Exam 4 Β· Week 9 Β· Standalone study page
M9 Β· Hematologic Disorders
This page keeps all of the original course information, while reducing the decision to one module: blood cells, clotting, transfusion and safety.
βΈM9Hematologic DisordersWeek 9
π‘ The one idea
Anemia is not one disease β it is three different failures. Not making cells, losing cells, or destroying cells. The cell size tells you which.
| Anemia | Cell size | Cause | Signature |
|---|---|---|---|
| Iron deficiency | Microcytic, small | Blood loss, poor intake | Most common; pica, spoon nails |
| B12 deficiency | Macrocytic, large | No intrinsic factor | Neuro signs β numbness, gait |
| Folate deficiency | Macrocytic | Poor diet, alcohol | Same but no neuro signs |
| Aplastic | Normocytic | Marrow fails | All three lines low |
| Sickle cell | Normocytic | Genetic Hgb S | Pain crises, triggered by hypoxia and dehydration |
β The distinction they test
B12 and folate look identical on a blood count. The difference is neurological: B12 deficiency causes numbness, tingling and gait problems. Folate does not.
Pernicious anemia is a lack of intrinsic factor, so oral B12 will not absorb β it needs lifelong IM injections.
π Iron teaching, four points
- Take with vitamin C (orange juice) β it doubles absorption
- Best on an empty stomach; with food if it upsets the gut
- Stools turn black and tarry β this is expected, not bleeding
- Liquid iron through a straw β it stains teeth. Z-track for IM
π¨ Transfusion reactions β first action is always the same
Never restart a transfusion after a reaction, and never flush the existing line - that pushes more blood in.
Stay with the patient for the first 15 minutes; that is when most severe reactions begin. Blood must infuse within 4 hours, and only normal saline may share the line.
π©Έ DIC β clotting and bleeding at once
Widespread clotting consumes the clotting factors and platelets, so the patient then bleeds everywhere. Labs: low platelets, low fibrinogen, prolonged PT/aPTT, high D-dimer.
Treatment is treat the cause β usually sepsis, obstetric emergency, or major trauma.
β High-yield β what the exam actually asks
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- MCV sorts the anemias: microcytic = iron deficiency; normocytic = chronic disease or kidney; macrocytic = B12, folate or alcohol. Ferritin low + TIBC high = iron deficiency. Hgb electrophoresis confirms sickle cell. Bone marrow biopsy (posterior iliac crest) diagnoses aplastic anemia and leukemia.
- Fatigue is the #1 anemia sign. Transfuse chronic anemia around Hgb
<7 g/dL; long-term management is subQ epoetin alfa. - Polycythemia vera is the opposite β marrow overproduces RBCs β thick blood, ruddy face, itching after a warm shower, splenomegaly, high clot risk. Therapeutic phlebotomy is the mainstay; nursing priority is clot prevention.
- Sickle cell crisis: IV fluids, IV opioids (PCA/morphine, not PO Tylenol β do not withhold opioids), oxygen, transfusion PRN. Ice is contraindicated. Prevention: avoid high altitude and temperature extremes.
- Leukemia crowds out normal marrow β the pancytopenia triad: infection, bleeding/bruising, fatigue.
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- Hodgkin lymphoma has Reed-Sternberg cells, painless cervical/supraclavicular nodes, B symptoms (fever, night sweats, weight loss), orderly contiguous spread, better prognosis. Non-Hodgkin has no Reed-Sternberg cells and spreads unpredictably.
- Multiple myeloma CRAB: Calcium elevated, Renal failure, Anemia, Bone lesions and pathologic fractures. Push fluids to protect the kidneys; fall and fracture precautions.
- Platelets normal
150,000β450,000/mmΒ³; fibrinogen170β340 mg/dL. Neutropenic precautions start at ANC<1,000/mmΒ³. - Thrombocytopenia precautions: electric razor, soft toothbrush, no NSAIDs/aspirin/heparin, stool softeners to prevent straining, minimize IV sticks, check stool for occult blood.
- Hemophilia: give clotting factor before and after any procedure. Priority labs are coags, not CBC (platelets are normal). Compression beats a factor injection if she is bleeding right now. Ice, not heat. No aspirin. Deep joint bleeds are ~
75%of bleeds.
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- Von Willebrand is the most common inherited bleeding disorder β heavy menses is often the presenting complaint. DDAVP for mild disease.
- DIC: bleeding and clotting at once from an underlying cause. Labs: PT/PTT/INR up, platelets down, fibrinogen down, FDPs up. Treat the cause first (antibiotics for sepsis) β fluids β heparin β blood products.
- Transfusions: two-nurse verification, 0.9% NS only (dextrose hemolyzes, LR clots), stay with her the first
15 min, infuse within4 hours. - Reactions: acute hemolytic (ABO mismatch β fever, chills, flank pain, hemoglobinuria); febrile non-hemolytic (most common); allergic/anaphylactic; TRALI (respiratory distress without overload signs); TACO (crackles, JVD, hypertension from too much too fast).
π§ From the LSC exam-prep recording
What the faculty actually said in the review session for this week β their numbers, their worked calculations, their priority rulings. On an exam, this beats the textbook.
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- HIT: platelets
220,000→90,000in 48 hours on day 7 of heparin. Stop the heparin, daily platelet counts, notify, and assess for thrombosis — HIT clots as well as bleeds. Do not give vitamin K (that is warfarin’s antidote) and do not start warfarin. Heparin is monitored with aPTT, not the platelet count. Warfarin → PT/INR. - Aplastic anemia hits all three cell lines. Masks, handwashing, transfusions, bleeding precautions. An iron-rich diet does nothing β the marrow is not short of raw material, it is shut down.
- DIC lab triad: βplatelets, βfibrinogen, βD-dimer. To address organ ischemia specifically the answer is oxygen and IV fluids β holding pressure and vitamin K do not perfuse organs.
- ITP: petechiae and a 10-minute nosebleed can wait. Severe headache with vomiting in a thrombocytopenic client means intracranial hemorrhage.
- Von Willebrand is treated with desmopressin β the same drug as DI. Avoid IM injections, aspirin and contact sports; soft toothbrush; watch for hematuria and melena.
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- Hemophilia: a clotting factor is missing, so the platelet plug never stabilizes. A hemarthrosis is not simply rested — elevate, give factor replacement, no ROM, because the joint is far too painful to exercise through. Never aspirin or NSAIDs.
- Pressure-holding times: 5 minutes for venipuncture, 10+ for arterial. "2 minutes" is a distractor.
- Platelets: under 20,000, and especially under 10,000, is significant bleeding risk. They used both 150,000β450,000 and 140,000β400,000 as "normal" and told students not to be thrown by lab-to-lab variation.
- Multiple myeloma trend case: calcium
10.2 β 11.6 β 13.2, creatinine1.1 β 1.6 β 2.4, with confusion, vomiting and falling urine output. The immediate-intervention findings are calcium, creatinine, confusion, decreased output. - Myeloma care: fluids 3 L/day to flush M proteins Β· fall precautions, because some fracture just standing up Β· a walker, not a cane or a wheelchair β a cane is not stable enough and a wheelchair deconditions her Β· monitor hypercalcemia Β· NSAIDs contraindicated.
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- Bisphosphonates: sit upright, full glass of water, stay upright 30β60 minutes.
- Calc (reconstitution): 1 g at 250 mg/mL β add
4 mL. 1.5 g to yield 300 mg per 2 mL β add10 mL.
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- Aplastic anemia: the marrow is not producing. Iron will not help β the building blocks are already there. More oxygen will not raise a hemoglobin either. She needs transfusion and marrow support, and she will not build stamina until the hemoglobin comes up.
- ITP: an immune destruction of platelets, commoner in children. Petechiae are expected; the feared event is intracranial hemorrhage. Short term steroids and IVIG; long term splenectomy, because the spleen is doing the destroying.
- Bleeding precautions: no intramuscular injections β bleeding into muscle is prolonged and painful β soft-bristled toothbrush, monitor for hematuria and melaena, and teach her the signs of internal bleeding.
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- TRALI: sudden dyspnea within hours of starting a transfusion. Stop the transfusion, keep the line open with normal saline, oxygen, notify. Do not flush the remaining blood through.
- Transfusion reactions by severity: a febrile reaction is the mildest and the transfusion may only be paused. A hemolytic reaction and TRALI are stop-immediately-and-do-not-restart.
- Urine output is the floor: 30 mL/hr is the minimum accepted. Below that the kidneys are being sacrificed to keep the heart and brain perfused.
- Sickle cell crisis: hydration and oxygen come before anything else — the cells are sickling precisely because they are short of oxygen and fluid.
- Reconstitution: read the target concentration, not the vial. If you hold 1 g and need 300 mg in every 2 mL, work to the concentration they asked for and stop when the units cancel.
β οΈ Exam traps
- TRALI vs TACO β the discriminator is whether there are fluid-overload signs.
- Hemophilia checks coags; thrombocytopenia checks platelets.
- For any suspected reaction: stop the transfusion, keep the line open with NS on new tubing, stay with her, then notify.
⚠️ What it turns into — the complication for each one
The disorder cards below run definition, causes, signs, diagnostics, management and nursing. This is the part they do not have, and it is where the exam lives: so what happens if this is missed or left? Too few red cells, too few platelets, too few neutrophils — each has its own emergency. In neutropenia a fever is the emergency, because there are no cells left to make the usual signs.
| Disorder | What it turns into |
|---|---|
| Iron deficiency anemia | High-output heart failure when the anemia is severe and long-standing, poor growth and developmental delay in a child, and the harms of pica itself |
| Vitamin B12 deficiency and pernicious anemia | Neurologic damage that does not reverse — paraesthesia, ataxia, loss of proprioception and cognitive change. This is why B12 deficiency must not be treated with folate alone: the blood picture improves while the nerves keep dying. Raised gastric cancer risk |
| Sickle cell disease | Vaso-occlusive crisis, acute chest syndrome, stroke in children, splenic sequestration, aplastic crisis, priapism, and chronic damage to kidney, retina and bone. Functional asplenia means overwhelming infection by encapsulated organisms |
| Aplastic anemia and neutropenia | Neutropenic fever is a medical emergency — sepsis with no localising signs, no pus, sometimes no raised white count. Bleeding from thrombocytopenia, and dependence on transfusion or transplant |
| Thrombocytopenia and ITP | Spontaneous bleeding, intracranial hemorrhage, and GI bleeding. The number that changes the plan: spontaneous bleeding risk climbs sharply below 20,000 |
| Disseminated intravascular coagulation | Clotting and bleeding at the same time — microthrombi starving organs while the clotting factors run out and she bleeds from every puncture site. Organ failure and death; the treatment is treating the cause |
🩸 The hematologic disorders, section by section
The anemias first, grouped by what is missing, then the marrow and platelet problems, then DIC. Same six sections every time.
Iron Deficiency AnemiaOpenClose
Definition and Overview
Too little iron to build hemoglobin, so red cells come out small and pale — microcytic and hypochromic. It is the commonest anemia in the world. The important clinical point is that in an adult, especially a man or a postmenopausal woman, iron deficiency is a symptom of blood loss until proved otherwise, and the search for the source matters more than the iron tablets.
Causes and Risk Factors
Chronic blood loss — heavy menstrual bleeding, gastrointestinal bleeding from ulcers, cancer, or long-term NSAID or aspirin use, and repeated blood donation. Inadequate intake in restrictive diets, poverty and food insecurity. Malabsorption after gastric surgery, with celiac disease, or with long-term proton pump inhibitors. Increased demand in pregnancy, infancy and adolescence.
Clinical Manifestations
Fatigue, pallor (check conjunctivae, palms and nail beds, not just the face), exertional dyspnea, tachycardia, headache, dizziness and cold intolerance. More specifically: spoon-shaped nails (koilonychia), cracks at the corners of the mouth, a smooth sore tongue, and pica — craving ice, clay or starch. It comes on slowly, so people accommodate to it and describe themselves as fine.
Assessment and Diagnostic Findings
Low hemoglobin and hematocrit, low MCV and MCH, high RDW, low serum ferritin (the most useful single test), low serum iron, high total iron-binding capacity and low transferrin saturation. Then find the bleeding: faecal occult blood testing, endoscopy and colonoscopy in adults. Reticulocyte count to watch the response to treatment.
Medical Management
Treat the cause, then replace the iron. Oral ferrous sulfate is first line; intravenous iron for malabsorption, intolerance or ongoing heavy loss. Transfusion only for symptomatic severe anemia. Continue iron for 3 to 6 months after the hemoglobin normalises to refill the stores — stopping when the count is normal is why it recurs.
Nursing Management and Client Education
Teach how to take iron so it actually works: on an empty stomach, with vitamin C or orange juice, which increases absorption; away from milk, antacids, calcium, tea, coffee and whole grains, which block it; and with food only if the stomach cannot tolerate it otherwise. Warn that it turns the stools black and causes constipation, so start fiber and fluids at the same time — and that black stools from iron are expected, but tarry, sticky or foul-smelling stools are bleeding and must be reported. Liquid iron is taken through a straw and the teeth rinsed afterwards to prevent staining. Keep iron out of children's reach — iron overdose is a leading cause of poisoning death in young children. Teach iron-rich foods: red meat, liver, beans, lentils, dark leafy greens and fortified cereals. Plan rest around activity, and expect the energy to take weeks, not days, to come back.
Vitamin B12 Deficiency and Pernicious AnemiaNeuro damage is permanentOpenClose
Definition and Overview
Too little vitamin B12, so red cells are made large and immature — megaloblastic, macrocytic. Pernicious anemia is the specific autoimmune form: antibodies destroy the gastric parietal cells, so no intrinsic factor is made and B12 cannot be absorbed in the ileum however much is eaten. The critical difference from other anemias is that B12 deficiency also damages the nervous system, and that damage becomes permanent.
Causes and Risk Factors
Pernicious anemia (autoimmune, associated with other autoimmune disease, more common with age). Loss of the absorbing surface: gastrectomy or bariatric surgery, ileal resection, Crohn disease, celiac disease. Drugs: metformin and long-term proton pump inhibitors. Diet: strict vegan diet without supplementation. Alcohol use disorder.
Clinical Manifestations
The anemia symptoms — fatigue, pallor, dyspnea, tachycardia — plus two things that mark it out. A smooth, beefy red, sore tongue, and neurological signs: symmetrical numbness and tingling in the hands and feet, loss of position and vibration sense, an unsteady wide-based gait, muscle weakness, and memory loss, irritability or confusion. Giving folic acid alone corrects the blood picture while the neurological damage continues silently — which is why the two deficiencies must be told apart before treatment. Mild jaundice and pallor together give the classic lemon-yellow tint.
Assessment and Diagnostic Findings
Low hemoglobin with a high MCV, hypersegmented neutrophils on the film, low serum B12, and raised methylmalonic acid and homocysteine, which rise before B12 falls. Intrinsic factor antibodies and anti-parietal cell antibodies confirm pernicious anemia; the Schilling test is historical. Check folate at the same time. Neurological examination including gait, vibration and proprioception, and a documented fall risk.
Medical Management
Vitamin B12 replacement — and in pernicious anemia it must bypass the gut, so it is given by intramuscular injection, monthly and for life, or as high-dose oral or intranasal B12 where absorption allows. Dietary deficiency is corrected with oral supplementation and diet. Treat the underlying bowel disease or stop the offending drug where possible. Recheck the blood count and reticulocytes to confirm response.
Nursing Management and Client Education
Say plainly that the injections are lifelong. Clients stop them when they feel better, and the anemia returns while the nerve damage worsens; that is the single most important piece of teaching on this card. Teach self-injection or arrange a reliable schedule. Fall precautions while position sense is impaired — good lighting, no loose rugs, well-fitting shoes, an assistive device if the gait is unsteady. Because sensation is reduced, teach the client to check the water temperature with a thermometer or an unaffected part of the body, and to inspect the feet daily. Gentle mouth care with a soft brush and bland foods for the sore tongue. Teach B12-rich foods — meat, fish, eggs, dairy, fortified cereals — and for vegans, that supplementation is not optional. Pace activity and rest, and reassure that the anemia symptoms improve within weeks even though the neurological recovery is slower and may be incomplete.
Sickle Cell DiseaseHydration and oxygenOpenClose
Definition and Overview
An inherited disorder of hemoglobin: hemoglobin S distorts red cells into a rigid sickle shape when it gives up oxygen. The sickled cells block small vessels, causing ischemic pain and organ damage, and they break down early, causing a chronic haemolytic anemia. It is autosomal recessive — two copies give the disease, one copy gives sickle cell trait, which is usually asymptomatic.
Causes and Risk Factors
Inherited, and most common in people of African, Mediterranean, Middle Eastern and Indian ancestry. A crisis is precipitated by anything that increases oxygen demand or reduces oxygen supply: infection, dehydration, hypoxia, high altitude, cold exposure, strenuous exercise, stress, alcohol, smoking, pregnancy and surgery.
Clinical Manifestations
Vaso-occlusive crisis is the commonest: sudden severe pain in the bones, joints, chest, back or abdomen, with swelling of the hands and feet in small children (dactylitis). Chronic anemia with jaundice, gallstones and delayed growth. Then the organ damage: acute chest syndrome — chest pain, fever, cough and hypoxia, and the leading cause of death; stroke; splenic sequestration; priapism; leg ulcers; retinopathy; and renal failure. Fever in sickle cell disease is an emergency — the spleen is functionally absent, so overwhelming infection can kill within hours.
Assessment and Diagnostic Findings
Hemoglobin electrophoresis is the diagnostic test; newborn screening finds most cases. During a crisis: pain score using the client's own scale, oxygen saturation, temperature, CBC and reticulocytes, and hydration status. Chest x-ray for any chest symptom, fever or hypoxia, looking for acute chest syndrome. Transcranial Doppler in children to predict stroke risk. Annual eye examination, renal function and hearing.
Medical Management
Hydration, oxygen and analgesia are the management of a crisis. Hydroxyurea raises fetal hemoglobin and markedly reduces crises and acute chest syndrome. Transfusion or exchange transfusion for severe crisis, stroke and acute chest syndrome. Folic acid. Penicillin prophylaxis in young children and full immunisation including pneumococcal and meningococcal vaccines. Newer agents (L-glutamine, crizanlizumab, voxelotor); haematopoietic stem cell transplant and gene therapy are curative options for selected clients.
Nursing Management and Client Education
Believe the pain and treat it properly. These clients are chronically undertreated and wrongly labelled drug-seeking; a crisis is severe ischemic pain and usually needs scheduled intravenous opioids, often client-controlled analgesia, not as-needed doses and not intramuscular injections. Add generous hydration, oxygen for hypoxia, warmth, and rest, plus non-drug measures — warm compresses, never cold, because cold causes further sickling. Watch closely for acute chest syndrome and encourage incentive spirometry, which helps prevent it. Teach the triggers and how to avoid them: fluids, warmth, no smoking, avoid high altitude and extreme exertion, and treat infections early. Teach that any fever means going to hospital the same day. Genetic counselling for the family. Address the toll honestly — missed school and work, chronic pain, and the experience of being disbelieved.
Aplastic Anemia and NeutropeniaFever is an emergencyOpenClose
Definition and Overview
Aplastic anemia is failure of the bone marrow itself, so all three cell lines fall — pancytopenia: too few red cells, too few white cells and too few platelets. Neutropenia is a low neutrophil count specifically, and it is the one that determines infection risk. Febrile neutropenia is an oncological and haematological emergency.
Causes and Risk Factors
About half of aplastic anemia is idiopathic, and much of it is autoimmune. Identified causes: chemotherapy and radiation, chloramphenicol, some antiepileptics and sulfonamides, benzene and other industrial chemicals, viral hepatitis, Epstein–Barr virus, HIV and parvovirus B19, pregnancy, and inherited syndromes such as Fanconi anemia. Neutropenia most often follows chemotherapy, with the nadir around 7 to 14 days after a cycle.
Clinical Manifestations
The findings follow the missing cells. Low red cells: fatigue, pallor, dyspnea, tachycardia. Low platelets: bruising, petechiae, nosebleeds, bleeding gums, heavy periods, and blood in urine or stool. Low neutrophils: infection — but without neutrophils there is little inflammation, so there may be no pus, no redness, no swelling and no cough. A single temperature of 100.4°F (38°C) may be the only sign, and it is an emergency.
Assessment and Diagnostic Findings
CBC with differential and the absolute neutrophil count: below 1000 is neutropenia, below 500/mm³ is severe and high risk. Reticulocyte count is low, which is what marks marrow failure rather than destruction. Bone marrow aspiration and biopsy confirm aplastic anemia. Culture everything before antibiotics; inspect mouth, perineum, IV sites, skin folds and any wound every shift. Vital signs frequently, and a careful drug and exposure history.
Medical Management
Remove the cause where one is identified. Immunosuppressive therapy (antithymocyte globulin and ciclosporin) or haematopoietic stem cell transplantation, which is curative and preferred in younger clients with a matched donor. Growth factors — filgrastim — to raise the neutrophil count. Transfusion of red cells and platelets as needed, using irradiated leucocyte-reduced products in transplant candidates. Empiric broad-spectrum antibiotics within one hour of febrile neutropenia, after cultures.
Nursing Management and Client Education
Neutropenic precautions: private room, meticulous hand hygiene, no visitors with infections, no fresh flowers, plants, standing water, or raw fruit, vegetables and undercooked food. No rectal temperatures, suppositories, enemas or vaginal examinations — breaking that mucosa lets bacteria straight into the blood. Meticulous mouth care with a soft brush and no alcohol-based mouthwash. Bleeding precautions while platelets are low: soft toothbrush, electric razor, no flossing, no intramuscular injections, no aspirin or NSAIDs, apply pressure for at least 5 minutes after any needlestick, and prevent constipation and falls. Teach the client to take their temperature and to call for a single reading of 100.4°F rather than waiting to see, and to report bleeding, bruising or black stools. Teach food safety, crowd avoidance during the nadir, no gardening or litter trays, and no live vaccines. Plan rest and pace activity.
Thrombocytopenia and ITPBleeding precautionsOpenClose
Definition and Overview
A platelet count below 150,000/mm³. Immune thrombocytopenia (ITP) is the autoimmune form: antibodies coat the platelets and the spleen destroys them, so production is normal but survival is short. Heparin-induced thrombocytopenia (HIT) is the dangerous exception — the platelet count falls but the client clots rather than bleeds.
Causes and Risk Factors
Decreased production: marrow failure, leukemia, chemotherapy, radiation, alcohol, B12 or folate deficiency. Increased destruction: ITP, HIT, DIC, thrombotic thrombocytopenic purpura, sepsis, viral infection including HIV and hepatitis C, and drugs — heparin, quinine, sulfonamides, some antiepileptics. Sequestration in an enlarged spleen from liver disease.
Clinical Manifestations
Bleeding risk tracks the count: above 50,000 usually no spontaneous bleeding; 20,000–50,000 bleeding with trauma; below 20,000 spontaneous bleeding; below 10,000 risk of intracranial hemorrhage. Look for petechiae, purpura, easy bruising, nosebleeds, bleeding gums, heavy menstrual bleeding, blood in urine or stool, and the change in level of consciousness, headache or new focal deficit that signals intracranial bleeding — assess neurological status, not just the skin. In HIT, look instead for a new thrombosis and a platelet drop of more than half, typically 5 to 10 days after heparin started.
Assessment and Diagnostic Findings
CBC with platelet count and a peripheral blood film; coagulation studies are normal in ITP, which helps distinguish it from DIC. Test for HIV, hepatitis C and H. pylori. Review every drug the client is taking, and specifically every heparin exposure including flushes. Bone marrow examination in unclear cases. Neurological checks, stool and urine for occult blood, and quantified menstrual loss.
Medical Management
ITP: corticosteroids first line, then intravenous immunoglobulin or anti-D for a rapid rise, then rituximab, thrombopoietin receptor agonists (romiplostim, eltrombopag), and splenectomy for refractory disease. Platelet transfusion only for serious bleeding or before a procedure. HIT: stop all heparin immediately, including flushes and heparin-coated lines, and start a non-heparin anticoagulant such as argatroban — and do not give platelets, which fuels the clotting. Otherwise, treat the cause and stop the offending drug.
Nursing Management and Client Education
Bleeding precautions are the core of the nursing care: soft toothbrush, electric razor only, no flossing, no rectal temperatures, suppositories or enemas, no intramuscular injections, pressure for 5 to 10 minutes after any needlestick, stool softeners to prevent straining, and a safe environment to prevent falls and bumps. No aspirin or NSAIDs, and check every over-the-counter and herbal product. Assess neurological status each shift while the count is very low. Teach the client to report headache, visual change, confusion, black or bloody stools, blood in urine, or bleeding that will not stop, and to avoid contact sports and activities with a fall risk. On steroids, teach infection risk, glucose and never stopping abruptly. After splenectomy, teach lifelong infection risk, pneumococcal, meningococcal and Hib vaccination, and carrying medical identification.
Disseminated Intravascular CoagulationClotting and bleeding at onceOpenClose
Definition and Overview
A catastrophic derangement of coagulation in which the clotting cascade is switched on throughout the circulation at once. Microclots form everywhere, consuming platelets and clotting factors, and the clot-dissolving system then runs unopposed — so the client clots and bleeds simultaneously. It is always secondary to something else, and it is the something else that must be treated.
Causes and Risk Factors
Sepsis is the commonest trigger. Then major trauma, burns, crush injury, obstetric emergencies (abruption, amniotic fluid embolism, retained products, severe pre-eclampsia), malignancy especially acute promyelocytic leukemia, ABO-incompatible transfusion reaction, snake envenomation, and massive transfusion.
Clinical Manifestations
Bleeding from everywhere at once: oozing from IV sites, venepunctures, gums and the surgical wound, epistaxis, haematuria, gastrointestinal bleeding, and widespread petechiae, purpura and ecchymoses. At the same time clotting: cool mottled or cyanotic fingers and toes, acral gangrene, dyspnea and chest pain from pulmonary microthrombi, oliguria from renal microthrombi, and altered mental status. Bleeding from three unrelated sites in a septic or post-obstetric client is DIC until proved otherwise.
Assessment and Diagnostic Findings
The lab pattern is the diagnosis: platelets low and falling, PT and aPTT prolonged, fibrinogen low, and D-dimer and fibrin degradation products markedly high. Serial measurements matter more than any single set, because the trend is what shows it. Also hemoglobin, schistocytes on the film, renal and liver function, and ABGs. Assess every possible bleeding site and every extremity for perfusion, hourly urine output, and neurological status.
Medical Management
Treat the underlying cause — that is the only thing that stops DIC. Antibiotics and source control for sepsis, delivery for an obstetric cause, treatment of the malignancy. Supportive replacement for a client who is bleeding: platelets, fresh frozen plasma and cryoprecipitate for low fibrinogen, and red cells for anemia. Heparin is used cautiously and only in the thrombotic presentation. Oxygen and hemodynamic support throughout.
Nursing Management and Client Education
Handle the client as gently as possible: minimal needlesticks, avoid intramuscular injections, apply firm pressure for at least 10 minutes after any puncture, use a soft toothbrush or sponge swabs and an electric razor, avoid tape on fragile skin, and turn and position carefully. Do not remove clots that have formed — dislodging them restarts the bleeding. Measure and record blood loss rather than estimating it. Check perfusion in every limb hourly and report cool, dusky or painful extremities. Neurological checks for intracranial bleeding. Strict hourly intake and output. Monitor closely during transfusion for reaction and for fluid overload. This is frightening to watch — keep the family informed in plain words, and get support to them, because DIC often accompanies an already critical illness.
Polycythemia VeraOpenClose
Definition and Overview
A chronic myeloproliferative disorder: the bone marrow overproduces red cells, and usually white cells and platelets too. It is the mirror image of anemia — too much blood rather than too little — and everything that goes wrong follows from one fact: the blood becomes thick, so it moves slowly and clots. Most cases carry the JAK2 mutation. It is a cancer of the marrow, not a reaction to anything, which is what separates it from secondary polycythemia.
Causes and Risk Factors
Primary (polycythemia vera) is a clonal marrow disorder, most often with a JAK2 V617F mutation, and is commoner after about age 60. Secondary polycythemia is the marrow responding appropriately to chronic hypoxia — COPD, long-standing smoking, sleep apnoea, high altitude, cyanotic heart disease — by making more erythropoietin. Relative polycythemia is not extra red cells at all, only dehydration concentrating the ones that are there.
Clinical Manifestations
A ruddy, flushed, purple-red face and hands from the sheer volume of red cells. Itching, classically after a warm bath or shower (aquagenic pruritus) — a distinctive enough clue that exams lean on it. Splenomegaly, and a feeling of fullness after small meals. Headache, dizziness, tinnitus, blurred vision and fatigue from sluggish flow. Hypertension. Burning pain and redness in the hands and feet (erythromelalgia). And, at the same time, a bleeding tendency — epistaxis, gum bleeding, bruising — because the platelets are numerous but do not work properly.
Assessment and Diagnostic Findings
High hemoglobin, high hematocrit and high red cell mass, often with a raised white count and platelet count. Low or normal erythropoietin in polycythemia vera, which is how it is separated from secondary polycythemia, where erythropoietin is high. JAK2 mutation testing. Bone marrow biopsy shows a hypercellular marrow. Raised uric acid from rapid cell turnover.
Medical Management
Therapeutic phlebotomy is the mainstay — blood is removed to bring the hematocrit down and thin the blood, repeated as often as the count demands. Low-dose aspirin to reduce clotting, unless bleeding forbids it. Myelosuppressive therapy (hydroxyurea) or a JAK inhibitor for higher-risk disease. Allopurinol for the raised uric acid. Antihistamines for the itching.
Nursing Management and Client Education
The nursing priority is preventing clots, and the teaching is almost entirely about circulation.
- Elevate the legs when sitting and avoid crossing them — this promotes venous return and is the single most-tested self-care measure.
- Drink at least 3 litres of fluid a day unless it is restricted. One litre is not enough — hydration is what keeps the blood from thickening further.
- Avoid tight or restrictive clothing, including wearing support hose continuously — anything that constricts encourages stasis.
- Keep moving. Walk regularly, and never sit still for long stretches, in the car or on a plane.
- No flossing. Use a soft toothbrush and an electric razor — the platelets do not work properly and gums and skin bleed easily.
- Report both directions. Clot signs: calf pain or swelling, chest pain, breathlessness, one-sided weakness or slurred speech. Bleeding signs: nosebleeds, bleeding gums, black stools, unusual bruising.
- Warm, not hot. Cool or tepid showers and starch baths reduce the itching; hot water provokes it.
- Keep every phlebotomy appointment even when feeling well, and expect fatigue afterwards.
π§ Mind maps 2
One per disorder, built from the structure of your ATI chapter.
π― Who gets it
- Blood-loss risk: trauma, menorrhagia, GI bleeding (ulcer, tumor), surgical loss, or chemical/radiation exposure.
- Rapid metabolic demand raises anemia risk: pregnancy, adolescence, or infection.
- Sickle-cell disease: malformed RBCs during hypoxia block capillaries in joints and organs.
- G6PD deficiency impairs glycolysis, which raises the risk for hemolysis.
π What you see
- Mild anemia may cause few or no symptoms at all.
- Common findings include pallor, fatigue, somnolence, headache, irritability, and dyspnea on exertion.
- Anemia can cause limb numbness/tingling and increased sensitivity to cold.
- Sickle-cell crisis brings severe pain along with tissue hypoxia.
π§ͺ What confirms it
- Hgb carries oxygen/CO2 and indicates blood's oxygen-carrying capacity.
- Hct is the percentage of RBCs within total blood volume.
- MCV shows RBC size: normocytic, microcytic, or macrocytic.
- MCH shows Hgb per RBC: normochromic (normal) or hypochromic (low).
π©Ί What you do
- Encourage more dietary intake of the deficient nutrient: iron, B12, or folic acid.
- Monitor oxygen saturation to decide if oxygen therapy is needed.
- Give anemia medications at the right time and technique for best absorption.
- Teach energy conservation and warn about dizziness risk when standing.
π Drugs
- Oral iron (ferrous sulfate, fumarate, gluconate) replenishes iron stores needed for Hgb and O2 transport.
- Parenteral iron (iron dextran) is reserved for severe anemia only.
- Give parenteral iron using the Z-track injection method.
- Normal indices (normocytic, normochromic) point to bleeding, sickle-cell disease, long-term illness, or aplastic anemia.
π¬ What you teach
- Recheck hemoglobin in
4-6 weeksto confirm iron therapy is working. - Taking vitamin C alongside iron supplements boosts oral absorption.
- Take iron supplements between meals if tolerated, to improve absorption.
Read left to right: who gets it β what you see β what confirms it β what you do β what goes wrong. Cover a column and rebuild it out loud.
π― Who gets it
- ITP most often develops in people assigned female at birth, ages
20-50. - ITP risk: certain medications, viral infection (HIV, hepatitis C), or another autoimmune disorder.
- In children, ITP often follows a recent viral illness.
- The main TTP risk factor is having another autoimmune disorder.
π What you see
- Watch for spontaneous gum or nose bleeding along with oozing from incisions or cuts.
- Look for petechiae and ecchymoses on the extremities, upper chest, and neck.
- Hematuria and excess bleeding from IV sites, injections, or minor trauma can occur.
- Expect tachycardia, hypotension, and diaphoresis as bleeding or shock develops.
π§ͺ What confirms it
- Hemoglobin drops with DIC and ITP; normal is
14-18 g/dL(male),12-16 g/dL(female). - Platelets fall (thrombocytopenia) with DIC, TTP, and ITP; normal range is
150,000-400,000/mm3. - Fibrinogen drops with DIC; normal range is
200-400 mg/dL. - Prothrombin time rises with DIC; normal range is
11.0-12.5 sec.
π©Ί What you do
- In DIC, treat the underlying cause (sepsis, malignancy, hemorrhage) to stop the clotting cascade.
- In DIC, work to prevent organ damage from microemboli and replace lost clotting factors.
- Watch for microemboli signs: cyanotic nail beds and localized pain.
- Recheck vital signs and hemodynamic status often in DIC, HIT, ITP, and TTP.
π Drugs
- ITP is treated with corticosteroids and immunosuppressant medications.
- TTP is treated with antiplatelet medications such as aspirin, alprostadil, or plicamycin.
- TTP: immunosuppressive therapy lessens the severity of complications.
- HIT is treated with direct thrombin inhibitors: argatroban, lepirudin, or bivalirudin.
Read left to right: who gets it β what you see β what confirms it β what you do β what goes wrong. Cover a column and rebuild it out loud.
🎥 Lecture recordings 2
Tap a card to open that recording in Google Drive. The same list lives in the lecture library.
All NUR 258 recordings →🖼️ Infographics & deep dives 5
The blood and clotting pages already on this site.
📄 Simple Nursing handouts for this module — 2 of them, straight from your Drive.
π Active Learning Templates 2
One per disorder. Every row is filled from that section of the ATI chapter β print it, cover the right, rebuild it.
📋 Anemias6 parts
Filled from ATI chapter 42, row by row from that chapterβs own sections β 12 of 12 rows have content.
π§ What it isAlterations in Health (Diagnosis) Β· Health Promotion & Disease Prevention
Alterations in Health (Diagnosis)
- Covers anemia's causes (blood loss, poor RBC production, hemolysis, nutrient deficiency), risk factors, expected findings, lab workup (CBC, RBC indices, iron studies), and treatments including iron, B12, folic acid, and transfusions, plus heart failure risk.
Health Promotion & Disease Prevention
- Pregnant or menstruating clients need iron-rich foods or an iron supplement.
- If cholesterol is high, get iron from fortified cereal, fish, poultry, or legumes instead of red/organ meat.
- Eat folate-rich foods like spinach, lentils, bananas, and folic-acid-fortified grains or juice regularly.
π How it shows upAssessment β Risk Factors Β· Assessment β Expected Findings
Assessment β Risk Factors
- Blood-loss risk: trauma, menorrhagia, GI bleeding (ulcer, tumor), surgical loss, or chemical/radiation exposure.
- Rapid metabolic demand raises anemia risk: pregnancy, adolescence, or infection.
- Sickle-cell disease: malformed RBCs during hypoxia block capillaries in joints and organs.
- G6PD deficiency impairs glycolysis, which raises the risk for hemolysis.
- Hemolysis can follow transfusion reactions, autoimmune disease, a mechanical valve, or cardiopulmonary bypass.
- Pernicious anemia stems from a lack of intrinsic factor needed to absorb vitamin B12.
- Pica means eating nonfood items for at least
1 month, which can crowd out nutritious choices. - Bone marrow suppression from radiation or chemical exposure can cause aplastic anemia.
Assessment β Expected Findings
- Mild anemia may cause few or no symptoms at all.
- Common findings include pallor, fatigue, somnolence, headache, irritability, and dyspnea on exertion.
- Anemia can cause limb numbness/tingling and increased sensitivity to cold.
- Sickle-cell crisis brings severe pain along with tissue hypoxia.
- Exam findings include tachycardia, palpitations, and orthostatic hypotension on standing.
- Watch for dizziness or fainting when standing or exerting.
- Pallor shows in nail beds and mucous membranes; skin feels cool to touch.
- Chronic anemia can cause spoon-shaped nail deformities over time.
π§ͺ How it is confirmedLaboratory Tests Β· Diagnostic Procedures
Laboratory Tests
- Hgb carries oxygen/CO2 and indicates blood's oxygen-carrying capacity.
- Hct is the percentage of RBCs within total blood volume.
- MCV shows RBC size: normocytic, microcytic, or macrocytic.
- MCH shows Hgb per RBC: normochromic (normal) or hypochromic (low).
- MCHC shows the percent of Hgb relative to cell size.
Diagnostic Procedures
- Bone marrow aspiration/biopsy diagnoses aplastic anemia, where marrow fails to make RBCs, platelets, and WBCs.
π©Ί What you doNursing Care Β· Medications Β· Therapeutic Procedures
Nursing Care
- Encourage more dietary intake of the deficient nutrient: iron, B12, or folic acid.
- Monitor oxygen saturation to decide if oxygen therapy is needed.
- Give anemia medications at the right time and technique for best absorption.
- Teach energy conservation and warn about dizziness risk when standing.
- Teach the client the expected time frame for anemia to resolve.
- With erythropoietin, monitor blood pressure and check Hgb/Hct weekly.
- Watch for a cardiovascular event if Hgb rises more than
1 g/dLin2 weekson erythropoietin. - Give B12 by the route matching the cause: oral, parenteral, or intranasal.
- Give parenteral B12 IM or deep subQ, and never mix it with other drugs in the syringe.
Medications
- Oral iron (ferrous sulfate, fumarate, gluconate) replenishes iron stores needed for Hgb and O2 transport.
- Parenteral iron (iron dextran) is reserved for severe anemia only.
- Give parenteral iron using the Z-track injection method.
- Normal indices (normocytic, normochromic) point to bleeding, sickle-cell disease, long-term illness, or aplastic anemia.
- Microcytic, hypochromic anemia (low indices) suggests iron deficiency, thalassemia, or chronic blood loss.
Therapeutic Procedures
- Blood transfusion rapidly improves cell counts and anemia symptoms.
- Transfusions are reserved for clients with significant anemia symptoms, given infection risk.
π¬ Around the patientClient Education Β· Interprofessional Care
Client Education
- Recheck hemoglobin in
4-6 weeksto confirm iron therapy is working. - Taking vitamin C alongside iron supplements boosts oral absorption.
- Take iron supplements between meals if tolerated, to improve absorption.
- Iron supplements can turn stools green to black.
- Epoetin alfa is a growth factor that boosts RBC production.
- B12 therapy for intrinsic-factor loss or irreversible malabsorption continues lifelong.
- Ongoing B12 replacement is given as a monthly injection.
Interprofessional Care
From this module β built from the notes above on this page, not a section of the ATI chapter.
- Hematologist for inherited anemias and for anything not responding to replacement.
- Dietitian for iron, B12 and folate intake, and for the restricted diets that cause deficiency.
- Gastroenterology β unexplained iron deficiency in an adult means looking for a bleeding source.
- Transfusion service; genetic counseling for inherited disorders.
- Social work where food insecurity is the underlying cause.
β οΈ What goes wrongComplications
Complications
From this module β built from the notes above on this page, not a section of the ATI chapter.
- Heart failure and angina from sustained high-output demand, particularly in older adults.
- Sickle cell: vaso-occlusive crisis, acute chest syndrome, stroke, splenic sequestration, priapism.
- Pernicious anemia: neurological damage can become permanent β paraesthesia, ataxia and cognitive change β if B12 is not replaced.
- Thalassemia: iron overload from repeated transfusion, needing chelation.
- Falls and injury from fatigue and dizziness; delayed wound healing.
📋 Coagulation Disorders6 parts
🖼️ InfographicsLabs - Lab Values - WBC & Coagulation Panel
Filled from ATI chapter 43, row by row from that chapterβs own sections β 12 of 12 rows have content.
π§ What it isAlterations in Health (Diagnosis) Β· Health Promotion & Disease Prevention
Alterations in Health (Diagnosis)
- Coagulopathies involve platelet or clotting-factor problems that impair or overdrive clotting. Covers ITP, TTP, HIT, DIC, and hemophilia β their causes, mortality risk, and why some cause bleeding while others trigger dangerous clots simultaneously.
Health Promotion & Disease Prevention
From this module β built from the notes above on this page, not a section of the ATI chapter.
- Bleeding precautions: soft toothbrush, electric razor, no contact sport, no rectal temperatures or suppositories.
- No aspirin or NSAIDs in a bleeding disorder unless specifically prescribed.
- Medical alert identification; tell every dentist and surgeon before any procedure.
- Genetic counseling for hemophilia, which is X-linked β carrier mothers, affected sons.
- For anticoagulation: consistent vitamin K intake, adherence to monitoring, and awareness of interacting drugs.
π How it shows upAssessment β Risk Factors Β· Assessment β Expected Findings
Assessment β Risk Factors
- ITP most often develops in people assigned female at birth, ages
20-50. - ITP risk: certain medications, viral infection (HIV, hepatitis C), or another autoimmune disorder.
- In children, ITP often follows a recent viral illness.
- The main TTP risk factor is having another autoimmune disorder.
- HIT risk factors include female sex assigned at birth.
- HIT risk rises with heparin exposure over
1 week; unfractionated heparin is more likely to trigger it. - HIT risk also rises with postsurgical thromboprophylaxis (clot-prevention therapy).
- DIC can follow septicemia, cardiac arrest, or major trauma (hemorrhage, burns, crush injury).
Assessment β Expected Findings
- Watch for spontaneous gum or nose bleeding along with oozing from incisions or cuts.
- Look for petechiae and ecchymoses on the extremities, upper chest, and neck.
- Hematuria and excess bleeding from IV sites, injections, or minor trauma can occur.
- Expect tachycardia, hypotension, and diaphoresis as bleeding or shock develops.
- Microemboli can cause organ failure and respiratory distress.
- Cyanotic, dark, or gray nail beds signal microvascular clotting.
- HIT causes redness, warmth, swelling, and pain in the lower legs.
π§ͺ How it is confirmedLaboratory Tests Β· Diagnostic Procedures
Laboratory Tests
- Hemoglobin drops with DIC and ITP; normal is
14-18 g/dL(male),12-16 g/dL(female). - Platelets fall (thrombocytopenia) with DIC, TTP, and ITP; normal range is
150,000-400,000/mm3. - Fibrinogen drops with DIC; normal range is
200-400 mg/dL. - Prothrombin time rises with DIC; normal range is
11.0-12.5 sec. - Partial thromboplastin time rises with DIC; normal aPTT is
30-40 sec, PTT60-70 sec.
Diagnostic Procedures
From this module β built from the notes above on this page, not a section of the ATI chapter.
- PT/INR for the extrinsic pathway and warfarin; aPTT for the intrinsic pathway and heparin.
- PTβwarfarin, aPTTβheparin.
- Platelet count, fibrinogen and D-dimer β in DIC the platelets and fibrinogen fall while D-dimer rises.
- Specific factor assays to identify hemophilia A (VIII) or B (IX).
- Imaging for suspected internal or joint bleeding.
π©Ί What you doNursing Care Β· Medications Β· Therapeutic Procedures
Nursing Care
- In DIC, treat the underlying cause (sepsis, malignancy, hemorrhage) to stop the clotting cascade.
- In DIC, work to prevent organ damage from microemboli and replace lost clotting factors.
- Watch for microemboli signs: cyanotic nail beds and localized pain.
- Recheck vital signs and hemodynamic status often in DIC, HIT, ITP, and TTP.
- Watch for organ failure or intracranial bleed: falling urine output, declining level of consciousness.
- Trend clotting lab values closely to catch a worsening coagulopathy.
- Give fluid volume replacement as ordered to support perfusion.
- Transfuse blood, platelets, and other clotting products as needed.
- Watch closely for complications from any blood product transfusion.
Medications
- ITP is treated with corticosteroids and immunosuppressant medications.
- TTP is treated with antiplatelet medications such as aspirin, alprostadil, or plicamycin.
- TTP: immunosuppressive therapy lessens the severity of complications.
- HIT is treated with direct thrombin inhibitors: argatroban, lepirudin, or bivalirudin.
- DIC: heparin can limit new microclot formation and clotting-factor depletion.
Therapeutic Procedures
- TTP can be treated with plasma exchange therapy.
- ITP: splenectomy may be performed if medical management fails.
π¬ Around the patientClient Education Β· Interprofessional Care
Client Education
From this module β built from the notes above on this page, not a section of the ATI chapter.
- Recognize and report bleeding: bruising, gum or nose bleeding, blood in urine or stool, black tarry stools, and unexplained headache.
- Hemophilia: a swollen, warm, painful joint is a bleed β factor first, then rest, ice and elevation.
- Apply firm pressure for
10 minutesto any bleeding site, and seek help if it does not stop. - Warfarin: keep vitamin K intake steady rather than avoiding greens entirely; attend every INR check.
- A head injury in anyone with a bleeding disorder or on anticoagulation is assessed, not watched at home.
Interprofessional Care
From this module β built from the notes above on this page, not a section of the ATI chapter.
- Hematologist and a specialist hemophilia center.
- Pharmacist for anticoagulant dosing, reversal agents and the long list of interactions.
- Physiotherapy after joint bleeds to preserve function.
- Genetic counseling for inherited disorders.
- Dentist and surgeon informed in advance, with a factor cover plan agreed.
β οΈ What goes wrongComplications
Complications
From this module β built from the notes above on this page, not a section of the ATI chapter.
- Intracranial hemorrhage β the most feared, and often with little external sign.
- Hemarthrosis with repeated bleeds leading to permanent joint destruction.
- DIC β simultaneous clotting and bleeding, with organ failure.
- Heparin-induced thrombocytopenia β platelets fall and the client clots rather than bleeds. Stop all heparin.
- Transfusion reactions and inhibitor development in hemophilia.
π Notes & key concepts
The lines from this module that carry a number, a dose or an absolute rule β the ones that decide questions. Everything else is on the cards above.
- MCV sorts the anemias: microcytic = iron deficiency; normocytic = chronic disease or kidney; macrocytic = B12, folate or alcohol. Ferritin low + TIBC high = iron deficiency. Hgb electrophoresis confirms sickle cell. Bone marrow biopsy (posterior iliac crest) diagnoses aplastic anemia and leukemia.
- Fatigue is the #1 anemia sign. Transfuse chronic anemia around Hgb
<7 g/dL; long-term management is subQ epoetin alfa. - Polycythemia vera is the opposite β marrow overproduces RBCs β thick blood, ruddy face, itching after a warm shower, splenomegaly, high clot risk. Therapeutic phlebotomy is the mainstay; nursing priority is clot prevention.
- Sickle cell crisis: IV fluids, IV opioids (PCA/morphine, not PO Tylenol β do not withhold opioids), oxygen, transfusion PRN. Ice is contraindicated. Prevention: avoid high altitude and temperature extremes.
- Platelets normal
150,000β450,000/mmΒ³; fibrinogen170β340 mg/dL. Neutropenic precautions start at ANC<1,000/mmΒ³. - Hemophilia: give clotting factor before and after any procedure. Priority labs are coags, not CBC (platelets are normal). Compression beats a factor injection if she is bleeding right now. Ice, not heat. No aspirin. Deep joint bleeds are ~
75%of bleeds. - DIC: bleeding and clotting at once from an underlying cause. Labs: PT/PTT/INR up, platelets down, fibrinogen down, FDPs up. Treat the cause first (antibiotics for sepsis) β fluids β heparin β blood products.
- Transfusions: two-nurse verification, 0.9% NS only (dextrose hemolyzes, LR clots), stay with her the first
15 min, infuse within4 hours. - HIT: platelets
220,000 β 90,000 in 48 hours on day 7 of heparin. Stop the heparin, daily platelet counts, notify, and assess for thrombosis β HIT clots as well as bleeds. Do not give vitamin K (that is warfarin's antidote) and do not start warfarin. Heparin β aPTT. Warfarin β PT/INR. - DIC lab triad: βplatelets, βfibrinogen, βD-dimer. To address organ ischemia specifically the answer is oxygen and IV fluids β holding pressure and vitamin K do not perfuse organs.
- ITP: petechiae and a 10-minute nosebleed can wait. Severe headache with vomiting in a thrombocytopenic client means intracranial hemorrhage.
- Hemophilia hemarthrosis: elevate, give factor replacement, no ROM, never aspirin or NSAIDs.
- Pressure-holding times: 5 minutes for venipuncture, 10+ for arterial. "2 minutes" is a distractor.
- Platelets: under 20,000, and especially under 10,000, is significant bleeding risk. They used both 150,000β450,000 and 140,000β400,000 as "normal" and told students not to be thrown by lab-to-lab variation.
π― Module quiz
Questions for this module. They also feed the Mega Quiz.
Nothing here yet β drop it in when you have it