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Oral Medicine > Topic 52 > Flashcards

Topic 52 Flashcards

1
Q

Acrodermatitis enteropathica (etiology)

A
  1. autosomal recessive hereditary disease
    - caused by zinc deficiency
    - in infancy and childhood untreated may be lethal
  2. in adulthood due to :
    - parenteral feeding
    - malabsorbtion
    - inflammatory bowel diseases
    - chronic alkcoholism
    - hepatic diseases
    - special diets
    - anorexia nervosa
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2
Q

Acrodermatitis enteropathica (symptoms)

A

-acral dermatitis
-periorificial dermatitis
-alopecia
-diarrhea
-retardation of growth
-prolonged wound healing
-predisposition to infections
-peeling of hans and soles
-paronychia
-photophobia
-psychic disorder
-vesicles, bullae, pustules
on the basis of erythema
-crusty, scaly psoriasis after a couple of
days
-bacterial and fungal symptomes
(nose, mouth, anal and genital regions)
-around mouth: pustules similar to
impetigo on an erythema
-ulcerativ fissural angular cheilitis
(perleche)
-edema and erythemas on the mucosa
of the lips and the oral cavity
-aphtous ulcers
-whitish pseudomembranous
candidiasis (buccal mucosa and
tongue)

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3
Q

Acrodermatitis enteropathica (differential diagnosis)

A
  • psoriasis
  • candidiasis
  • eczema
  • perioral dermatitis
  • bullous epidermolysis
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4
Q

Acrodermatitis enteropathica (therapy)

A
  • Zinc substitution
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5
Q

Amyloidosis (etiology)

A 
-overproduction of
immunglobulines
due to disturbances of
protein metabolism
-amyloid (a chemical compound made of immunglobulines and carbohydrates)
-deposits within the skin
-in the subcutaneous layers
-gastrointestinal tract
-inner organs
-bones
-nerves
-vessels
-muscles
Predisposing fastors: 
-rheumatoid arthritis
-multiple myeloma
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6
Q

Amyloidosis (clinical forms)

A
  • primary (systemic/localized)
  • secondary (systemic/localized)
  • familial
  • senile
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7
Q

Primary Systemic Amyloidosis (symptoms)

A

Primary systemic amyloidosis:

  • periorbital and perinasal transparent papules
  • macroglossia
  • amyloid deposits (muscles- tongue)
  • enlarged tongue, hard to touch, retains of the teeth
  • reddish-yellowish nodules appear on lateral sides of the tongue
  • atrophy of lingual papillae, purpuras
  • petechiae, purpuras, ecchymoses („pinch purpuras”)
  • haemorrhagic bullae
  • swollen minor and major salivary glands
  • regional swelling of lymphatic glands
  • xerostomia
  • wax-like yellow skin
  • within the oral cavity: dark, reddish tone
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8
Q 
Secondary Systemic Amyloidosis (symptoms)
accompanying chronic diseases:
- Hodgkin’s disease
- tuberculosis
- rheumatoid arthritis
- regional ileitis
A
  • gingival swelling (apart from macroglossia)
  • nodules on mucosa
  • plaques, papules, bullae
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9
Q

Amyloidosis (diagnosis)

A
  • histological examination (obtained from biopsy)

- Congo red, thioflavine+ stains

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10
Q

Amyloidosis (differential diagnosis)

A
  • scleroderma
  • myxoedema
  • sarcoidosis
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11
Q

Amyloidosis (therapy)

A

symptomatic treatment

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12
Q

Lipoid proteinosis-hyalinosis of the skin and mucosae-Urbach-Wiethe disease (pathogenesis)

A
  • unknown etiology
  • hyalin-like lipoprotein is deposited within tissue
    layers of GI, respiratory tract, skin, mucosa
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13
Q

Lipoid proteinosis-hyalinosis of the skin and mucosae-Urbach-Wiethe disease (symptoms)

A

-in childhood: hoarseness
-yellowish-whitish papules
on the eyelids
-rigid and mottled facial skin
-papules, nodules, pustules and later scars on the skin

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14
Q

Lipoid proteinosis-hyalinosis of the skin and mucosae-Urbach-Wiethe disease (oral symptoms)

A
  • nodular, papular, whitish, yellowish on buccal
    mucosa, tongue, lips, palate
  • streak like, reddish-yellow, drip-like hyalinization
    of gingiva
  • atrophic, hard, enlarged tongue
  • short, thick frenulums (partial immobilization)
  • hyalin deposits become harder and resemble scars
  • oral infections and ulcers
  • obstruction of the parotid passage
  • reoccuring painful swelling of the parotid gland
  • dental enamel hypoplasia, hypodontia
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15
Q

Lipoid proteinosis-hyalinosis of the skin and mucosae-Urbach-Wiethe disease (diagnosis)

A
  • hystopathology
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16
Q

Lipoid proteinosis-hyalinosis of the skin and mucosae-Urbach-Wiethe disease (differential diagnosis)

A
  • amyloidosis
  • scleroderma
  • porphyria
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17
Q

Lipoid proteinosis-hyalinosis of the skin and mucosae-Urbach-Wiethe disease (therapy)

A
  • supportiv therapy
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18
Q

Waldenström’s macroglobulinaemia (etiology)

A

-chronic, often lethal disease
-charactized by the overproduction of IG-s
(gammopathy)
-proliferation of pathological
lymphoid cells
(hybrid cells with features of
B and plasma cells)

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19
Q

Waldenström’s macroglobulinaemia (pathogenesis)

A
  • macroglobulines create a complex with blood clotting factors
  • macroglobulines linked to the surface of erythrocytes
  • damage the capillary wall
  • cause hemophilia or hemolytic anaemia
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20
Q

Waldenström’s macroglobulinaemia (symptoms)

A

-mainly by elderly men
-purpuras all over the body
-dypnoea
-loss of weight
-fatigue
-hepato-splenomegaly
-anaemi
-thrombocytopenia
-granulocytopenia
-nasal and oral mucosa
bleedings

21
Q

Waldenström’s macroglobulinaemia (oral symptoms)

A 
-petechiae, ecchymoses, sugillations in
groups or extended clusters,
-may meld to each other: finally become
ulcerative and painful
-gingival hemorrhage
-prolonged bleeding after extraction
Rarely:
-swelling of salivary glands and
xerostomia
- generalized lymphadenopathy
-increased predisposition for thrombosis
22
Q

Waldenström’s macroglobulinaemia (differential diagnosis)

A
  • Werlhov’s disease
  • amyloidosis
  • Osler’s disease
23
Q

Waldenström’s macroglobulinaemia (therapy)

A
  • plasmaferesis
  • transfusions
  • the prognosis is poor
24
Q

Hyperuricemia-gout (etiology)

A
  • accumulation of uric acid

- commonly caused by familial factors

25
Q

Hyperuricemia-gout (predisposing factors)

A

-DM
-alcoholism
-psoriasis
-multiple myeloma
-haemolytic anaemia
-pharmaceutical products (diuretics, chemotherapeutic drugs
aspirin, nicotinicacid)
-carcinoma
-sarcoma
-leukaemia
-lymphoma
-lead poisoning

26
Q

Hyperuricemia-gout (symptoms)

A

-arthritis (joint of leg: ankles, knee) pain, accompanied with minor swelling
-tophi various sizes appear on the hands and legs (deposition of urate crystals within
periarticular tissue layers)
-urate deposition on skin, cartilage, bones,
inner organs (kidneys- gout associated nephropathy)
-bilateral swelling of the parotid gland
(sialadenosis)

27
Q

Hyperuricemia-gout (diagnosis)

A
  • elevated levels of serum uric acid
  • X-ray examination (radiolucent urate tophy)
  • biopsy from the tophy
28
Q

Hyperuricemia-gout (differential diagnosis)

A
  • rheumatoid arthritis
  • multiple myeloma
  • Hand-Schüller-Christian disease
  • inflammatory disease of parotid gland
  • cancerous disease of the parotid gland
29
Q

Hyperuricemia-gout (therapy)

A
  • NSAID
  • corticosteroids
  • analgetics
  • diet
30
Q

Porphyria cutanea tarda-Chronic hepatic porphyria (etiology)

A
  1. congenital, erythropoietic form (uncommon)
  2. hepatic porphyria cutanea tarda (common)
    Predisposing factors:
    -liver diseases (alcohol)
    -iron deficiencies
    -effect of drugs
    (tetracyclin, chloroquin,
    piridoxine)
31
Q

Porphyria cutanea tarda-Chronic hepatic porphyria (symptoms)

A
  1. congenital form:
    - reddish-brown discoloration of the teeth
    - splenomegaly
    - haemolytic anaemy
  2. both form:
    - the skin is excessively sensitive to light
    - vesicles, bullae, erosions
    - ulcerations covered by bloody crusts
    - scarring
    - alopecia
    - periorbital hyperpigmentosis
    - hypertrichosis
32
Q

Porphyria cutanea tarda-Chronic hepatic porphyria (oral symptoms)

A

-erythema, vesiculo-bullous alterations
(labial mucosa, gingiva, commisures,lips)
-brownish-black haemorrhages
-crusty erosions
-ulcers
-the tongue becomes atrophic erythematous
-candidiasis

33
Q

Porphyria cutanea tarda-Chronic hepatic porphyria (differential diagnosis)

A

-pemphigus
-herpetiform dermatitis
-other vesiculobullous
dermatosis

34
Q

Porphyria cutanea tarda-Chronic hepatic porphyria (therapy)

A

-Internal and dermatological, local

antiseptic and antimicotic treatment

35
Q

Hypercarotinaemia-carotene jaundice (etiology)

A
  • carotene accumulated in the blood

- consumption of excess amounts of carrots, eggs, pumpkins, oranges

36
Q

Hypercarotinaemia-carotene jaundice (symptoms)

A

-yellowish discoloration of palms, soles, palate
-sclera will not become yellow (distinction from
jaundice)

37
Q

Hypercarotinaemia-carotene jaundice (differential diagnosis)

A

-hepatitis

38
Q

Haemochromatosis-bronze diabetes (etiology)

A

-genetic disorder of iron metabolism
-haemosiderin from nutrition is accumulated excessively in the liver, kidney, pancreas, inner organs, skin, mucosa
-occours in a secondary manner too:
transfusions, long iron derivate th.

39
Q

Haemochromatosis-bronze diabetes (pathogenesis)

A

-liver, heart, pancreas failure may develop
-DM and its complications
-hepatic cirrhosis and its complication
(hepatic carcinoma) may develop

40
Q

Haemochromatosis-bronze diabetes (symptoms)

A

Brownish-grey spots containing hemosiderin on

the oral mucosa- not protruding from the level of the surrounding mucosa.

41
Q

Haemochromatosis-bronze diabetes (diagnosis)

A
  • histopathology
42
Q

Haemochromatosis-bronze diabetes (differential diagnosis)

A
  • haematoma
  • melanoplakia
  • malignant lentigo
  • amalgam tattoo
  • Addison’s disease
43
Q

Haemochromatosis-bronze diabetes (therapy)

A
  • Blood transfusions

- Deferoxamin injection

44
Q

Protein deficiency (etiology)

A

-decreased intake of protein
-malabsorbtion
-metabolic disorder
-chronic disorder
(hepatic or renal)
-malignancies

45
Q

Protein deficiency (symptoms)

A
  • dry and hyperpigmented skin and hair
  • edemas
  • muscle wasting
  • hypotension
  • anaemia
  • hypoglicemia
46
Q

Protein deficiency (oral symptoms)

A
  • atrophic oral mucosa and tongue
  • painful inflammation of fungiform papillae
  • fissures (rhagades) in the commisure of the lips
  • swelling of the parotid gland
47
Q

Protein deficiency (differential diagnosis)

A
  • vitamin deficiencies (B2,B3)
  • anaemia
  • candidiasis
48
Q

Protein deficiency (therapy)

A

-Protein rich nutrition

Oral Medicine (4 decks)

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