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Dermatology 2 > Autoimmune and Immune mediated skin diseases > Flashcards

Autoimmune and Immune mediated skin diseases Flashcards

Autoimmune, immune mediated,

1
Q

When investigating a pruritic dog, in what order should which investigations take place?

A

1: Investigate cause of pruritus e.g. Malassezia dermatitis
2: Investigate potential underlying causes for this e.g. ectoparasites, environmental atopy, food atopy, endocrinopathy, immune mediated
3: If no ectoparasites found, carry out diet exclusion trial to rule in/out food atopy
4: If ineffective, and have ruled out all other causes, can diagnose as environmental atopy
5: Can investigate specific allergen or choose not to and control clinical signs

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2
Q

Describe the options for carrying out a food exclusion trial

A
  • home cooked using novel proteins e.g. white fish, pork, rabbit etc., restricted to single protein source, single carbohydrate source and water. Start at 150% of original commercial diet, increase if weight loss. Minimum 3, up to 10 weeks
  • OR commercial diets containing novel or hydrolysed proteins. Minimum 8 weeks. If no response try home cooked
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3
Q

What are the 2 methods for investigating allergens?

A

Intradermal allergy testing and serological tests

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4
Q

How does intradermal allergy testing work?

A
  • shows type 1 hypersensitivities

- Tests capacity of skin to react to allergens

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5
Q

Discuss the disadvanages of intradermal allergy testing

A
  • Time consuming
  • Requires clipping and sedation
  • Cannot be performed in lichenified, hyperpigmented, inflamed skin, widespread pyoderma or seborrhoea
  • Allergens may be expensive to obtain
  • Rare risk of anaphylaxis
  • Harder in cats
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6
Q

Describe the method for intradermal allergy testing

A
  • Introduce allergen into skin of animal, mark location on a sheet
  • Measure degree of swelling, indicating inflammation and therefore allergic reaction to allergen to identify if reaction has occurred indicating allergy
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7
Q

How does serology testing for allergy work?

A
  • Measure serum IgE alone, but may not correlate to levels in the skin
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8
Q

Compare the variations of serology testing for allergens

A
  • Polyclonal: may measure trace IgG and give false positives
  • Monoclonal: less sensitive, false negatives
  • Mixed allergens: avoided as do not identify specific allergens
  • Mast cell receptor molecule for specific IgE: better, but more expensive
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9
Q

What medical treatments are available for environmental atopy?

A
  • Steroid creams
  • Ciclosporin
  • Glucocorticoids
  • Lokivetmab
  • Oclacitanib
  • Immunotherapy/hyposensitisation
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10
Q

Identify actions an owner can take to avoid exposure of a dog to common allergens e.g. house dust mites

A
  • Freeze bedding and any soft toys for 24 hours after washing
  • Do not allow dogs in bedroom
  • Hypoallergenic mattress and pillow covers for human bedding
  • Wash human and dog bedding >70degressC
  • Anti-dust mite sprays
  • Remove carpets
  • Socks for going on walks
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11
Q

Describe the immunotherapy/hyposensitisation protocol for an allergy

A
  • Shots recommended if allergic to pollens, dust mites
  • 17 injections at 3 day intervals, last 3 at 10, 20, 30 days intervals
  • then injections every 2-3 weeks for 2-3 years
  • High cost
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12
Q

What are the differentials for a dog with erythema, alopecia, hyperpigmentation on legs, crusting, lichenification

A
  • Mange
  • Fleas
  • Bacterial skin infection
  • Allergy
  • Mites
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13
Q

In a case of environmental atopy where the owner has little money available for treatment, what actions would you advise?

A
  • Glucocorticoids (short term)
  • Anti-histamines e.g. piriton
  • Good ectoparasite control
  • Careful management of heat, humidity and stress
  • Supplement EFAs, moisturisse
  • Shampoo to remove allergens in coat
  • Hypoallergenic diet may help
  • Steroid cream in flare up areas
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14
Q

Outline an example of an immune mediated skin disease of cows

A
  • Bovine leukocyte adhesion deficiency
  • Genetic, and once gene identified was bred out
  • Was due to BLAD gene, which led to a replacement of cytosine by a guanosine in the CD18 gene
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15
Q

Give examples of primary immunodeficiency disorders of the skin in small animals

A
  • Severe combined immunodeficiency disease (SCID)
  • Lethal acrodermatitis in English bull terriers
  • Defective neutrophil function in Weimaraners
  • Leukocyte adhesion deficiency in Irish setters
  • Canine granulocytopathy syndrome in Irish setters with juvenile bacterial pyoderma
  • Canine cyclic haematopoiesis of gray Collies
  • Hypotrichosis and thymic aplasia in Birman kittens
  • Chediak Higashi syndrome of cats
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16
Q

Identify the points in the immune system where development blocks may lead to immunodeficiencies

A
  • Lymphoid precursor dysfunction can lead to combined immunodeficiency
  • Myeloid precursor defects may lead to neutrophil defects
  • Issues with “Bursal” processing may lead to agammaglobulinaemia
  • Issues with B cells during development can lead to deficiencies in individual immunoglobulin classes
  • Thymic aplasia leads to lack of thymic processing and T cell defects
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17
Q

Explain what is meant by a primary immuno-deficiency condition

A

A genetic defect in the immune system leading to clinical disease, rare

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18
Q

Explain what is meant by a secondary immuno-deficiency condition

A

Impairment of the immune system due to factors such as viral and other infections, endogenous hormones, drugs, age and malnutrition. Leads to the development of various uncommon conditions

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19
Q

Identify the general mechanisms that may cause autoimmune diseases

A
  • Normal responses that go awry or abnormal responses
  • Immune dysfunction
  • Genetics
  • Environmental triggers
  • Inflammation
  • Trauma
  • Infection
  • Neoplasia
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20
Q

Give examples of ways in which a normal immune response can go awry and lead to autoimmune disease

A
  • Immune response to previously hidden antigens, which may appear due to tissue damage, molecular alterations, or newly synthesised antigens
  • Or response to molecular mimicry as a result of microbial cross reactions
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21
Q

Give an overview as to how an abnormal immune response may occur, leading to autoimmune disease

A
  • Self reactive T cells and lymphoid tumours
  • Failure of apoptosis, viral infections, microchimerism
  • Hormonal influences, genetic predisposition
  • Failure of regulatory control
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22
Q

Give an example how neoplasia can lead to autoimmune disease

A

Thymoma in cats, develop skin diseases, mechanism poorly understood, but removal of thymoma leads to resolution of skin disease
- T cells called to skin, target follicles leading to alopecia

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23
Q

Name the structures that act as autoantigens in the following conditions

a: Pemphigus
b: Pemphigoig
c: Linear IgA dermatitis
d: Epidermolysis bullosa acquista

A

a: Desmosomes
b: Hemidesmosomes
c: Lamina lucida
d: Type VII collagen fibres below the lamina densa

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24
Q

Which structure of the skin is a common target of immune disease and what is the result?

A

Desmosomes, leads to skin falling apart

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25
Q

Which forms of pemphigus are more, and which are less, common in dogs?

A
  • Vulgaris rare in animals (common in people)
  • Foliaceous common in dogs
  • Also erthematosus more common in dogs
  • Uncertain regardin vegetans
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26
Q

Describe the aetiology of pemphigus

A
  • Usually unknown

- Associated wirh abnormal immune regulation or antigenic stimulation

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27
Q

List the factors that are recognised as causes of pemphigus in animals

A
  • Neoplasia
  • Infectious agents
  • Drugs (antibiotics, vaccines, wormers)
  • Chronic skin disease
  • (In people: autoimmune disorders, certain haplotypes, pregnancy)
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28
Q

Compare the pathogenesis of pemphigus vularis and foliaceous

A
  • Autoantibodies bind to all suprabasal layers of stratified squamous epithlium
  • Desmoglein 3 mainly in lower layers (vulgaris, split near bottom of epiderms)
  • Desmoglein 1 mainly in superficial layers (foliaceous, split near top)
  • Desmocollin 1 is major autoantigen in canine pemhigus foliaceous
  • Desmosome break apart = pustules, ulcerations
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29
Q

Describe the clinical signs of canine pemphigus foliaceous

A
  • Leaf-like pustule appearance
  • Erythema around pustules intense
  • Sterile pus in skin
  • Crusting occurs as pustule disappears
  • Pyrexia, inappetance, depressed
  • Lesions on face ad feet
  • Pruritus is a major feature
  • No response to antibactieral therapy
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30
Q

What is the signalment for canine pemphigus foliaceous?

A
  • Any breed, but Cockers predisposed
  • Onset from 2-7yrs
  • Disease chronic in 75% of cases
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31
Q

Outline feline pemphigus foliaceous

A
  • Little understood re. pathogenesis
  • Assumed some features of canine apply
  • PF is most common form of auto-immune skin condition in the cat
  • Drug eruption documented as underlying case, incl. antibiotics
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32
Q

Describe the pathogenesis of pemphigus vulgaris

A
  • Autoimmune blistering skin disease
  • Generation of autoantibodies that target transmembrane desmosomal proteins in the epithlium
  • Desmoglein 3 at the bottom of the epidermis affected, leading to lifting of the entire epidermis
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33
Q

Describe canine discoid lupus erythematosus (DLE) (appearance, prevalence, disease process, cause)

A
  • Long nosed dogs
  • Leads to crusty nosed appearnce, erythematous
  • May be as common as pemphigus foliaceous
  • Photosensitive dermatosis that involves the nasal planum
  • Can be related to stress
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34
Q

Outline the pathogenesis of plasma cell pododermatitis

A
  • Immune mediated? Aetiology unknown

- Leads to lymphocytosis of affected tissues and positive ANA titres

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35
Q

Give an example of a primary vasculitis in animals

A

Multisystemic necrotising vasculitis of small vessels in beagles = Juvenile Polyarteritis syndrome (JPS)

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36
Q

Compare the prevalence of primary and secondary cutaneous vasculopathies

A

Usually secondary to an underlying process

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37
Q

List potential causes of secondary vasculities in veterinary medicine

A
  • Infection
  • Vaccination
  • Drugs:
  • Allergy
  • Immune mediated
  • Other
  • Idiopathic
  • Sepsis and vascular toxins
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38
Q

Give examples of infections that may cause vasculitis

A
  • Bacterial (incl. endocarditis via Staphylococus intermedius)
  • Mycobacterial
  • Funga
  • Viral (FIP, FeLV, FIV, parvo)
  • Protozoa (e.g. Leishmaniasis0
  • Rickettshial (RMSF, Ehrlichia, Borrelia)
  • Sarcocystis
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39
Q

Give examples of vaccinations that may cause vasculitis

A
  • Rabies
  • Hyposensitisation
  • Sera
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40
Q

Give examples of drugs that may cause vasculitis

A
  • Antibiotics
  • Ivermectin
  • Vaccines
  • Metronidazole
  • Phenobarbitol
  • Frusemide
  • Itraconazole
  • Phenylbutazone
  • Enalapril
  • Imodium
  • Metoclopramide
  • Fenbendazole
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41
Q

Give examples of allergies that may cause vasculitis

A
  • Food
  • Insect/arthropod
  • Eosinophilic granuloma
  • Severe scabies
  • Flea hypersensitivity
42
Q

Give examples of immune mediated diseases that may cause vasculitis

A
  • SE
  • DLE
  • Rheumatoid arthritis
43
Q

Give examples of non-immune mediated conditions that may cause vasculitis

A
  • Plasma cell pododermatitis
  • malignancies
  • Ulcerative colitis
  • JPS of beagles
44
Q

What is vasculitis?

A

An accumulation of cells within the vessel wall, causing injury with necrosis and degeneration of endothelial smooth muscle cells and fibrin deposition

45
Q

What is fibrinoid necrosis in vasculitis?

A

Association of complement, fibrin, immunoglobulins, platelets within vessel wall and lumen, that appears as an eosinophilic mush

46
Q

Describe the histological changes that occur with vasculitis

A
  • Frequently transient and are followed by signs of vasculopathy where tissue changes suggest vascular compromise
  • Variety of distinct histological changes
47
Q

What therapy is required in cases of auto-immune and immune mediated skin disease?

A

Immunosuppressives

48
Q

List the methods used in the diagnosis of canine pemphigus foliaceous

A
  • Tzanck prep of pustule
  • Bacterial swab and culture and sensitivity testing
  • Skin biopsy for histopathology
49
Q

What results would be expected in a Tzanck prep of a pustule in the case of canine pemphigus foliaceous?

A
  • Numerous acantholytic keratinocytes
  • Neutrophils
  • Eosinophils in some cases
  • No cocci should be observed
50
Q

What may complicate the diagnosis of pemphigus foliaceous and what should be done to avoid this?

A
  • PF lesions can involve substantial secondary bacterial infection, so cocci may be seen
  • Treat for microbial infection first, then collect samples
51
Q

Explain the use of a skin biopsy for the diagnosis of canine pemphigus foliaceous

A
  • For histopath, bacterial and fungal culture
  • Use punch, may require 8mm to encompass pustule
  • Pustules delicate and readily traumatised by biopsy collection, may need several samples
52
Q

Describe the clinical signs of feline pemphigus foliaceous

A
  • Very similar to dermatophytosis
  • Involvement of claw beds of several feeet, also pinnae
  • May wax and wane
53
Q

List the methods used for the diagnosis of feline pemphigus foliaceous

A
  • Haematology
  • ANA
  • Fungal culture
  • Skin biopsies
  • Cytology from undisturbed neutrophils
54
Q

What results would be expected for all diagnostic tests carried out in the investigation of feline pemphigus foliaceous?

A
  • Haematology: eosinophilia
  • ANA: negative
  • Fungal culture: negative
  • Cytology: neutrophils, sometimes eosinophils, acantholytic keratinocytes
55
Q

From what area are pustules likely to be most useful in the diagnosis of feline pemphigus foliaceous

A

From top of head or base of pinnae, require punch or excision, will require anaesthesia
Ideally multiple samples and 6mm punch

56
Q

List the differential diagnoses for pemphigus vulgaris

A
  • Cutaneous manifestations of lupus erythemotus
  • Epitheliotropic lymphosarcoma (T cell lymphoma)
  • Uveodermatological syndrome (Japanese Akitas)
  • Nasal aspergillosis
  • Erythema multiforme
  • Mucous membrane pemphigoid
57
Q

What histological pattern is seen in canine DLE?

A

Interface dermatitis, hydropic/lichenoid

58
Q

In what conditions is an interface dermatitis pattern seen on histology?

A
  • Muco-cutaneous lupus
  • Pemphigu erythematosus
  • P. foliaceous
  • Mucocutaneous pyoderma
59
Q

What is required for the diagnosis of canine DLE?

A
  • NOT ANA; non-specific, raised in systemic disease

- Diagnosis based on assessment of response to antibacterial agents

60
Q

What are the differentials for plasma cell pododermatitis in the cat?

A
  • Eosinophilic granuloma complex
  • Pemphigus foliaceous
  • Viral infection with cowpox
  • Multicentric tumours
  • Contact dermatitis (rare in cats)
  • metabolic deposits
  • Vasculitis
61
Q

How would you go about making a diagnosis of feline plasma cell pododermatitis?

A
  • Collection of deep biopsies from pads

- Demonstration of numerous plasma cells and lymphocytes in the dermis

62
Q

What methods are used in the diagnosis of Idiopathic Symmetric Lupoid Onychodystrophy (ILSO)?

A
  • Histopathology: dew claw easiest to amputate, submit whole nail and third distal phalanx for histology
  • Bacterial and fungal cultures carried out
63
Q

List the differentials for vasculitis

A
  • Cold agglutinin disease
  • DIC
  • Coagulopathy
  • SLE
  • Lymphoreticular neoplasia
  • Frostbite
64
Q

Why does vasculitis present a diagnostic challenge?

A
  • Small blood vessel damage is a consequence of a variety of disease processes
  • Vasculitis often transient, followed by more chronic change aka vasculopathy, biopsy may not show active inflammation
65
Q

What samples are required for the diagnosis of vasculitis?

A
  • Skin, organ, lymph node biopsies

- Blood samples

66
Q

What blood findings would be consistent with vasculitis?

A
  • Lymphopaenia, eosinopaenia, leukopaenia, neutropaenia, monocytosis
  • Leukocytosis with left shift
  • Normochromic, normocytic anaemia
  • Thrombocytopaenia
  • Increased serum liver enzymes, TAGs
  • Hypoalbuminaemia
  • Hyperglobulinaemia
  • Hyperfibrinogenaemia
67
Q

Describe the clinical signs of feline pemphigus foliaceous

A
  • Skin lesions usually observeed around head, esp. pinnae, planum nasale, also claw beds
  • Pustules and vesicles, transient and replaced by erosions and overlying crusts
  • Nail beds have thick caseous green purulent discharge (paronychia) on multiple digits and feet, claws themselves are normal appearance
  • Lesions can extend to rest of face, tail, ventral abdomen, incl around nipples
68
Q

Describe the clinical signs of equine pemphigus foliaceous

A
  • Covered in scale and crusting

- Histology shows acantholytic keratinocytes

69
Q

Describe the histological appearance of canine pemphigus foliaceous

A

Intraepidermal and/or intrafollicular pustules with abundant acantholytic keratinocytes in granular or upper spinous cell layers

70
Q

What is meant by acantholytic?

A

Loss of intercellular connections

71
Q

How can keratinocytes be identified as acantholytic?

A
  • Think fried eggs
  • Large blue cells with nuclei normal for keratinocytes in stratum granulosum and spinosum
  • In stratum corneum, normal keratinocytes have no nuclei
  • Presence of nucleus shows that these have shed too early, and desmosomal connections have broken
72
Q

Describe the results of direct immunofluorescence in canine pemphigus foliaceous, and state where immunopathology would be used

A
  • Anti-keratinocyte membrane auto-antibodies demonstrated
  • Usually IgG, occasionally IgM or IgA or C3 associated, target desmocollin 1
  • Only used in reaserch, not a diagnostic tool
73
Q

Describe the clinical signs of canine pemphigus vulgaris

A
  • Lesions (pustules, vesicles, erosions, ulcers) at mucosal and mucocutaneous junctions (eyes, lips, nose, pepuce, anus)
  • Rare cases affected with varient of PV without oral or mucosal involvement
  • May also see inside mouth
  • Paronychia sometimes seen
74
Q

Describe the clinical appearance of canine discoid lupus erythematosus

A
  • Hypopigmentation
  • Erythema
  • Scaling
  • Erosions
  • Very similar appearance to pemphigus erythematosus, little importance, treat the same
75
Q

Describe the histological appearance of canine DLE

A
  • Lymphoplasmacytic
  • Lichenoid pattern
  • Interface dermatitis
76
Q

Describe the clinical signs of plasma cell pododermatitis

A
  • Gross swelling of multiple metacarpal/tarsal pads, occasionally foot pads
  • Ulceration, lameness, pain, occasionally pruritus
  • Occasionally pad ulceration
77
Q

Describe the histological appearance of plasma cell pododermatitis

A

Full of plasma cells

78
Q

Describe the clinical signs of idiopathic symmetric lupod onychodystrophy

A
  • Typical history of naisl progressive becoming loose or splitting, incl, dew claws
  • Some nairls lost altogether
  • Extremely painful when nails start to lift off
79
Q

Describe the histological appearance of vasculitis

A
  • Dermal oedema
  • Collagen smudging
  • Hair follicle atrophy
  • Degeneration of vessel walls
  • Perivascular cuffing with mononuclear cells
80
Q

Describe the clinical appearance of vasculitis

A
  • Skin becomes necrotic, hair follicles shut down, crusting, ulceration
  • Skin affected in dependent areas and extremities, esp. paws (incl. sloughing pads), claws, pinnae, lips, tail, scrotum, oral mucosa
  • Skin lesions include purpura, macules, plaques, haemorrhagic bullae, papules, pustules, necrosis, ulcers, acrocyanosis
  • oedematous plaques, urticaria, lymphoedema, pain , erythema
  • Septa vasculitis and panniculitis
  • Pitting oedema of limbs, ventral trunk, head and scrotum
  • Anorexia, depression, pyrexia, pain, pruritus
  • Polyarthropathy, myopathy, neuropathy,, hepatopathy, thrombocytopaenia, anaemia, lymphadenopathy
  • Change in skin colour to blue, black, red
81
Q

Discuss the management of feline pemphigus foliaceous (licensing, side effects, other difficulties)

A
  • Ciclosporin off license
  • Licensed in cats for allergy
  • Side effects: GI disruption (V/D)
  • Only for use where are confident will see patient regularly
  • Very expensive
82
Q

List the treatment options for pemphigus

A
  • Glucocorticoids
  • Ciclosporin
  • Azathioprine
  • Gold salts (aurothioglucose)
  • Chlorambucil (cats)
  • Oclacitanib (Apoquel)
  • Adjunctive therapy
83
Q

Outline the use of glucocorticoids in the treatment of pemphigus

A
  • Pred/methylpred
  • <2mg/kg/day divided until in remission (care re. doses >2mg/kg)
  • Then alternate day therapy
  • Slowly reduce dose
84
Q

What considerations should be taken into account when using glucocorticoids inthe treatment of pemphigus?

A
  • Reduce slowly to avoid relapse (every 2-3 weeks)

- Inform owners of risk of iatrogenic Cushings or Addison’s, as well as risk of diabetes

85
Q

Outline the use of ciclosporin in the treatment of pemphigus

A
  • Dose required unclear
  • Use 5mg/kg/day for allergies
  • Good to minimise side effects from treatment
86
Q

Outline the use of azathioprine inthe treatment of pemphigus

A
  • Not recommended in cats
  • Historical treatment
  • In dogs: 3mg/kg orally q24-48 hours
  • Frequent monitoring required
  • Slow onset of action (3-6 weeks for clinical effects)
87
Q

What are the potential adverse effects of azathioprine treatment for pemphigus?

A
  • Myelosuppression
  • Pancreatitis (may lead to diabetes)
  • Panniculitis
  • Hepatotoxicity
88
Q

Describe the monitoring required when using azathioprine as a treatment for pemphigus

A
  • CBC and platelet count initially q2 weeks for 2 months

- Then q2-3 months

89
Q

Explain the mechanism of action of Gold salts (Aurothioglucose) for the treatment of pemphigus

A

Influences neutrophil migration, lymphocyte function and immunoglobulin production

90
Q

Describe the protocol for the use gold salts in the treatment of pemphigus

A
  • Weekly dose of 1.0mg/kg IM, to once every 2 or 4 weeks
  • May take 6-12 weeks to see full response
  • Monitoring every 2 weeks
91
Q

List the adverse effects of gold salts in the treatment of pemphigus

A
  • Glomerulonephritis
  • Bone marrow suppression
  • Thrombocytopaenia
  • Cutaneous eruptions
  • Injections themselves are painful
92
Q

What monitoring is required during the use of gold salts for pemphigus?

A
  • Every 2 weeks require haematology, serum biochem, urinalysis
  • This is the expensive part, not the drug
93
Q

Describe the use of chlorambucil for the treatment of feline pemphigus

A
  • Daily or every other day therapy, in combination with steroids
  • 0.1-0.2mg/kg, tablet is 2mg so most cats receive half a tablet/day
  • Therapy for 4-8 weeks
  • Regular monitoring required
94
Q

Describe the adverse effects of chlorambucil

A
  • Vomiting
  • Diarrhoea
  • Anorexia
  • Bone marrow suppression
95
Q

What monitoring is required while using chlorambucil?

A

Haematology every 2 weeks

96
Q

Discuss the use of oclacitanib in the treatment of pemphigus

A
  • Suggested, but no studies

- Only effective against the pruritus via IL-13 block (is an allergy medication)

97
Q

Explain the adjunctive therapies used for pemphigus

A
  • Chlorhexidine based shampoo to prevent secondary bacterial component and remove crust/scale
  • Antibiotics for 3 weeks e.g. cefalexin 20mg/kg BID
  • Gut protectants to e.g. cimetidine omeprazole to reduce risk of side effects
  • Methylprednisolone equivalent dose of 0.8-1mg of prednisolone
98
Q

Outline the treatment options for CLE/DLE

A
  • Topical glucocorticoids
  • Topical ciclosporin (Tacrolimus)
  • Topical sunblockers
  • Vitamine E 400-800mg/day
  • Essential fatty acids
  • Niacinamide and tetracycline
  • Oral glucocorticoids
  • Azathioprine
  • Chlorambucil
  • Nasal flap plastic surgery
99
Q

Discuss the use of topical ciclosporin in the treatment of CLE/DLE

A
  • Not licensed in animals
  • Protopic ointment
  • used for perianal fistulas/anal furunculosis, CLE/DLE, pemphigus erythematosus
  • Apply once/twice daily for 4-8 weeks
  • Burns in humans, none noted in aanimals
  • No significant toxic absorption and no side effects in animals
100
Q

Outline the use of niacinamide in the treatment of CLE/DLE

A
  • Aka nicotinamide (vit B3)
  • mode of action and efficacy unsure
  • No side effects
  • Dose: 3xdaily, 250mg<10kg or 500mg>10kg for 6-8 weeks

Dermatology 2 (23 decks)

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