Abscesses

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Abscesses

CONA CM

CONA CM

Anemia: Clinical
Microcytic anemia: Pathology review
Intrinsic hemolytic normocytic anemia: Pathology review
Extrinsic hemolytic normocytic anemia: Pathology review
Non-hemolytic normocytic anemia: Pathology review
Macrocytic anemia: Pathology review
Myeloproliferative disorders: Pathology review
Myeloproliferative neoplasms: Clinical
Leukemias: Pathology review
Leukemia: Clinical
Lymphoma: Clinical
Plasma cell disorders: Pathology review
Plasma cell disorders: Clinical
Platelet disorders: Pathology review
Thrombocytopenia: Clinical
Bleeding disorders: Clinical
Thrombosis syndromes (hypercoagulability): Pathology review
Thrombophilia: Clinical
Peripheral vascular disease: Clinical
Venous thromboembolism: Clinical
Deep vein thrombosis and pulmonary embolism: Pathology review
Thrombolytics
Antiplatelet medications
Anticoagulants: Warfarin
Anticoagulants: Heparin
Anticoagulants: Direct factor inhibitors
Blood products and transfusion: Clinical
Vaccinations: Clinical
Pneumonia: Clinical
Abscesses
Infective endocarditis: Clinical
Skin and soft tissue infections: Clinical
Septic arthritis
Osteomyelitis
Fever of unknown origin: Clinical
Diarrhea: Clinical
Gastroenteritis
Clostridium difficile (Pseudomembranous colitis)
Urinary tract infections: Clinical
Sexually transmitted infections: Clinical
Meningitis, encephalitis and brain abscesses: Clinical
Clostridium tetani (Tetanus)
Clostridium botulinum (Botulism)
Salmonellosis
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Pediatric upper airway conditions: Clinical
Pediatric lower airway conditions: Clinical
HIV (AIDS)
Herpes simplex virus
Varicella zoster virus
Herpesvirus medications
Epstein-Barr virus (Infectious mononucleosis)
Cytomegalovirus
Coccidioidomycosis and paracoccidioidomycosis
Aspergillus fumigatus
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Plasmodium species (Malaria)
Antimalarials
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Toxoplasma gondii (Toxoplasmosis)
Ascaris lumbricoides
Ancylostoma duodenale and Necator americanus
Strongyloides stercoralis
Enterobius vermicularis (Pinworm)
Anthelmintic medications
Bites and stings: Clinical
Cytomegalovirus infection after transplant (NORD)
Mechanisms of antibiotic resistance
Streptococcus pyogenes (Group A Strep)
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Candida
Staphylococcus aureus
Pediatric infectious rashes: Clinical
ECG basics
ECG normal sinus rhythm
ECG rate and rhythm
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ECG intervals
ECG QRS transition
ECG cardiac hypertrophy and enlargement
ECG cardiac infarction and ischemia
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Wolff-Parkinson-White syndrome
Ventricular tachycardia
Brugada syndrome
Premature ventricular contraction
Long QT syndrome and Torsade de pointes
Ventricular fibrillation
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Bundle branch block
Heart blocks: Pathology review
Pulseless electrical activity
Supraventricular arrhythmias: Pathology review
Ventricular arrhythmias: Pathology review
Heart failure
Heart failure: Pathology review
Heart failure: Clinical
Dilated cardiomyopathy
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Endocarditis
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Pericarditis and pericardial effusion
Cardiac tamponade
Dressler syndrome
Pericardial disease: Clinical
Myocardial infarction
Coronary artery disease: Clinical
Renal artery stenosis
Hypertension: Clinical
Aortic aneurysms and dissections: Clinical
Pulmonary hypertension
Peripheral artery disease
Chronic venous insufficiency
Leg ulcers: Clinical
Congenital heart defects: Clinical
Lymphedema
Syncope: Clinical
Tuberculosis: Pathology review
Asthma: Clinical
Diffuse parenchymal lung disease: Clinical
Bronchiectasis
Obstructive lung diseases: Pathology review
Restrictive lung diseases: Pathology review
Lung cancer: Clinical
Pleural effusion: Clinical
Anatomy clinical correlates: Pleura and lungs
Pleural effusion, pneumothorax, hemothorax and atelectasis: Pathology review
Sleep apnea
Respiratory distress syndrome: Pathology review
Acute respiratory distress syndrome: Clinical
Chronic obstructive pulmonary disease (COPD): Clinical
Pneumothorax: Clinical
Acute kidney injury: Clinical
Chronic kidney disease: Clinical
Nephritic and nephrotic syndromes: Clinical
Hypernatremia: Clinical
Hyponatremia: Clinical
Hyperkalemia: Clinical
Hypokalemia: Clinical
Parathyroid conditions and calcium imbalance: Clinical
Metabolic and respiratory alkalosis: Clinical
Metabolic and respiratory acidosis: Clinical
Kidney stones: Clinical
Esophageal disorders: Clinical
Esophageal surgical conditions: Clinical
Esophagitis: Clinical
Gastroesophageal reflux disease (GERD): Clinical
Peptic ulcers and stomach cancer: Clinical
Malabsorption syndromes: Pathology review
Inflammatory bowel disease: Clinical
Irritable bowel syndrome
Viral hepatitis: Clinical
Jaundice: Clinical
Cirrhosis: Clinical
Pancreatitis: Clinical
Alcohol-associated liver disease
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Antiphospholipid syndrome
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Joint pain: Clinical
Scleroderma: Pathology review
Sjogren syndrome: Clinical
Seronegative arthritis: Clinical
Vasculitis: Clinical
Inflammatory myopathies: Clinical
Sarcoidosis
Gout and pseudogout: Pathology review
Antigout medications
Fibromyalgia
Hypopituitarism: Clinical
Thyroid nodules and thyroid cancer: Clinical
Hypothyroidism and thyroiditis: Clinical
Hyperthyroidism: Clinical
Adrenal masses and tumors: Clinical
Adrenal insufficiency: Clinical
Congenital adrenal hyperplasia: Clinical
MEN syndromes: Clinical
Cushing syndrome: Clinical
Pituitary adenomas and pituitary hyperfunction: Clinical
Diabetes mellitus: Clinical
Hypercholesterolemia: Clinical
Osteoporosis
Hemochromatosis
Seizures: Clinical
Cerebral vascular disease: Pathology review
Stroke: Clinical
Headaches: Clinical
Dementia and delirium: Clinical
Alzheimer disease
Parkinson disease
Hypokinetic movement disorders: Clinical
Hyperkinetic movement disorders: Clinical
Trigeminal neuralgia
Bell palsy
Multiple sclerosis
Guillain-Barre syndrome
Muscle weakness: Clinical
Myasthenia gravis
Lambert-Eaton myasthenic syndrome
Shock: Clinical
Disorders of consciousness: Clinical
Subarachnoid hemorrhage

Flashcards

Abscesses

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Everyone who has ever had a pimple has had an abscess, even though they’re tiny, they’re still abscesses.

An abscess forms when normal tissue, like skin for example, is split apart and that new space is invaded by nearby pathogens like bacteria.

And there are roughly ten bacterial cells for every one human cell and they cover every surface of the human body.

So any cut or break in the skin or closed off area within the body is an invitation for bacteria to dive in and multiply.

When that happens the immune system typically responds and a battle ensues with the result being pus - a mixture of bacteria, immune cells, and dead tissue.

So, in response to an injury, the tissue releases small chemicals in the local area called cytokines, like tumor necrosis factor, interleukin-1, interleukin-6 and interleukin-17, and chemokines which attract nearby white blood cells which are part of the immune system. It’s kinda like yelling for help and being heard by the nearby police.

In addition to attracting immune cells, the cytokines also dilate nearby capillaries - which brings more blood to the site, and make the capillaries more leaky, so that the white blood cells that do show up, can slip out of the blood and get into the tissue more easily.

Often times, the first immune cells at the scene are neutrophils, which release chemicals and enzymes that kill bacteria and dissolve pieces of of dead cells, creating a pool of dead material.

This is a specific type of acute inflammatory response called suppurative inflammation, which simply means that pus is created in the process.

From a macroscopic view, this is sometimes referred to a liquefactive necrosis, because the area of dead tissue turns to liquid.

As those immune cells get to a point where they can’t withstand the environment, they die too, and become part of that pool.

Initially the debris might be intermixed with healthy tissue, but over time it can coalesce into a single area - a process that is often sped up when more immune cells get involved.

Around this pool of pus, a wall of fibrinogen - which is the same protein that holds together blood clots - starts to harden into a barrier.

Occasionally sheets of fibrin form septations, creating loculations or pockets of pus within the abscess itself...kinda like an abscess within an abscess.

Even though the pus is largely dead material, there are still plenty of live bacteria within the pus, which makes it highly infectious if it gets spread from one place to another.

One of the most common bacteria found in abscesses, especially in the skin or underlying soft tissue, is Staphylococcus aureus.

In fact, Staphylococcus aureus releases the enzyme coagulase, which helps speed up the process of building the fibrinogen wall.

In contrast to an abscess near the skin, ones that originate deeper in the body often occur in spaces that are already relatively walled off.

For example, in the gallbladder, if a stone blocks bile from flowing out, it essentially becomes a new home for bacteria.

Bacteria from the nearby small intestine can easily sneak past the stone, crawl into the gallbladder, and multiply, which causes an inflammatory response, and eventually an abscess might form.

Typically these deep infections are a mix of aerobic bacteria that use up all of the available oxygen, and anaerobic bacteria that can only live in its absence.

Sources

  1. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  2. "CURRENT Medical Diagnosis and Treatment 2020" McGraw-Hill Education / Medical (2019)
  3. "Yen & Jaffe's Reproductive Endocrinology" Saunders W.B. (2018)
  4. "Bates' Guide to Physical Examination and History Taking" LWW (2016)
  5. "Robbins Basic Pathology" Elsevier (2017)
  6. "Etymologia:<i>Staphylococcus</i>" Emerging Infectious Diseases (2013)
  7. "Patterns of Contrast Enhancement in the Brain and Meninges" RadioGraphics (2007)
  8. "A play in four acts: Staphylococcus aureus abscess formation" Trends in Microbiology (2011)