1. Bedside procedures and monitoring
   • Blood-group determination
   • Blood transfusion
   • Blood-pressure measurement
   • ECG registration
2. Acute coronary syndrome
   • Laboratory changes
   • Troponin types, testing, interpretation
3. Acute cardiac emergencies
   • Pulmonary edema
   • Cardiogenic shock
4. Hematology: anemia
   • Iron-deficiency anemia
   • Vitamin B12 and folate-deficiency anemia
   • Congenital hemolytic anemia
   • Acquired hemolytic anemia
5. Hematology: leukemia
   • Acute leukemia
   • Chronic leukemia
6. Valvular heart disease
   • Mitral stenosis
   • Mitral regurgitation
   • Aortic stenosis
   • Aortic regurgitation
7. Inflammatory bowel disease
   • Ulcerative colitis: endoscopy, imaging, pathology
   • Crohn disease: endoscopy, imaging, pathology

1. Bedside procedures and monitoring
   • Blood-group determination
   • Blood transfusion
   • Blood-pressure measurement
   • ECG registration
2. Acute coronary syndrome
   • Laboratory changes
   • Troponin types, testing, interpretation
3. Acute cardiac emergencies
   • Pulmonary edema
   • Cardiogenic shock
4. Hematology: anemia
   • Iron-deficiency anemia
   • Vitamin B12 and folate-deficiency anemia
   • Congenital hemolytic anemia
   • Acquired hemolytic anemia
5. Hematology: leukemia
   • Acute leukemia
   • Chronic leukemia
6. Valvular heart disease
   • Mitral stenosis
   • Mitral regurgitation
   • Aortic stenosis
   • Aortic regurgitation
7. Inflammatory bowel disease
   • Ulcerative colitis: endoscopy, imaging, pathology
   • Crohn disease: endoscopy, imaging, pathology

1. Topics 1-5: Blood grouping, transfusion, BP measurement, ECG, ACS troponin
2. Topics 6-7: Pulmonary edema and cardiogenic shock
3. Topics 8-13: Anemias and leukemias
4. Topics 14-17: Mitral and aortic valve lesions
5. Topics 18-19: Ulcerative colitis and Crohn disease

1. Determination of blood group

Purpose

• To identify ABO blood group and Rh(D) status before transfusion, pregnancy care, and transplantation.
• Always perform ABO forward grouping, reverse grouping where applicable, and RhD typing. Confirm unexpected results before issuing blood.

Preparation

• Verify patient identity using two identifiers.
• Collect correctly labeled venous blood, usually EDTA sample.
• Check reagent validity, storage, controls, and sample quality.
• Use anti-A, anti-B, anti-D reagents; follow local laboratory protocol.

Principle

• Forward grouping: patient red cells are tested against known antisera.
• Reverse grouping: patient serum/plasma is tested against known A and B reagent red cells.
• Rh typing: patient red cells are tested with anti-D reagent.

Slide/tube technique - basic viva steps

1. Label the test areas or tubes.
2. Add antisera: anti-A, anti-B, anti-D.
3. Add patient red-cell suspension.
4. Mix gently and observe for agglutination. Tube/gel methods are more reliable than slide testing.
5. Record results and correlate with reverse grouping.
6. If results disagree, do not report or issue non-emergency routine blood until resolved.

Interpretation

Important precautions

• Clerical identification error is a major cause of fatal ABO-incompatible transfusion.
• Use controls and repeat discrepant/weak reactions.
• In a life-threatening emergency, give uncrossmatched emergency blood according to local policy, commonly group O red cells, while samples are processed.

2. Blood transfusion

Definition

Indications

• Red blood cells (RBCs):
  • Acute major hemorrhage.
  • Symptomatic severe anemia or inadequate oxygen delivery.
  • Stable adults often use a restrictive threshold around Hb <7 g/dL, with clinical context and higher thresholds in selected cardiac/operative settings.
• Platelets:
  • Severe thrombocytopenia with bleeding.
  • Prophylaxis at very low platelet counts in marrow failure.
  • Before invasive procedures when platelet count is inadequate.
• Fresh frozen plasma (FFP):
  • Bleeding with multiple coagulation-factor deficiency, such as DIC, liver failure, or massive transfusion.
  • Urgent reversal of warfarin when prothrombin complex concentrate is unavailable.
• Cryoprecipitate/fibrinogen concentrate:
  • Hypofibrinogenemia with bleeding, for example massive obstetric hemorrhage or DIC.

Contraindications

• Do not use RBC transfusion simply to expand volume.
• Do not use FFP for nutritional support, hypoalbuminemia, or minor isolated laboratory abnormalities without bleeding/procedure risk.
• Use caution in heart failure, chronic kidney disease, and elderly patients because of transfusion-associated circulatory overload (TACO).
• In a patient with previous severe allergic or hemolytic reaction, obtain specialist transfusion advice and suitable modified components.

Methodology

1. Confirm indication, informed consent where feasible, prescription, blood group, antibody screen, and crossmatch.
2. At bedside, two trained staff members or validated electronic system verify:
   • Patient identity using two identifiers.
   • Compatibility label, unit number, ABO/Rh type, expiry date, and component.
3. Record baseline temperature, pulse, respiratory rate, blood pressure, and oxygen saturation if indicated.
4. Use a dedicated blood administration set with filter and 0.9% saline only if a compatible fluid is required.
5. Start slowly and observe closely, especially during the first 15 minutes.
6. Monitor vital signs per local policy and document start/finish time.
7. Complete RBC transfusion within the institutionally specified period, commonly no longer than 4 hours after removal from controlled storage.
8. Never add drugs to blood bags or run blood through the same line as incompatible solutions such as dextrose-containing fluids.

Complications

• Acute hemolytic transfusion reaction: usually ABO incompatibility. Features: fever, chills, back/flank pain, hypotension, hemoglobinuria, DIC, acute kidney injury.
• Febrile nonhemolytic reaction: fever/chills without hemolysis.
• Mild allergic reaction: itching, urticaria.
• Anaphylaxis: wheeze, shock, angioedema.
• Bacterial contamination/sepsis: high fever, rigors, hypotension.
• TACO: dyspnea, hypertension, pulmonary edema, raised JVP.
• TRALI: acute hypoxemia and noncardiogenic pulmonary edema during or within 6 hours of transfusion.
• Electrolyte/metabolic complications in massive transfusion: hypocalcemia from citrate, hyperkalemia, hypothermia, acidosis, dilutional coagulopathy.

• Delayed hemolytic reaction.
• Alloimmunization.
• Iron overload with repeated transfusions.
• Transfusion-transmitted infection, now rare but not zero.
• Transfusion-associated graft-versus-host disease in susceptible patients receiving nonirradiated cellular products.

If a transfusion reaction is suspected

1. Stop the transfusion immediately.
2. Keep IV access open with normal saline.
3. Recheck patient and unit identification.
4. Assess ABCs, vital signs, and treat anaphylaxis/shock if present.
5. Notify the clinician and blood bank urgently.
6. Send the blood bag, tubing, and appropriate post-reaction samples as per protocol.
7. Document and do not restart the same unit unless the blood bank/clinician confirms a non-serious cause.

3. Measurement of blood pressure

Preparation and rules

• Patient should avoid smoking, caffeine, and exercise for at least 30 minutes beforehand where possible.
• Allow the patient to rest quietly for at least 5 minutes.
• Patient seated with back supported, feet flat on floor, legs uncrossed.
• Arm bare, relaxed, and supported at heart level.
• Use correct cuff size:
  • Bladder width about 40% of arm circumference.
  • Bladder length about 80% of arm circumference.
• At the first visit, measure BP in both arms. Use the higher-reading arm for future measurements.
• Do not talk during measurement.

Auscultatory technique

1. Palpate brachial artery and place cuff snugly 2-3 cm above the antecubital fossa.
2. Estimate systolic BP by palpation: inflate until radial pulse disappears, then add 20-30 mmHg.
3. Place stethoscope over the brachial artery, not under the cuff.
4. Deflate slowly at about 2-3 mmHg per second.
5. First Korotkoff sound = systolic BP.
6. Disappearance of Korotkoff sounds, phase V = diastolic BP in most adults.
7. Record to nearest 2 mmHg, arm used, body position, cuff size if nonstandard, and device.

Interpretation and repeat readings

• Take at least two readings 1 minute apart; average them.
• If readings differ significantly, take additional readings.
• Confirm hypertension using repeated clinic measurements and preferably ambulatory or home BP monitoring unless severe hypertension or acute organ damage is suspected.

Common errors

• Cuff too small: falsely high BP.
• Cuff too large: falsely low BP.
• Arm below heart level: falsely high BP.
• Talking, pain, anxiety, recent exercise, full bladder: falsely high reading.
• Deflating too fast: may underestimate systolic and overestimate diastolic BP.

4. ECG registration: rules and technique

Purpose

Preparation

• Explain procedure and obtain cooperation.
• Patient supine, relaxed, warm, and still.
• Expose chest appropriately, preserve privacy.
• Clean and dry skin; shave excessive hair if needed.
• Remove metal objects or minimize electrical interference.
• Ensure correct patient name, date, time, calibration, and clinical details.

Standard settings

• Paper speed: 25 mm/s.
• Calibration: 10 mm = 1 mV.
• At 25 mm/s:
  • One small square = 0.04 s.
  • One large square = 0.20 s.

Electrode placement

• RA: right arm.
• LA: left arm.
• RL: right leg, ground.
• LL: left leg.

• V1: 4th right intercostal space, right sternal border.
• V2: 4th left intercostal space, left sternal border.
• V3: midway between V2 and V4.
• V4: 5th left intercostal space, midclavicular line.
• V5: same horizontal level as V4, anterior axillary line.
• V6: same horizontal level as V4/V5, midaxillary line.

Technique

1. Attach electrodes securely.
2. Check for artifact and baseline stability.
3. Ask patient not to move, talk, or tense muscles.
4. Record all 12 leads.
5. Label the ECG and inspect tracing quality before removing electrodes.
6. If ACS is suspected, obtain ECG immediately and repeat serially if symptoms or findings evolve.

Common errors

• V1/V2 placed too high can mimic ischemia or produce misleading patterns.
• Reversal of right and left arm leads may cause inverted lead I and abnormal aVR.
• Poor skin contact, tremor, movement, and mains interference cause artifacts.
• Incorrect gain or paper speed causes incorrect measurements.

5. Laboratory changes in acute coronary syndrome and troponin test

ACS definition

• ST-elevation myocardial infarction (STEMI)
• Non-ST-elevation myocardial infarction (NSTEMI)
• Unstable angina

Key laboratory findings in ACS

• Cardiac troponin I or T: rises in myocardial injury. Preferred biomarker.
• CK-MB: may rise, but is less sensitive and specific than troponin. Can sometimes assist in suspected reinfarction when serial dynamics are needed.
• Myoglobin: early but nonspecific, now rarely used for diagnosis.
• Supportive, nonspecific findings:
  • Mild leukocytosis.
  • Elevated glucose due to stress hyperglycemia.
  • Raised CRP later.
  • Possible elevated BNP/NT-proBNP if heart failure is present.
  • Lipid profile should be measured early, although values may fall after acute MI.

Troponin: types

• Cardiac troponin I (cTnI)
• Cardiac troponin T (cTnT)
• High-sensitivity troponin I/T (hs-cTn): detects much lower concentrations and permits faster rule-out/rule-in pathways.

Indications for troponin testing

• Suspected ACS: chest pain, dyspnea, diaphoresis, syncope, unexplained nausea, or ischemic ECG changes.
• Suspected myocardial injury in critically ill patients.
• Risk stratification in confirmed ACS.
• Not appropriate as a screening test in asymptomatic low-risk people.

Methodology

• Venous blood sample is analyzed by an immunoassay.
• Obtain sample at presentation and repeat using the assay-specific protocol, commonly a rapid 0/1-hour or 0/2-hour high-sensitivity troponin pathway, or longer serial testing where required.
• Interpret using the laboratory-specific 99th percentile upper reference limit (URL) and the absolute or relative change on serial measurements.

Evaluation of results

• Myocardial injury: troponin above the 99th-percentile URL.
• Acute myocardial injury: a rise and/or fall on serial testing.
• Myocardial infarction: acute myocardial injury plus clinical evidence of ischemia, such as ischemic symptoms, new ischemic ECG changes, imaging evidence of new loss of viable myocardium/regional wall-motion abnormality, or coronary thrombus.
• A single normal early troponin does not exclude MI if symptom onset was recent. Repeat testing is essential.
• Stable, chronically elevated troponin may occur in chronic kidney disease, heart failure, structural heart disease, or other chronic injury.

Causes of raised troponin other than type 1 MI

• Myocarditis.
• Tachyarrhythmia or severe bradyarrhythmia.
• Pulmonary embolism.
• Acute heart failure.
• Sepsis, shock, severe hypoxemia, or severe anemia.
• Hypertensive emergency.
• Chronic kidney disease.
• Takotsubo syndrome.
• Cardiac trauma or cardiac procedures.

1. Blood group determination

• Correct patient identification and labeled EDTA blood sample.
• Anti-A, anti-B, anti-D reagents; check expiry and controls.

• Mix patient RBCs separately with anti-A, anti-B, and anti-D.
• Look for agglutination.
• Confirm with reverse grouping and crossmatch when transfusion is planned.

• Anti-A positive: Group A.
• Anti-B positive: Group B.
• Both positive: Group AB.
• Neither positive: Group O.
• Anti-D positive: Rh positive.

2. Blood transfusion

• Acute major bleeding.
• Symptomatic severe anemia.
• Platelets for severe thrombocytopenia/bleeding.
• FFP for bleeding with coagulation-factor deficiency.

• Do not use blood as a volume expander.
• Avoid unnecessary transfusion in stable mild anemia.
• Use cautiously in heart failure/renal failure due to fluid overload risk.

1. Confirm indication, consent, blood group, crossmatch.
2. Check patient identity, unit number, ABO/Rh, expiry date.
3. Record baseline vitals.
4. Use blood set with filter; use only normal saline with blood.
5. Start slowly for first 15 minutes and monitor.
6. Complete within local protocol, commonly within 4 hours.

• Acute hemolytic reaction: fever, chills, back pain, hypotension, hemoglobinuria.
• Febrile nonhemolytic and allergic reactions.
• Anaphylaxis.
• Sepsis from contaminated unit.
• TACO: circulatory overload/pulmonary edema.
• TRALI: acute noncardiogenic pulmonary edema.
• Delayed hemolysis, iron overload, alloimmunization.

3. Blood pressure measurement

• Rest 5 minutes.
• No caffeine, smoking, or exercise for 30 minutes if possible.
• Seated, back supported, feet on floor, arm at heart level.
• Use correct cuff size.

1. Place cuff 2-3 cm above elbow crease.
2. Palpate brachial artery.
3. Inflate 20-30 mmHg above estimated systolic pressure.
4. Deflate at 2-3 mmHg/second.
5. First Korotkoff sound = systolic BP.
6. Disappearance of sound = diastolic BP.

• Take at least two readings and average them.
• Measure both arms initially.
• Cuff too small gives falsely high BP.
• Record arm, position, reading, and cuff if unusual size.

4. ECG registration

• Explain procedure; patient supine, relaxed, and still.
• Clean/dry skin and ensure correct patient details.
• Standard setting: 25 mm/s; 10 mm = 1 mV.

• V1: 4th right intercostal space, sternal border.
• V2: 4th left intercostal space, sternal border.
• V3: midway between V2 and V4.
• V4: 5th left intercostal space, midclavicular line.
• V5: anterior axillary line, level with V4.
• V6: midaxillary line, level with V4.

• Attach limb and chest electrodes correctly.
• Ask patient not to talk or move.
• Check for artifacts and record all 12 leads.
• Label ECG with name, date, time, and calibration.

5. ACS laboratory changes and troponin

• Suspected ACS: chest pain, dyspnea, sweating, ischemic ECG changes.
• Risk stratification in ACS.

• Troponin I.
• Troponin T.
• High-sensitivity troponin assays are preferred.

• Blood sample at presentation and repeat after 1-3 hours according to local assay protocol.
• Interpret using the assay-specific 99th-percentile upper reference limit and serial rise/fall.

• Raised troponin = myocardial injury.
• Rise/fall + ischemic symptoms/ECG/imaging evidence = myocardial infarction.
• Normal early result does not exclude MI: repeat sample needed.

• CK-MB may rise but is less useful than troponin.
• Mild leukocytosis, hyperglycemia, and raised CRP may occur.

• Myocarditis, heart failure, pulmonary embolism, sepsis, renal failure, tachyarrhythmia, severe anemia.

6. Acute pulmonary edema

• Acute left ventricular failure: acute MI, hypertensive crisis, arrhythmia.
• Acute mitral regurgitation or severe aortic valve disease.
• Fluid overload, renal failure.
• Noncardiogenic: ARDS, sepsis, aspiration, TRALI.

• Sudden severe breathlessness, orthopnea, anxiety.
• Tachypnea, tachycardia, cyanosis.
• Cough with pink frothy sputum.
• Bilateral fine basal crepitations.
• Raised JVP, S3 gallop, peripheral edema if cardiogenic.

• Pulse oximetry/ABG: hypoxemia.
• ECG and troponin: rule out ACS.
• Chest X-ray: bilateral perihilar “bat-wing” opacities, cardiomegaly, Kerley B lines, pleural effusions.
• Echo: assess LV function and valve lesion.

1. Sit patient upright, give oxygen if hypoxemic.
2. Continuous monitoring, IV access, ECG.
3. Noninvasive ventilation, CPAP/BiPAP, if severe respiratory distress.
4. IV loop diuretic, for example furosemide, if fluid overload/congestion.
5. IV nitrates if hypertensive and BP adequate.
6. Treat cause: ACS, arrhythmia, hypertensive emergency, valve lesion.
7. If hypotension/shock: avoid nitrates, consider ICU, vasopressor/inotrope support.

7. Cardiogenic shock

• Extensive acute MI: most common cause.
• Mechanical MI complications: ventricular septal rupture, papillary muscle rupture causing acute MR, free-wall rupture.
• Severe acute heart failure/cardiomyopathy.
• Serious arrhythmias.
• Acute severe valvular disease.
• Massive pulmonary embolism or right ventricular infarction.

• Persistent hypotension: SBP <90 mmHg or need for vasopressors.
• Signs of poor perfusion: cold clammy skin, altered mental status, oliguria, weak pulse, raised lactate.
• Tachycardia, tachypnea.
• Pulmonary edema and raised JVP may be present.
• Echo may show poor LV/RV function or mechanical complication.

• ECG, serial troponin.
• ABG and serum lactate.
• Renal function, electrolytes, CBC.
• Urgent echocardiography.
• Coronary angiography if ACS is suspected.

1. ABC approach, ICU/cardiac shock team, continuous monitoring.
2. Oxygen and ventilatory support if needed.
3. Cautious fluid bolus only if hypovolemia or RV infarction is suspected. Avoid excess fluids.
4. Norepinephrine is usually first-line vasopressor for severe hypotension.
5. Add inotrope such as dobutamine if low cardiac output persists with adequate BP.
6. Urgent revascularization by PCI/CABG in MI-related shock.
7. Treat cause: reperfusion, correct arrhythmia, repair mechanical defect.
8. Consider mechanical circulatory support in refractory shock.

8. Iron-deficiency anemia: CBC changes and treatment

• Low hemoglobin and hematocrit.
• Low MCV: microcytic anemia.
• Low MCH/MCHC: hypochromic anemia.
• Increased RDW: variable red-cell size, often early.
• Low reticulocyte count or inappropriately normal count.
• Smear: microcytes, hypochromia, anisopoikilocytosis, pencil cells/elliptocytes.
• Platelets may be increased: reactive thrombocytosis.

• Low serum ferritin: best indicator of depleted iron stores.
• Low serum iron.
• Raised TIBC/transferrin.
• Low transferrin saturation.

• Chronic blood loss: menstrual or gastrointestinal.
• Increased requirement: pregnancy, growth.
• Poor dietary intake.
• Malabsorption: celiac disease, post-gastrectomy.

1. Identify and treat the cause of iron loss, especially GI bleeding in men and postmenopausal women.
2. Oral iron is first line if tolerated.
3. Take iron away from tea, coffee, calcium, and antacids; vitamin C may improve absorption.
4. Continue therapy after Hb normalizes to replenish iron stores.
5. IV iron if oral iron is ineffective, not tolerated, malabsorption exists, or rapid replacement is needed.
6. RBC transfusion only for severe symptomatic anemia, hemodynamic instability, or active major bleeding.

6. Pulmonary edema

• Acute LV failure, MI, hypertension, arrhythmia.
• Acute mitral regurgitation, fluid overload, renal failure.

• Sudden dyspnea, orthopnea, tachypnea.
• Pink frothy sputum, cyanosis.
• Bilateral basal crepitations.
• Hypoxemia; CXR: bilateral “bat-wing” opacities.

• Sit upright, oxygen if hypoxemic, monitoring.
• CPAP/BiPAP if severe distress.
• IV furosemide if fluid overloaded.
• Nitrates if hypertensive and BP is adequate.
• Treat cause. Avoid nitrates in hypotension/shock.

7. Cardiogenic shock

• Extensive acute MI: most common.
• Mechanical MI complication, severe valve lesion.
• Arrhythmia, myocarditis, severe heart failure.

• SBP <90 mmHg, cold clammy skin.
• Confusion, oliguria, raised lactate.
• Weak pulse, tachycardia, pulmonary edema.

• ABC, ICU monitoring, oxygen/ventilation if needed.
• Cautious fluids only if hypovolemia/RV infarction.
• Norepinephrine for hypotension; dobutamine for low cardiac output.
• Urgent PCI/CABG if MI-related.
• Treat arrhythmia or mechanical cause.

8. Iron-deficiency anemia

• Low Hb and hematocrit.
• Low MCV: microcytic.
• Low MCH/MCHC: hypochromic.
• High RDW.
• Smear: pencil cells, microcytes, hypochromia.
• Sometimes reactive thrombocytosis.

• Low ferritin, serum iron, transferrin saturation.
• High TIBC.

• Find and treat cause, especially menstrual or GI blood loss.
• Oral iron first line.
• IV iron if malabsorption, intolerance, or need for rapid correction.
• Transfuse only if severe symptomatic anemia/instability.

9. Vitamin B12 and folate-deficiency anemia

• Low Hb, high MCV: macrocytic anemia.
• Macro-ovalocytes and hypersegmented neutrophils.
• May cause leukopenia and thrombocytopenia.

• B12 deficiency: neurological signs may occur, such as paresthesia and ataxia.
• Folate deficiency: no neurological manifestations.

• Replace vitamin B12, usually IM initially if severe/malabsorption.
• Folic acid orally for folate deficiency.
• Treat cause.
• Do not give folate alone until B12 deficiency is excluded, as neurologic damage may progress.

10. Congenital hemolytic anemia

• Anemia with increased reticulocyte count.
• Raised indirect bilirubin and LDH; low haptoglobin.
• Smear varies:
  • Spherocytes: hereditary spherocytosis.
  • Target cells/microcytosis: thalassemia.
  • Sickle cells: sickle-cell disease.

• Folic acid.
• Avoid triggers in G6PD deficiency.
• Transfusion when indicated.
• Specific therapy: hydroxyurea in sickle-cell disease; splenectomy in selected hereditary spherocytosis; iron chelation in transfusion-dependent thalassemia.

11. Acquired hemolytic anemia

• Autoimmune hemolytic anemia.
• Drugs, infections, mechanical hemolysis, microangiopathy.

• Anemia with reticulocytosis.
• Raised indirect bilirubin, LDH; low haptoglobin.
• Spherocytes in warm autoimmune hemolysis.
• Schistocytes in microangiopathic/mechanical hemolysis.
• Direct Coombs test positive in autoimmune hemolytic anemia.

• Treat underlying cause and stop offending drug.
• Warm autoimmune hemolysis: corticosteroids first line.
• Rituximab/splenectomy for refractory cases.
• Transfuse compatible blood if severe.

12. Acute leukemia

• Anemia and thrombocytopenia.
• WBC may be high, normal, or low.
• Blasts in peripheral blood.
• Neutropenia may occur.

• Infection/sepsis due to neutropenia.
• Bleeding due to thrombocytopenia/DIC.
• Tumor lysis syndrome.
• Leukostasis if very high WBC count.

• Urgent hematology referral.
• Confirm with bone marrow examination, flow cytometry, cytogenetics.
• Induction chemotherapy followed by consolidation.
• Supportive care: antibiotics, blood/platelet transfusion, tumor-lysis prevention.
• Acute promyelocytic leukemia: start ATRA urgently if suspected.

13. Chronic leukemia

CML

• Marked leukocytosis with granulocytes at all maturation stages.
• Basophilia, eosinophilia; often thrombocytosis.
• Philadelphia chromosome/BCR-ABL positive.

• Tyrosine kinase inhibitor, for example imatinib.
• Stem-cell transplant in resistant/advanced disease.

CLL

• Persistent lymphocytosis.
• Smudge cells.
• May develop anemia and thrombocytopenia later.

• Observation if asymptomatic early disease.
• Targeted therapy or chemoimmunotherapy when symptomatic/progressive.
• Treat infections and autoimmune cytopenias.

14. Mitral stenosis

• Loud S1.
• Opening snap after S2.
• Low-pitched mid-diastolic rumbling murmur at apex.
• Best heard with bell in left lateral position.
• Presystolic accentuation if sinus rhythm.

• Thickened, fused mitral leaflets with reduced opening.
• “Hockey-stick” anterior leaflet.
• Reduced mitral valve area.
• Left atrial enlargement, pulmonary hypertension.

15. Mitral regurgitation / insufficiency

• Soft S1.
• High-pitched pansystolic murmur at apex.
• Radiates to left axilla.
• May have S3 due to volume overload.

• Incomplete mitral leaflet closure.
• Regurgitant jet from LV to LA on color Doppler.
• LA and LV dilatation in chronic MR.
• Assess cause: prolapse, rheumatic disease, ischemia, chordal rupture.

16. Aortic stenosis

• Harsh ejection systolic murmur.
• Best heard at right 2nd intercostal space.
• Radiates to carotid arteries.
• Soft/absent A2 in severe disease.
• Slow-rising, low-volume pulse: pulsus parvus et tardus.

• Thickened/calcified aortic valve with reduced opening.
• High transvalvular velocity and pressure gradient.
• Reduced aortic valve area.
• LV hypertrophy.

17. Aortic regurgitation / insufficiency

• High-pitched, early diastolic decrescendo murmur.
• Best heard at left sternal border with patient sitting forward in expiration.
• Wide pulse pressure, bounding pulse.
• Austin Flint murmur may occur at apex in severe AR.

• Diastolic regurgitant jet from aorta to LV on color Doppler.
• LV dilatation due to volume overload.
• Assess aortic root dilatation, valve morphology, and severity of regurgitation.

18. Ulcerative colitis

• Continuous inflammation starting from rectum.
• Diffuse erythema, edema, loss of vascular pattern.
• Friability, superficial ulcers, spontaneous bleeding.
• Pseudopolyps in chronic disease.

• Loss of haustrations: “lead-pipe colon”.
• Mucosal granularity, ulcers.
• Toxic megacolon in severe disease.

• Inflammation limited to mucosa and submucosa.
• Cryptitis and crypt abscesses.
• Continuous lesions.
• No transmural inflammation or granulomas.

19. Crohn disease

• Skip lesions with normal bowel between affected areas.
• Aphthous ulcers, deep linear/serpiginous ulcers.
• Cobblestone appearance.
• Strictures, fistulas, perianal disease.
• Commonly affects terminal ileum and colon.

• “String sign” of terminal ileum due to stricture.
• Bowel-wall thickening, strictures, fistulas.
• “Comb sign” on CT: engorged mesenteric vessels.

• Transmural inflammation.
• Deep fissuring ulcers.
• Noncaseating granulomas may be present.
• Fibrosis, strictures, fistula formation.