Pallor examination

Splenomegaly can be due to several mechanisms but is almost always a sign of a systemic condition. Patient habits, travel, and medical conditions can increase risk of splenomegaly and suggest etiology. Symptoms can suggest infectious, malignant, hepatic, or hematologic causes. Physical examination will typically reveal splenomegaly, but abdominal ultrasonography is recommended for confirmation. Physical examination should also assess for signs of systemic illness, liver disease, and anemia or other hematologic issues. The most common causes of splenomegaly in the United States are liver disease, malignancy, and infection. Except for apparent causes such as infectious mononucleosis, basic laboratory analysis and ultrasonography are the first-line steps in determining etiology. Malaria and schistosomiasis are common in tropical regions, where as many as 80% of people may have splenomegaly. Management of splenomegaly involves treating the underlying disease process. Splenectomies and spleen reduction therapies are sometimes performed. Any patient with limited splenic function requires increased vaccination and prophylactic antibiotics for procedures involving the respiratory tract. Acute infections, anemia, and splenic rupture are the most common complications of splenomegaly, and people with splenomegaly should refrain from participating in contact sports to decrease risk of rupture. Clinical recommendation Evidence rating Comments – , C Expert opinion based on cirrhosis bei...

Anemia is defined as a hemoglobin level of less than the 5th percentile for age. Causes vary by age. Most children with anemia are asymptomatic, and the condition is detected on screening laboratory evaluation. Screening is recommended only for high-risk children. Anemia is classified as microcytic, normocytic, or macrocytic, based on the mean corpuscular volume. Mild microcytic anemia may be treated presumptively with oral iron therapy in children six to 36 months of age who have risk factors for iron deficiency anemia. If the anemia is severe or is unresponsive to iron therapy, the patient should be evaluated for gastrointestinal blood loss. Other tests used in the evaluation of microcytic anemia include serum iron studies, lead levels, and hemoglobin electrophoresis. Normocytic anemia may be caused by chronic disease, hemolysis, or bone marrow disorders. Workup of normocytic anemia is based on bone marrow function as determined by the reticulocyte count. If the reticulocyte count is elevated, the patient should be evaluated for blood loss or hemolysis. A low reticulocyte count suggests aplasia or a bone marrow disorder. Common tests used in the evaluation of macrocytic anemias include vitamin B 12 and folate levels, and thyroid function testing. A peripheral smear can provide additional information in patients with anemia of any morphology. Anemia is usually classified based on the size of RBCs, as measured by the mean corpuscular volume (MCV). Anemia can be microcytic ...

1. Optic disc pallor in excess of cupping. Various insults can occur to the optic nerve and manifest ophthalmoscopically as pallor, atrophy, cupping and notching. By far, the most common optic nerve affliction is glaucoma. Glaucoma presents with a very characteristic cavernous atrophy, commonly termed “cupping” or “notching.” This distinctive neuropathy presents with enlargement of the optic disc cup—preferentially at the inferior and superior regions—with an enlarged vertical cupping pattern and compromise or obliteration of the neuroretinal rim. In this chronic disease, there typically is an absence of pallor. The rim tissue remains well perfused, although focal damage occurs to the superior and inferior neuroretinal rim. Occasionally, patients will present with glaucomatous-type optic nerves and exhibit additional features, such as pallor, which indicate the presence of another condition entirely or an entity in addition to glaucoma. There are also several clinical entities and situations in which the optic nerve can be compromised and superficially resemble glaucoma. It is imperative to correctly differentiate these non-glaucomatous neuropathies from glaucoma. Is There Optic Disc Pallor? Identifying optic disc pallor sometimes is difficult when the condition is subtle, or there are media and cataract issues impairing judgment. It can also be challenging to differentiate true disc pallor from mimics. For example, after cataract extraction, there is a loss of the light-a...

Cardiovascular examination frequently appears in OSCEs and you’ll be expected to pick up the relevant clinical signs using your examination skills. This cardiovascular examination OSCE guide provides a clear step-by-step approach to examining the cardiovascular system, with an included video demonstration. Download the cardiovascular examination Introduction Wash your hands and don PPE if appropriate. Introduce yourself to the patient including your name and role. Confirm the patient’s name and date of birth. Briefly explain what the examination will involve using patient-friendly language. Gain consent to proceed with the examination. Adjust the head of the bed to a 45° angle. Adequately expose the patient’s chest for the examination (offer a blanket to allow exposure only when required and if appropriate, inform patients they do not need to remove their bra). Exposure of the patient’s lower legs is also helpful to assess for peripheral oedema and signs of peripheral vascular disease. Ask the patient if they have any pain before proceeding with the clinical examination. You might also be interested in our over 2000 flashcards that cover clinical examination, procedures, communication skills and data interpretation. General inspection Clinical signs Inspect the patient from the end of the bed whilst at rest, looking for clinical signs suggestive of underlying pathology: • Cyanosis: a bluish discolouration of the skin due to poor circulation (e.g. peripheral vasoconstrictio...

Contents • 1 Disease Entity • 1.1 Etiology • 1.2 Risk Factors • 1.3 General Pathology • 1.4 Primary prevention • 2 Diagnosis • 2.1 History • 2.2 Physical examination • 2.3 Signs • 2.4 Symptoms • 2.5 Clinical diagnosis • 2.6 Diagnostic procedures • 2.7 Laboratory test • 2.8 Differential diagnosis • 3 Management • 3.1 Prognosis • 4 Additional Resources • 5 References Disease Entity Optic atrophy refers to the death of the retinal ganglion cell axons that comprise the optic nerve with the resulting picture of a pale optic nerve on fundoscopy. Optic atrophy is an end stage that arises from myriad causes of optic nerve damage anywhere along the path from the retina to the lateral geniculate. Since the optic nerve transmits retinal information to the brain, optic atrophy is associated with vision loss. Optic atrophy is somewhat of a misnomer as atrophy implies disuse, and thus optic nerve damage is better termed optic neuropathy. Etiology Anything that can compromise ganglion cell function can cause (over time) optic atrophy (and more broadly optic neuropathy). Optic atrophy can occur due to damage within the eye (glaucoma, optic neuritis, papilledema, etc.), along the path of the optic nerve to the brain (tumor, neurodegenerative disorder, trauma, etc.), or it can be congenital (Leber’s hereditary optic atrophy, autosomal dominant optic atrophy). Risk Factors Risk factors run the gamut from increased intraocular pressure (glaucoma), ischemia, compression (tumors), inflammation,...

Careful examination of the oral cavity may reveal findings indicative of an underlying systemic condition, and allow for early diagnosis and treatment. Examination should include evaluation for mucosal changes, periodontal inflammation and bleeding, and general condition of the teeth. Oral findings of anemia may include mucosal pallor, atrophic glossitis, and candidiasis. Oral ulceration may be found in patients with lupus erythematosus, pemphigus vulgaris, or Crohn disease. Additional oral manifestations of lupus erythematosus may include honeycomb plaques (silvery white, scarred plaques); raised keratotic plaques (verrucous lupus erythematosus); and nonspecific erythema, purpura, petechiae, and cheilitis. Additional oral findings in patients with Crohn disease may include diffuse mucosal swelling, cobblestone mucosa, and localized mucogingivitis. Diffuse melanin pigmentation may be an early manifestation of Addison disease. Severe periodontal inflammation or bleeding should prompt investigation of conditions such as diabetes mellitus, human immunodeficiency virus infection, thrombocytopenia, and leukemia. In patients with gastroesophageal reflux disease, bulimia, or anorexia, exposure of tooth enamel to acidic gastric contents may cause irreversible dental erosion. Severe erosion may require dental restorative treatment. In patients with pemphigus vulgaris, thrombocytopenia, or Crohn disease, oral changes may be the first sign of disease. Clinical recommendation Evidence...

Contents • 1 Disease Entity • 1.1 Etiology • 1.2 Risk Factors • 1.3 General Pathology • 1.4 Primary prevention • 2 Diagnosis • 2.1 History • 2.2 Physical examination • 2.3 Signs • 2.4 Symptoms • 2.5 Clinical diagnosis • 2.6 Diagnostic procedures • 2.7 Laboratory test • 2.8 Differential diagnosis • 3 Management • 3.1 Prognosis • 4 Additional Resources • 5 References Disease Entity Optic atrophy refers to the death of the retinal ganglion cell axons that comprise the optic nerve with the resulting picture of a pale optic nerve on fundoscopy. Optic atrophy is an end stage that arises from myriad causes of optic nerve damage anywhere along the path from the retina to the lateral geniculate. Since the optic nerve transmits retinal information to the brain, optic atrophy is associated with vision loss. Optic atrophy is somewhat of a misnomer as atrophy implies disuse, and thus optic nerve damage is better termed optic neuropathy. Etiology Anything that can compromise ganglion cell function can cause (over time) optic atrophy (and more broadly optic neuropathy). Optic atrophy can occur due to damage within the eye (glaucoma, optic neuritis, papilledema, etc.), along the path of the optic nerve to the brain (tumor, neurodegenerative disorder, trauma, etc.), or it can be congenital (Leber’s hereditary optic atrophy, autosomal dominant optic atrophy). Risk Factors Risk factors run the gamut from increased intraocular pressure (glaucoma), ischemia, compression (tumors), inflammation,...

Cardiovascular examination frequently appears in OSCEs and you’ll be expected to pick up the relevant clinical signs using your examination skills. This cardiovascular examination OSCE guide provides a clear step-by-step approach to examining the cardiovascular system, with an included video demonstration. Download the cardiovascular examination Introduction Wash your hands and don PPE if appropriate. Introduce yourself to the patient including your name and role. Confirm the patient’s name and date of birth. Briefly explain what the examination will involve using patient-friendly language. Gain consent to proceed with the examination. Adjust the head of the bed to a 45° angle. Adequately expose the patient’s chest for the examination (offer a blanket to allow exposure only when required and if appropriate, inform patients they do not need to remove their bra). Exposure of the patient’s lower legs is also helpful to assess for peripheral oedema and signs of peripheral vascular disease. Ask the patient if they have any pain before proceeding with the clinical examination. You might also be interested in our over 2000 flashcards that cover clinical examination, procedures, communication skills and data interpretation. General inspection Clinical signs Inspect the patient from the end of the bed whilst at rest, looking for clinical signs suggestive of underlying pathology: • Cyanosis: a bluish discolouration of the skin due to poor circulation (e.g. peripheral vasoconstrictio...

Careful examination of the oral cavity may reveal findings indicative of an underlying systemic condition, and allow for early diagnosis and treatment. Examination should include evaluation for mucosal changes, periodontal inflammation and bleeding, and general condition of the teeth. Oral findings of anemia may include mucosal pallor, atrophic glossitis, and candidiasis. Oral ulceration may be found in patients with lupus erythematosus, pemphigus vulgaris, or Crohn disease. Additional oral manifestations of lupus erythematosus may include honeycomb plaques (silvery white, scarred plaques); raised keratotic plaques (verrucous lupus erythematosus); and nonspecific erythema, purpura, petechiae, and cheilitis. Additional oral findings in patients with Crohn disease may include diffuse mucosal swelling, cobblestone mucosa, and localized mucogingivitis. Diffuse melanin pigmentation may be an early manifestation of Addison disease. Severe periodontal inflammation or bleeding should prompt investigation of conditions such as diabetes mellitus, human immunodeficiency virus infection, thrombocytopenia, and leukemia. In patients with gastroesophageal reflux disease, bulimia, or anorexia, exposure of tooth enamel to acidic gastric contents may cause irreversible dental erosion. Severe erosion may require dental restorative treatment. In patients with pemphigus vulgaris, thrombocytopenia, or Crohn disease, oral changes may be the first sign of disease. Clinical recommendation Evidence...

Splenomegaly can be due to several mechanisms but is almost always a sign of a systemic condition. Patient habits, travel, and medical conditions can increase risk of splenomegaly and suggest etiology. Symptoms can suggest infectious, malignant, hepatic, or hematologic causes. Physical examination will typically reveal splenomegaly, but abdominal ultrasonography is recommended for confirmation. Physical examination should also assess for signs of systemic illness, liver disease, and anemia or other hematologic issues. The most common causes of splenomegaly in the United States are liver disease, malignancy, and infection. Except for apparent causes such as infectious mononucleosis, basic laboratory analysis and ultrasonography are the first-line steps in determining etiology. Malaria and schistosomiasis are common in tropical regions, where as many as 80% of people may have splenomegaly. Management of splenomegaly involves treating the underlying disease process. Splenectomies and spleen reduction therapies are sometimes performed. Any patient with limited splenic function requires increased vaccination and prophylactic antibiotics for procedures involving the respiratory tract. Acute infections, anemia, and splenic rupture are the most common complications of splenomegaly, and people with splenomegaly should refrain from participating in contact sports to decrease risk of rupture. Clinical recommendation Evidence rating Comments – , C Expert opinion based on cirrhosis bei...