Exam 5 · Week 9 · BIO 280 Pathophysiology
M9 · Anemia · Blood Disorders · Hypertension
Why every anemia ends in tissue hypoxia, what platelets do when they fail, and why hypertension is called silent.
▸M9Anemia · Blood Disorders · HypertensionWeek 9
💡 The one idea
Every anemia, whatever its cause, ends in the same place: not enough oxygen reaching tissue. That is why they all share fatigue, pallor, tachycardia and breathlessness — and why the cause is what makes them different, not the symptoms.
Classify by cell size first: small, normal, or large. That one number narrows it immediately.
🩸 Anemia by cell size
| MCV | Type | Causes | Clue |
|---|---|---|---|
| Low microcytic | Small, pale cells | Iron deficiency (commonest of all), thalassemia, chronic disease | Pica, spoon nails (koilonychia), low ferritin |
| Normal normocytic | Normal size, too few | Acute blood loss, hemolysis, chronic kidney disease, aplastic anemia | In CKD the problem is erythropoietin, not iron |
| High macrocytic | Large, immature cells | B12 deficiency, folate deficiency | B12 causes neurological signs — numbness, tingling, gait and balance problems. Folate does not. |
Pernicious anemia is B12 deficiency caused by loss of intrinsic factor — so oral B12 cannot be absorbed and it must be given by injection, for life.
Giving folate to someone who is actually B12 deficient corrects the blood count and lets the neurological damage continue silently. Check both.
🪨 Sickle cell and thalassemia
Sickle cell is autosomal recessive. Under stress — hypoxia, dehydration, infection, cold, acidosis, high altitude — hemoglobin S polymerises, the cell stiffens into a sickle, and it jams small vessels.
- Vaso-occlusive crisis — severe pain, most often in bones, chest and abdomen. Treatment is hydration, oxygen, analgesia (opioids are appropriate) and warmth.
- Acute chest syndrome — chest pain, fever, hypoxia and a new infiltrate. A leading cause of death.
- Functional asplenia — repeated infarction destroys the spleen, so these patients are at high risk from encapsulated organisms. Vaccination matters enormously.
Cold and dehydration both trigger sickling. Never apply cold to a painful crisis — warmth and fluids, not ice.
🚨 Platelets and clotting
| Disorder | What happens | Key point |
|---|---|---|
Thrombocytopenia<150,000 |
Too few platelets — petechiae, purpura, bleeding gums | Spontaneous bleeding risk rises sharply below 20,000 |
| ITP | Autoimmune destruction of platelets | Otherwise well patient with a low count |
| DIC | Clotting and bleeding at the same time. Widespread microthrombi consume the clotting factors and platelets, so the patient then bleeds from everywhere. | Low platelets, low fibrinogen, high D-dimer, prolonged PT/aPTT. Triggered by sepsis, trauma, obstetric emergency, malignancy. |
| Hemophilia | X-linked recessive factor deficiency (A = factor VIII, B = factor IX) | Deep bleeding — into joints and muscle, not petechiae |
| Von Willebrand | Commonest inherited bleeding disorder | Mucosal bleeding, easy bruising, heavy periods |
Platelet problems bleed into the skin (petechiae, purpura, mucosa). Factor problems bleed deep (joints, muscles, after surgery). That distinction sorts most questions.
❤️ The healthy heart, in one card
Cardiac output = heart rate × stroke volume. Stroke volume depends on three things:
- Preload — how full the ventricle is before it contracts. Volume.
- Afterload — the resistance it must push against. Mostly blood pressure.
- Contractility — how hard the muscle squeezes.
Frank–Starling: more stretch gives a stronger contraction — up to a point. Past that point the fibers are overstretched and output falls. That failure point is heart failure.
Ejection fraction normal 55–70%. Below 40% is
systolic failure.
⭐ Hypertension — the silent one
| Category | Systolic | Diastolic | |
|---|---|---|---|
| Normal | <120 | and | <80 |
| Elevated | 120–129 | and | <80 |
| Stage 1 | 130–139 | or | 80–89 |
| Stage 2 | ≥140 | or | ≥90 |
| Crisis | >180 | and/or | >120 |
Primary (essential) hypertension is ~90–95% — no single identifiable cause. Secondary has one: renal disease, renal artery stenosis, hyperaldosteronism, phaeochromocytoma, sleep apnea, oral contraceptives.
It is called silent because it damages arteries for years without a single symptom. Headache and nosebleed are late, not early.
End-organ damage: heart (LVH, failure, MI), brain (stroke), kidney (nephropathy), eyes (retinopathy), vessels (aneurysm, peripheral arterial disease).
In a hypertensive emergency the pressure is lowered gradually. Dropping it too fast causes cerebral, cardiac and renal hypoperfusion — a stroke caused by the treatment.
🎯 Module quiz
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