Iron deficiency anemia (IDA)

A 35 year old woman presents to her primary care physician with a history of fatigue and generalized weakness for 6 months. She reports shortness of breath on exertion and has developed pica, specifically craving and eating ice. She follows a vegetarian diet. She also reports chronic rectal bleeding, noticing bright red blood on the toilet paper and on the surface of the stool. She denies pain during defecation but has anal itching and discomfort. She has a history of chronic constipation with straining. On examination, there is pallor of the skin and conjunctiva. No lymphadenopathy or hepatosplenomegaly is present. On per rectal examination, external hemorrhoids are noted. Laboratory studies show low hemoglobin with low MCV. Iron studies reveal low ferritin, low serum iron, high TIBC, and low transferrin saturation. Diagnosis?

Diagnosis is Iron deficiency anemia, most likely secondary to chronic blood loss, with hemorrhoids as a probable source; however, further evaluation for gastrointestinal bleeding is required.

1. Definition

Iron deficiency anemia is a microcytic hypochromic anemia caused by insufficient iron availability for hemoglobin synthesis.

2. Etiology

1. Chronic blood loss
• Gastrointestinal bleeding including hemorrhoids, but occult malignancy must be excluded
• Menstrual blood loss
2. Decreased iron intake
• Vegetarian diet
3. Increased requirements
• Pregnancy, growth
4. Malabsorption
• Celiac disease, post gastrectomy

3. Pathophysiology

1. Depletion of iron stores
2. Reduced heme synthesis
3. Decreased hemoglobin production
4. Formation of microcytic hypochromic red blood cells
5. Iron is primarily absorbed in the duodenum

4. Clinical Features

1. Fatigue and weakness
2. Dyspnea on exertion
3. Pallor
4. Pica, especially pagophagia
5. Koilonychia
6. Glossitis and angular cheilitis

Associated syndrome:

• Plummer Vinson syndrome
• Iron deficiency anemia
• Esophageal webs
• Dysphagia

5. Diagnosis

5.1 Complete Blood Count

1. Low hemoglobin
2. Low MCV <80 fL
3. Increased RDW

5.2 Iron Studies

1. Low ferritin (most specific)
2. Low serum iron
3. High TIBC
4. Low transferrin saturation

5.3 Additional Tests

1. Elevated soluble transferrin receptor
2. Increased free erythrocyte protoporphyrin
3. Mentzer index >13 suggests iron deficiency over thalassemia
4. Possible reactive thrombocytosis

6. Management

1. Identify and treat the underlying cause
• Evaluate for gastrointestinal bleeding, including endoscopic assessment if indicated
2. Iron replacement therapy
• Oral iron such as ferrous sulfate is first line
• Take with vitamin C to enhance absorption
3. Intravenous iron
• For intolerance, malabsorption, or severe deficiency
4. Monitoring response
• Reticulocytosis occurs within 5 to 7 days
• Hemoglobin improves over weeks

7. Complications

1. Severe anemia leading to cardiac strain
2. Impaired cognitive and physical performance
3. Restless leg syndrome

8. Key Clinical Insight

Microcytic anemia with low ferritin and pica in a patient with chronic rectal bleeding strongly indicates iron deficiency anemia, but gastrointestinal malignancy must be excluded in adults

9. Exam Level Pearls

1. Low ferritin is the most specific marker of iron deficiency anemia
2. Pica, especially ice craving, is a classic feature
3. High TIBC differentiates iron deficiency from anemia of chronic disease
4. Mentzer index >13 favors iron deficiency over thalassemia
5. Always evaluate chronic blood loss anemia in adults for occult gastrointestinal malignancy

Kawasaki disease

A 5-year-old female child presents to the emergency department with a history of high-grade fever and red eyes for 6 days. Examination reveals red, cracked lips, a strawberry tongue, and a faint maculopapular rash that began on the trunk and has spread to the limbs. Her palms and soles are erythematous and swollen. She also has cervical lymphadenopathy. Laboratory studies show elevated inflammatory markers (CRP and ESR). Echocardiography demonstrates coronary artery aneurysms. Diagnosis?

Diagnosis is Kawasaki disease.

1. Definition

Kawasaki disease is an acute, self-limited medium-vessel vasculitis of unknown etiology that primarily affects children and has a predilection for the coronary arteries.
It is the leading cause of acquired heart disease in children.

2. Etiology

1. Unknown etiology
2. Likely infectious trigger in genetically predisposed individuals
3. Immune-mediated vascular inflammation

3. Pathophysiology

Kawasaki disease involves immune activation with subsequent cytokine release, leading to endothelial injury and inflammation of medium-sized vessels. This results in coronary arteritis, which weakens the vessel wall and predisposes to the formation of coronary artery aneurysms.

4. Clinical Features

4.1 Diagnostic Criteria (CRASH)

Fever ≥5 days + ≥4 of the following:

1. Conjunctivitis (bilateral, non-purulent)
2. Rash (polymorphous, non-vesicular)
3. Adenopathy (cervical lymphadenopathy >1.5 cm, usually unilateral)
4. Strawberry tongue (± red/cracked lips)
5. Hands/feet changes (erythema, edema ± desquamation)

Diagnosis can be made with fewer criteria if coronary artery abnormalities are present.

4.2 Additional Features

1. Occurs in children <5 years
2. Symptoms appear sequentially
3. Irritability
4. Periungual desquamation in subacute phase

5. Diagnosis

Diagnosis is clinical; investigations support and assess complications.

5.1 Laboratory Findings

1. Leukocytosis
2. Elevated CRP and ESR
3. Thrombocytosis (subacute phase)

5.2 Echocardiography

1. Coronary artery aneurysms
2. May show myocarditis

6. Management

1. IVIG: 2 g/kg single infusion (within 7–10 days of fever onset)
2. Aspirin:
• High dose: 80–100 mg/kg/day (acute phase)
• Low dose: 3–5 mg/kg/day after afebrile for 48–72 hours

7. Complications

1. Coronary artery aneurysms (most important)
2. Myocardial infarction
3. Thrombosis

8. Key Clinical Insight

Child with prolonged fever + mucocutaneous findings + extremity changes + coronary involvement → Kawasaki disease

9. Exam Level Pearls

1. Fever ≥5 days is essential for diagnosis
2. Non purulent conjunctivitis distinguishes it from infection
3. Thrombocytosis occurs in the subacute phase
4. IVIG reduces risk of coronary artery aneurysms
5. Do not delay treatment if clinical suspicion is high

Atrial Fibrillation

A 55 year old female presents to the emergency department with sudden onset palpitations that began 30 minutes ago. She describes a sensation of heart racing and reports lightheadedness and dizziness, without chest pain, shortness of breath, or syncope. She has had similar self resolving episodes in the past and has a history of coronary artery disease. Vital signs show a pulse rate of 180 beats per minute, blood pressure of 110/70 mm Hg, respiratory rate of 16 breaths per minute, oxygen saturation of 96 percent on room air, and temperature of 98.2 F. Laboratory studies are within normal limits. ECG shows absent P waves, irregularly irregular rhythm, and narrow QRS complexes. Transesophageal echocardiography demonstrates a thrombus in the left atrium. Diagnosis?

Diagnosis is Atrial fibrillation with left atrial thrombus.

1. Definition

Atrial fibrillation is a supraventricular arrhythmia characterized by disorganized atrial electrical activity, resulting in an irregularly irregular ventricular rhythm and loss of effective atrial contraction.

2. Modern Classification

Atrial fibrillation is now considered a disease continuum:

1. Stage 1: At risk for AF
2. Stage 2: Pre AF with structural or electrical abnormalities
3. Stage 3: AF including paroxysmal, persistent, and long standing persistent AF
4. Stage 4: Permanent AF

This framework emphasizes risk factor modification, early detection, and treatment.

3. Etiology and Risk Factors

1. Coronary artery disease
2. Hypertension
3. Valvular heart disease, especially mitral stenosis
4. Thyrotoxicosis
5. Alcohol use
6. Obstructive sleep apnea
7. Obesity and metabolic syndrome

4. Pathophysiology

1. Ectopic impulses arise from the pulmonary veins
2. Cause chaotic atrial depolarization
3. Loss of atrial kick reduces cardiac output
4. Leads to blood stasis in the left atrium, especially the left atrial appendage
5. Results in thrombus formation and risk of embolic stroke

5. Clinical Features

1. Palpitations
2. Dizziness or lightheadedness
3. Fatigue
4. Shortness of breath
5. May be asymptomatic

6. Diagnosis

1. ECG findings
• Absent P waves
• Irregularly irregular rhythm
• Narrow QRS complexes
2. Echocardiography
• Detects left atrial thrombus
• Evaluates structural heart disease
3. Laboratory evaluation
• Rule out thyroid dysfunction and electrolyte abnormalities

7. Management

Management is based on rate control, rhythm control, and stroke prevention

7.1 Rate Control

1. Beta blockers
2. Non dihydropyridine calcium channel blockers
3. Digoxin in selected patients

7.2 Rhythm Control

1. Early rhythm control is recommended to reduce AF burden and progression
2. Electrical cardioversion
• Indicated if hemodynamically unstable
3. Pharmacologic cardioversion
• Amiodarone, flecainide, ibutilide
4. Key cardioversion principles
• AF <48 hours
• Cardioversion may be performed
• Anticoagulation should still be considered based on stroke risk
• AF >48 hours or unknown duration
• Requires
• TEE to exclude thrombus, or
• At least 3 weeks of anticoagulation before cardioversion
• If left atrial thrombus is present
• Cardioversion is contraindicated
• Requires adequate anticoagulation and confirmation of thrombus resolution before cardioversion

7.3 Anticoagulation

1. Use CHA2DS2 VASc score to assess stroke risk
2. Anticoagulation is indicated when
• Score ≥2 in men or ≥2 in women
3. Direct oral anticoagulants are preferred over warfarin in nonvalvular AF
4. Continue anticoagulation for at least 4 weeks after cardioversion

7.4 Interventional Therapy

1. Catheter ablation
• First line in selected symptomatic patients, especially paroxysmal AF
2. Left atrial appendage occlusion
• For patients with contraindications to long term anticoagulation

8. Complications

1. Ischemic stroke
2. Systemic embolism
3. Heart failure
4. Tachycardia induced cardiomyopathy

9. Key Clinical Insight

Irregularly irregular rhythm with absent P waves and presence of left atrial thrombus indicates atrial fibrillation with high embolic risk, requiring anticoagulation and delaying cardioversion until thrombus resolution

10. Exam Level Pearls

1. Irregularly irregular rhythm is diagnostic of atrial fibrillation
2. Left atrial appendage is the most common site of thrombus formation
3. Cardioversion is contraindicated in the presence of atrial thrombus
4. Anticoagulation is the most important step to prevent stroke
5. Early rhythm control improves long term outcomes