Chronic venous disease, Rash, pneumonia Flashcards

1
Q

Chronic Venous Disease (CVD)

A
  • A wide spectrum of morphologic and/or functional abnormalities of the veins of long duration
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2
Q

Types of veins

A
  1. Superificial veins - subcutaneous veins that are superficial to the deep muscular fasica (ex. great saphenous and small saphenous veins).
  2. Deep veins - either within the muscle or between the muscles (intermuscular)
    • Intermuscular are more important in the development of chronic venous disease (ex. anterior tibial, posterior tibial, peroneal, popliteal, and femoral).
  3. Perforating veins - communicate between and superficial venous system
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3
Q

What determines venous flow?

A
  1. Biscuspid venous valves - direct flow from distal to proximal and from superifical to deep
    • Valves prevent transmission of sudden incease in venous pressure and prevent backflow
  2. Venous pump - pumping effect of leg muscles on venous flow
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4
Q

Pathophysiology of chronic venous disease

A
  • Inadequate muscle pump, incompetent venous valves, and venous thrombosis or obstruction can result in elevated venous pressure (venous hypertension)
    • Mainly in deep veins
  • Venous hypertension results in anatomic, physiologic and histologic changes that result in vein dilation (and increased permeability/edema), skin changes, and/or skin ulceration.
  • Factors that determine if patient will have milde or severe form of CVD is unknown.
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5
Q

Risk factors for chronic venous disease

A
  • Age
  • Family history
  • Ligamentous laxity
  • Prolonged standing
  • Increased BMI
  • Smoking
  • Sedentary lifestyle
  • Lower extremity trauma
  • Prior venous thrombosis
  • Presence of arteriovenous shunt
  • High estrogen States
  • Pregnancy
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6
Q

Clinical Features of Chronic Venous Disease

A
  • Chronic venous disease is an entrie spectrum of disorders with a range of symptoms and severities
  • Symptoms:
    • Pain
    • Leg heaviness
    • Leg aching
    • Swelling
    • Dry skin
    • Trightness
    • Skin irritation
    • Muscle cramps
    • Itching
  • Clinical signs
    • Dilated veins
    • Edema
    • Lipodermatosclerosis - fibrosing dermatitis of subcutaneous tissue
    • Ulceration
    • Statis dermatitis
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7
Q

Diagnosis of Chronic venous disease

A
  • Diagnosis is made by the presence of typical symptoms and confirmed by presence of venous reflux (determined via duplex ultrasound).
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8
Q

Treatment Chronic Venous Disease

A
  • Conservative management
    • Leg elevation, exerciser, compression therapy
    • Topical dermatological agents for skin changes
    • Venous ulceration - ulcer wound management + compression therapy
  • Laser, surgery, ablation
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9
Q

Atopic Dermatitis (eczema)

A
  • A chronic, pruritic, inflammatory skin disease
  • Occurs most often in children, but also affects adults
  • Acute eczema - rapidly evolving red rash that might be blistered and swollen
  • Chronic eczema - longstanding irritable area
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10
Q

Pathophysiology Eczema

A
  • Often associated with elevated levels of IgE and personal or family history of atopy (group of disorders that include eczema, asthma, and allergic rhinitis).
  • Several factors are involved in the pathogensis of eczema including, skin barrier abnormalities, defects in innate immune response, and alterations in skin flora
    • Epidermis in patients with eczema tends to be imparied with increased transepidermal water loss
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11
Q

Clincial features Eczema

A
  • Skin dryness and pruritus are the main featues. Also see erythema, oozing, crusting, and lichenification (thickening).
  • Acute - intensely pruritic erythematous papules, vesicles with exudation and crusting
  • Chronic - dry, scaly, or excoriated eythematous papules
  • Atopic dermatitis has a chronic relapsing course over months to years. People with mild disease may have intermittent flares with spontaneous remission. However, patietns with moderate to severe eczema generally don’t clear without treatment.
  • Patients with eczema have increased incidence of bacterial and viral skin infection, due to “weaknesses” in skin barrier.
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12
Q

Treatment atopic dermatitis

A
  • Elmination of exacerbating factors
    • Avoidance of heat and low humidity
    • Treat skin infection
    • Use of antihistamines to control itching
    • Reduction of stress and anxiety
  • Skin hydration - important to use thick creams, with low water content, or ointments with zero water content. Skin hydration is especially important after bathing.
  • Topical corticosteriods - potency of the steriod depends on the severity of the eczema
  • Phototherapy - can be use in patients with moderate to severe atopic dermatitis who don’t respond to topical therapu (cannot be used in young children).
  • Oral cyclosporin - short term treatment options for patients with moderate to severe eczema who don’t repond to topical therapy and can’t use phototherapy
  • Other systemic immunosuppressants
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13
Q

Cellulitis and Skin Abscess

A
  • Cellulitis - A bacterial infection of the skin and tissue beneath the skin
  • Skin abscess - collection of pus within the dermis or the subcutaneous space
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14
Q

Risk factors for development of cellulitis or skin abscess

A
  • Skin barrier disruption due to trauma - abrasion, penetrating wound, pressure ulcer, venous leg ulcer, insect bite, injection drug use, etc.
  • Skin inflammation - eczema, radiation therapy
  • Edema due to impaired lymphatic drainage
  • Obesity
  • Immunosuppresion (ex. diabetes, HIV)
  • Breaks in skin between toes
  • Preexisting skin infection
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15
Q

Pathophysiology cellulitis

A
  • Most commonly caused by B-hemolytic streptococci and less commonly S. aureus or gram negative aerobic bacilli. However, many bacteria can result in cellulitis especially if the patient is immunocompromised.
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16
Q

Pathophysiology Skin abscess

A
  • Painful, fluctuant, erythematous nodule, with or without surrounding cellulitis
  • Regional adenopathy (swollen lymph nodes)
17
Q

Complications of cellulitis and abscess

A
  • Bacteremia, endocarditis, osteomyelitis, metastatic infection, sepsis, and toxic shock syndrome
18
Q

Treatment for skin abscess and cellulitis

A
  • Patients with nonpurulent infection - should be managed with empiric antibiotic therapy
  • Patients with drainable abscess - should undergo incision and drainage + antibiotic therapy
  • Patients with purulent cellulitis - antibiotic therapy
  • In mild infection, oral antibiotics are sufficent. Parenteral antibiotics are warrented when there are:
    • Systemic signs of toxicity - fever, hypotension, or sustained tachycardia.
    • Rapid progression of eythema
    • Progression of clinical findings after 48hrs of oral antibiotics
    • Inability to tolerate oral therapy
    • Promixity of lesion to indweling medical device
19
Q

Antibiotics for skin abscess and cellulitis

A
  1. If patient has signs indicating MRSA coverage (systemtic signs of toxicity, infection overlying medical device, etc).
    • Vancomycin (IV)
  2. No indication for MRSA coverage
    • B-lactam (cefazolin, naficillin, oxacillin)
    • Clindamycin (if patient has B-lactam allergy)
  3. Indication of oral antibiotics therapy with MRSA coverage (i.e., previous MRSA exposure)
    • Amoxiciliin + doxycyline
    • Clindamycin
  4. Indication for oral antibiotics with no MRSA coverage needed:
    • Dicloxacillin
    • Cefadroxil
    • Clindamycin
20
Q

Pitting Edema

A
  • Usually due to intravascular problems. Lymphatics are unblockers, so pushing on edema moves fluid into lymphatic vessels, resulting in pitting.
21
Q

Non-pitting edema

A
  • Lymphedema - Lyphmatic drainage is blocked, so pushing on edema does not push fluid into the lymph, and thus there is no pitting
  • Myxedema - Deposition of mucopolysaccarides in the dermis resulting in swelling (i.e., essentially, tissue is being deposited under the skin). “Edema” is not just fluid, so it doesn’t pit.
22
Q

Primary Immunodeficiency disorder (PID)

A
  • Heterogenous group of disorders that cause defects in immune system development and/or function.
  • Classified as disorders of adaptive immunity (T-cell, B-cell, or combined) or of innate immunity (ex. phagocyte or complement disorder).
  • PID should be susptected in patients with reccurent sinus or ear infection or pneumonias within 1 year period; failure to thrive; poor response to prolonged antibiotics use, persistent thrush or abscess, or family history.
23
Q

Empyema

A
  • Occurs when bacteria invades the pleural space resulting in the formation of pus
    • Can be a result onfparapneumonic effusion (effusion in pleural space adjacent to bacterial pneumonia)
24
Q
  1. Uncomplicated parapneumonic effusion
  2. Complicated parapneumonic effusion
  3. Thoracic empyema
A
  1. Forms when lung interstital fluid increases during pneumonia and moves across visceral pleural membrane. Fluid is exudative and sees an influx of neutrophils into pleural space. Effusion froms when resorptive capacity of pleural space is exceeded .
  2. Occurs when there is bacterial infection of the pleural space
  3. Occurs when there is bacterial infection of the pleural liquid resulting in either pur of presence of bacterial organism on Gram stain.
    • Positive culture is not needed for diagnosis
25
Q

Treament for empyema

A
  • Treatment involved antibiotics (same as those for pneumonia) as well as drainage of the pus
26
Q

Treatment for community acquired bacterial pneumonia

A
  • Outpatient without comorbidities
    • 1st line - Amoxicillin (for patients over age 50 where mycoplasama infection is less likely) or eythromycin or clarithromycin or azithromycin
    • 2nd line - doxycycline
  • Outpatient with comorbidities
    • Amoxicillin or amoxicillin/clavulanate or cefuroxime or cefporzile + clarithromycin or azithromycin or doxycycline. OR
    • Any one of the following Levofloxacin or moxifloxacin

* Antibiotic treatment is empiric and generally includes coverage for both typical and atypical organisms