so the child turns blue. Signs: bluish skin and "tet spells", where the blue deepens with crying or feeding. The child may squat to break a spell.
| Easy to confuse | The key difference |
|---|---|
| Iron deficiency vs thalassemia | Both are microcytic. Iron deficiency has a low ferritin. Thalassemia has normal iron and is inherited. |
| B12 vs folate | Both are macrocytic. Only B12 brings nerve signs. |
| Unstable angina vs NSTEMI | Both bring pain at rest with no ST elevation. Only NSTEMI has a positive troponin, which means muscle died. |
| NSTEMI vs STEMI | STEMI has ST elevation and a total blockage, so open the artery right away. |
| Systolic vs diastolic HF | Systolic is a weak squeeze, with a low EF. Diastolic is a stiff heart that cannot fill, with a normal EF. |
| Left vs right HF | Left means Lungs, with crackles and shortness of breath. Right means the Rest of the body, with bulging neck veins and swelling. |
| Preload vs afterload | Preload is the volume coming in, which stretches the heart. Afterload is the resistance it pushes against, and high blood pressure raises it. |
| AFib vs VFib | AFib brings a stroke risk, so give blood thinners. VFib is cardiac arrest, so defibrillate. |
| Effusion vs tamponade | An effusion is just fluid. A tamponade is fluid squeezing the heart, which gives Beck's triad, and it is an emergency. |
| PAD (arterial) vs venous insufficiency | Arterial means cool and pale, with claudication and toe ulcers. Venous means swelling, brown skin, and ankle ulcers. |
| Cyanotic vs non-cyanotic defects | Left to right means no blue skin, as in VSD, ASD, and PDA. Right to left means blue skin, as in ToF and transposition. |
Anemia: the blood carries less oxygen, because the hemoglobin or the red cell count is low.
MCV: the average size of a red cell. It sorts anemia into microcytic, normocytic, or macrocytic.
Ferritin: stored iron. It runs low in iron-deficiency anemia.
Intrinsic factor: a stomach protein the body needs to absorb B12. It is lost in pernicious anemia.
von Willebrand factor: the protein that helps platelets stick. There is too little of it in vWD.
DIC: disseminated intravascular coagulation. Clotting breaks out everywhere, then the patient bleeds.
Polycythemia vera: a JAK2 mutation makes too many red cells, so the blood turns thick and clots form.
Atherosclerosis: fatty plaque building up inside artery walls.
Troponin: a protein released when heart muscle is injured. It rises in a heart attack and in myocarditis.
STEMI / NSTEMI: a complete versus a partial blockage of a coronary artery, both causing an infarct.
Ejection fraction: the percent of blood the ventricle pushes out per beat. It drops in systolic heart failure.
Preload / Afterload: the volume filling the ventricle / the resistance it pushes against.
BNP: a peptide the heart releases when it is stretched. It runs high in heart failure.
Atrial fibrillation: disorganized electrical activity in the atria, which brings a clot and stroke risk.
Cardiac tamponade: fluid around the heart squeezing it, which gives Beck's triad.
Claudication: leg pain with walking that eases with rest, seen in PAD.
Tetralogy of Fallot: a cyanotic defect with pulmonary stenosis, right ventricular hypertrophy, an overriding aorta, and a VSD.