Malignant melanoma

D E FI N I T ION

 Malignancy arising from neoplastic transformation of melanocytes, the

pigment-forming cells of the skin. The leading cause of death from skin disease.

AE T IOLOGY 

DNA damage in melanocytes caused by ultraviolet radiation results in

neoplastic transformation. 50 % arise in pre-existing naevi, 50 % in previously normal skin.

Four histopathological types:

1. Superficial spreading (70 %): Typically arises in a pre-existing naevus, expands in radial

fashion before vertical growth phase.

2. Nodular (15 %): Arises de novo, aggressive, no radial growth phase.

3. Lentigo maligna (10 %): More common in elderly with sun damage, large flat lesions,

follow an indolent growth course. Usually on the face.

4. Acral lentiginous (5 %): Arise on palms, soles and subungual areas. Most common type

in non-white populations.

E P IDEMIOLOGY

 Steadily increasing incidence, 6,000/year diagnosed in the United

Kingdom, lifetime risk 1 in 80 in the USA. White races have 20 times increased risk to

non-white races.

H ISTORY

 Change in size, shape or colour of a pigmented skin lesion, redness, bleeding,

crusting, ulceration.

EXAMINA T I ON ABCD 

criteria for examining moles:

A Asymmetry.

B Border irregularity/bleeding.

C Colour variation.

D Diameter >6mm.

E Elevation.

INVE S T I G A T IONS

Excisional biopsy: For histological diagnosis and determination of Clark’s levels or Breslow

thickness.

Lymphoscintigraphy: Radioactive compound is injected around lesion and dynamic images

are taken over the course of 30 min to trace the lymph drainage and the sentinel node(s).

Sentinel lymph node biopsy (if primary and < 1mm depth): Sentinal lymph nodes are

dissected and histologically examined for metastatic involvement.

Staging: Imaging by ultrasound, CT or MRI, CXR.

Blood: LFT (liver is a common site of metastases).

MANAGEMENT

Primary prevention: Limit sun overexposure, avoid sunburn.

Wide local excision, margin dependent on depth of invasion (< 1mm: 1 cm, 1–4 mm:

2 cm margin). Skin grafting may be required.

Chemotherapy: May be necessary as adjunctive treatment or in metastatic disease.

Commonly used agents used are dacarbazine (20%respond), cisplatin, temozolomide

and vinblastine.

Biological therapy: Interferon a-2b, IL-2, and bevacizumab (unlicensed) have been shown

to potentially beneficial.

COM P L IC A T I ONS 

Lymphoedema may result after block dissection of lymph nodes.

PROGNOSIS

 5-year survival 90–95 % for lesions < 1.4 mm, 40 % with node-positive

disease and mean survival of 9 months with metastatic disease.

Poorer prognostic indicators: Ulceration, " mitotic rate, trunk lesions compared with limb.

Males poorer prognosis than females.

DERMATOLOGY 303

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تابع القراءه

Pemphigoid

D E F I N I T I ON

 An autoimmune subepidermal blistering (bullous) disease of the skin.

AET IOLOGY 

Autoantibodies are formed against the basement membrane hemidesmosomal

glycoproteins BP180 and BP230. Serum levels of anti-BP180 antibodies (present in

65%patients) correlate with disease activity. MHC class II allele DQB10301 is a marker

for enhanced susceptibility to this disorder, possibly by facilitating presentation of BP180

proteins to T cells. Anti-BP230 antibodies may form as a consequence of keratinocyte

injury. Deposits of polyclonal IgG and complement at the junction of the dermis and

epidermis result in activation of the complement cascade, release of proteolytic enzymes

and destruction of the basement membrane. Mast cells appear to play an integral role in

this process.

Drug-induced bullous pemphigoid may be caused by penicillamine, furosemide, captopril,

penicillin, sulfasalazine. Most causative drugs contain sulfhydryl groups that cleave

epidermal intercellular substance, resulting in the production of the antibodies.

E P IDEMI OLOGY 

Incidence of 4.3 per 100,000 person-years was found in a populationbased

study from the United Kingdom. Median age at presentation was 80 years. More cases

occur in women than men (60 % versus 40 %).

H ISTORY 

Acute onset. The tense blisters are tender and can be very itchy.

New blisters can keep developing without adequate treatment.

EXAMI N A T ION 

Primary lesions are often erythematous and eczematous plaques, generalized

on trunk and limbs. Large tense blisters then develop on these sites. (‘Cicatricial’

pemphigoid: Heals with scarring and may affect the eye and orogenital mucous membranes.)

I N V E S T IGATIONS

Skin biopsy:

A delicate 4-mm punch biopsy from the edge of an intact bulla: for light microscopy, to reveal

the ‘subepiderma’l blister.

A second biopsy for direct immunofluorescence (plus a biopsy of normal skin taken a few

millimeters from an involved area placed in Michel’s fixative). Deposits of IgG and

complement are seen in a linear pattern along the basement membrane zone.

MANAGEMENT

 Topical corticosteroid therapy e.g. clobetasol propionate cream.

Patients with disease affecting mucous membranes who cannot be treated topically are

treated with oral corticosteroids and steroid-sparing agents.

In patients with extensive involvement: management of fluid loss, pain, temperature control,

and septicemia.

COMPL I C A T IONS 

Fluid and electrolyte loss, secondary infections, complications of steroids

(diabetes mellitus, hypertension, gastric ulceration, osteoporosis).

P ROGNOS I S 

Good. Control of pemphigoid is easier than that of pemphigus. Complete

remission after 1 year is common.

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PH.Jafar Jassim 12/02/2020 01:09:00 ص

تابع القراءه

Erythroderma

D E F I N I T I ON

 Non-specific intense widespread reddening of the skin often preceded by

exfoliation.

AET IOLOGY

Pre-existing skin conditions: Eczema, psoriasis.

Malignancy: Cutaneous T-cell lymphoma, lymphoma, leukaemia.

Adverse drug reaction.

Infection: HIV, toxic shock syndrome.

Idiopathic.

E P IDEMI OLOGY 

Incidence: 1–2 in 100,000/year. 1 % of dermatological admissions.

Age usually > 40 years. < : ,¼2.5 : 1.

H ISTORY

 The skin feels hot and tight. Pruritus, erythema, scaling and shedding, fever and

shivering. Symptoms of cardiac failure. The history should also be directed towards establishing

aetiology.

EXAMI N A T ION

 The patient may be pyrexial or hypothermic.

Erythema and scaling of 90 % of the skin. Evidence of skin shedding.

The skin is hot and radiates warmth to the surroundings, can ! hypothermia.

Peripheral oedema, signs of volume depletion including # BP and tachycardia.

Signs of cardiac failure.

Signs of the underlying condition, e.g. psoriatic plaques.

PATHOLOGY/PATHOGENESIS 

Interaction of cytokines and cellular adhesion molecules

! "epidermal turnover rate ! severe scaling and shedding ! loss of fluid, electrolytes and

albumin. There is increased blood flow through the skin, which may cause temperature

dysregulation and high-output cardiac failure.

I N V E S T IGATIONS

Skin biopsy: In order to make a definitive diagnosis  lymph node biopsy if significant

lymphadenopathy.

Blood:

FBC: # Hb, " WBC if secondary infection, may reveal underlying haematological dyscrasia.

ESR, U&E: May have # Na

þ

, # K

þ

, " urea if lost through skin.

LFT: # Albumin loss through the skin  leakage to extracellular space from leaky capillaries.

Immunoglobulins: Hypergammaglobulinaemia, " IgE.

Blood film: For Sezary cells typical of T-cell lymphomas.

ABGs: For renal failure (metabolic acidosis) and ARDS.

Imaging: ECG, CXR or echocardiogram may show signs of cardiac failure.

MANAGEMENT 

This is a dermatological emergency.

1. Nurse the patient in a warm room.

2. Regularly monitor vital signs.

3. Catheterize and close fluid balance monitoring.

4. Treat the underlying cause if identified.

5. Continue only vital medications.

6. Swab the skin for secondary infection.

7. Ensure topical steroid and bandaging. Consider systemic steroid (controversial and never

used in cases of psoriatic erythroderma).

8. Use antihistamine for pruritus and sedative effect.

9. Managecomplications.

COMPL I C A T IONS

 Cardiac failure, renal failure, hypothermia, secondary infection, ARDS.

PROGNOSIS

 Mortality  20–40 %.

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PH.Jafar Jassim 8/22/2020 03:57:00 ص

تابع القراءه

Erythema nodosum

D E FI N I T ION

 Panniculitis (inflammation of the subcutaneous fat tissue) presenting as red

or violet subcutaneous nodules.

AE T IOLOGY

 Delayed hypersensitivity reaction to antigens associated with various infectious

agents, drugs, and other diseases.

Infection: Bacterial (Streptococcus, TB, Yersinia, rickettsia, Chlamydia, leprosy), viral (EBV),

fungal (histoplasmosis, blastomycosis, coccidioidomycosis), protozoal (toxoplasmosis).

Systemic disease: Sarcoidosis, IBD, Beh¸cet’s disease.

Malignancy: Leukaemia, Hodgkin’s disease.

Drugs: Sulphonamides, penicillin, oral contraceptive pills.

Pregnancy.

25 % of cases have no underlying cause identified.

E P IDEMIOLOGY

 Usually affects young adults. , : <  3: 1.

H ISTORY

 Tender red or violet nodules develop bilaterally on the shins and occasionally

on the thighs and forearms. Fatigue, fever, anorexia, weight loss and arthralgia are often

also present.

Symptoms of the underlying aetiology.

EXAMINA T I ON

 Crops of red or violet dome-shaped nodules usually present on both shins

(occasionally involving thighs or forearms) which are tender to palpation.

Low-grade pyrexia. Joints may be tender and painful on movement.

Signs of the underlying aetiology.

INVE S T I G A T IONS 

To determine the underlying aetiology.

Blood: Anti-streptolysin-O titre at diagnosis and 2–4 weeks later to assess for antecedent

streptococcal infection. FBC, U&Es, CRP, ESR, LFTs, serum ACE (" in sarcoidosis).

Throat swab and culture.

Mantoux/Heaf skin testing: For TB.

CXR: To look for hilar adenopathy or other evidence of pulmonary sarcoidosis, TB and fungal

infections.

MANAGEMENT 

Treat the cause. In most cases, manage conservatively.

NSAIDs or potassium iodide may be given for relief of the discomfort associated with the rash.

Persistent cases may require corticosteroids, colchicine, azathioprine or dapsone. When

considering corticosteroids, clinicians should assess the possibility of masking an underlying

malignant, inflammatory, or infectious condition.

COM P L IC A T I ONS 

None. Complications of the underlying cause.

PROGNOSIS

 The majority of cases resolve over 3–6 weeks leaving bruise marks.

Occasionally, nodules may persist or recur over several months, but they never ulcerate.

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تابع القراءه

Eczema

D E FI N I T ION 

A pruritic papulovesicular skin reaction to endogenous or exogenous agents.

AE T IOLOGY

 Numerous varieties caused by a diversity of triggers.

Exogenous: Irritant, contact, phototoxic.

Endogenous: Atopic, seborrhoeic, pompholyx, varicose, lichen simplex.1

Irritant: Prolonged skin contact with a cell-damaging irritant (e.g. ammonia in nappy rash).

Contact: Type IV delayed hypersensitivity to allergen (e.g. nickel, chromate, perfumes, latex

and plants).

Atopic: Two major models currently exist to explain the pathogenesis:

1 Impaired epidermal barrier function due to intrinsic structural and functional skin abnormalities

(predominant model).

2 Immune function disorder in which Langerhans cells, T cells and immune effector cells

modulate an inflammatory response to environmental factors (traditional model).

Seborrhoeic: Pityrosporum yeast seems to have a central role.

Varicose: Increased venous pressure in lower limbs.

E P IDEMIOLOGY

Contact: Prevalence 4 %.

Atopic: Onset is commonly in the first year of life. Childhood incidence 10–20 %.

H ISTORY 

Itching (can be severe), heat, tenderness, redness, weeping, crusting.

Enquire into occupational exposures or irritants used at home (e.g. bleach). Enquire into

family/personal history of atopy (e.g. asthma, hay fever, rhinitis).

EXAMINA T I ON

Acute: Poorly demarcated erythematous oedematous dry scaling patches. Papules, vesicles

with exudation and crusting, excoriation marks.

Chronic: Thickened epidermis, skin lichenification, fissures, change in pigmentation.

By type:

Contact and irritant: Eczema reaction occurs where irritant/allergen comes into contact

with the skin. In some cases, autosensitization (spread to other sites) can occur in contact

eczema.

Atopic: Particularly affects face and flexures.

Seborrhoeic: Yellow greasy scales on erythematous plaques, particularly in the nasolabial

folds, eyebrows, scalp and presternal area.

Pompholyx: Acute and often recurrent painful vesiculobullous eruption on palms and soles.

Varicose: Eczema of lower legs, usually associated with marked varicose veins.

Nummular: Coin shaped, on legs and trunk.

Asteatotic: Dry, ‘crazy paring’ pattern.

INVE S T I G A T IONS

Contact:

Skin patch testing: Disc containing postulated allergen is diluted and applied to back for 48 h.

Positive if allergen induces a red raised lesion.

Atopic: Laboratory testing, including IgE levels, are not used routinely and are not currently

recommended.

Swab for infected lesions (bacteria, fungi and viruses).

1 Lichen simplex is the thickening of skin secondary to a cycle of itch – scratch – itch, and is characterized by

well-demarcated hyperpigmented lichenified plaques.

Eczema (continued)

MANAGEMENT

Irritant or contact: Avoid precipitant. Barrier protection (e.g. gloves, barrier cream).

Atopic: Avoid precipitants. Topical steroids. Low potency steroids are used for face and skin

folds (areas at high risk for atrophy). The use of potent steroids in these areas should be

prescribed by a dermatologist. Tacrolimus (calcineurin inhibitor) ointment for moderate

to severe eczema not responding to potent steroids. Systemic immunosuppressants or

phototherapy may be helpful in very severe cases.

Topical or systemic antibiotics for secondary infection. Medicated bandages (e.g. zinc paste

for severe limb eczema). For pruritus, antihistamines. Emollients (in bath water, as soap

substitute or by direct application to affected area).

Seborrhoeic: Topical 1%hydrocortisone and antifungal. Ketoconazole shampoo for scalp

involvement.

Pompholyx: Potent topical steroids, potassium permanganate salts, systemic steroids in

severe attacks.

COMPL I C A T IONS

 Secondary infection, particularly from Staphylococcus aureus and HSV.

HSV superinfection can be life-threatening. " predisposition to Molluscum contagiosum.2

P ROGNOS I S

 Good prognosis for irritant eczema if the relevant agent is identified and

avoided. Endogenous eczema may have a chronic relapsing course. Of all patients, 90%with

atopic eczema recover by puberty.

Wiskott–Aldrich syndrome: Association of eczema, thrombocytopaenia, immunological

abnormalities and a predisposition to lymphoma and leukaemia.

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تابع القراءه

Basal cell carcinoma (skin)

D E F I N I T I ON

 Commonest form of skin malignancy; also known as a ‘rodent ulcer’.

AET IOLOGY

 Prolonged sun exposure or UV radiation.

Associated with abnormalities of the patched/hedgehog intracellular signaling cascade,

as seen in Gorlin’s syndrome (naevoid basal cell carcinoma syndrome). Other risk factors

include photosensitizing pitch, tar and arsenic.

Pathophysiology: Small dark blue staining basal cells growing in well-defined aggregates

invading the dermis with the outer layer of cells arranged in palisades. Numerous mitotic

and apoptotic bodies are seen. Growth rate is usually slow, but steady and insidious.

It does not metastasize, but has the potential to invade and destroy local tissues.

E P IDEMI OLOGY 

Common in those with fair skin and areas of high sunlight exposure,

common in the elderly, rare before the age of 40 years. Lifetime risk in Caucasians is 1:3.

H ISTORY 

A chronic slowly progressive skin lesion usually on the face but also on the scalp,

ears or trunk.

EXAMI N A T ION

Nodulo-ulcerative (most common): Small glistening translucent skin over a coloured

papule that slowly enlarges (early) or a central ulcer (‘rodent ulcer’) with raised pearly

edges. Fine telangiectatic vessels often run over the tumour surface. Cystic change may be

seen in larger more protuberant lesions.

Morphoeic: Expanding, yellow/white waxy plaque with an ill-defined edge (more

aggressive).

Superficial: Most often on trunk, multiple pink/brown scaly plaques with a fine ‘whipcord’

edge expanding slowly; can grow to more than 10 cm in diameter.

Pigmented: Specks of brown or black pigment may be present in any type of basal cell

carcinoma.

I N V E S T IGATIONS 

Biopsy is rarely necessary (diagnosis is based mainly on clinical

suspicion).

MANAGEMENT

 Cryotherapy, curettage, cauterization and photodynamic therapy are

used for small superficial lesions.

Surgical: Excision with a 0.5 cm margin of surrounding normal skin for discrete nodular or

cystic nodules in patients under 60 years; Mohs’ micrographic surgery, which includes

careful review of tissue excised under frozen section, is the treatment of choice for large

tumours (1 cm diameter) and lesions near the eyes, nose and ears. Excision and skin flap

coverage may be necessary.

Radiotherapy: Useful in basal cell carcinomas involving structures that are difficult to

surgically reconstruct (e.g. eyelids, tearducts). Repeated treatments may be necessary

as there is risk of side effects such as radiation dermatitis, ulceration or depilation.

COMPL I C A T IONS 

The tumour has a slow but relentless course. Can become disfiguring

on the face. Has the potential to invade, lead to loss of vision in the orbital region.

P ROGNOS I S 

Good with appropriate treatment. If left, may continue to grow, invade and

ulcerate. Regular follow-up is necessary to detect local recurrence or other lesions

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PH.Jafar Jassim 8/19/2020 02:59:00 ص

تابع القراءه

Acne vulgaris

D E FI N I T ION

 Inflammation of the pilosebaceous unit of the skin.

AE T IOLOGY 

Increased production and impaired normal flow of sebum (caused by

follicular hyperkeratinization and obstruction of the pilosebaceous duct) leading to inflammation

and formation of closed or open comedones. The bacteria Propionibacterium acnes,

Staphylococcus epidermidis and Pityrosporum yeast may be involved in pathogenesis.

Associated with polycystic ovarian syndrome, cortisol excess (Cushing’s syndrome), prolactinoma

and puberty.

E P IDEMIOLOGY

 Ubiquitous. Begins in puberty and tends to recede with age.

H ISTORY

 Usually self-diagnosed, acute onset, greasy skin, may be painful.

EXAMINA T I ON 

Open comedones (whiteheads: flesh-coloured papules), closed comedones

(blackheads: the black colour is caused by oxidation of melanin pigment), papules,

pustules, nodules, cysts and seborrhoea primarily affecting the face, neck, upper torso and

back. Three grades: mild, moderate and severe.

INVE S T I G A T IONS

 Normally none required, especially if experiencing puberty.

Blood: LH levels (increased LH: FSH ratio may be seen in PCOS), prolactin, sex-hormonebinding

globulin, testosterone, 17-OH-progesterone (9 a.m., follicular phase; if congential

adrenal hyperplasia is suspected).

Urine: 24-h urinary cortisol (if Cushing’s syndrome suspected).

Imaging: Pelvic ultrasound (if PCOS suspected).

MANAGEMENT

: Start treatment early to prevent scarring.

For mild/moderate acne: Over-the-counter preparations containing benzoyl peroxide,

azelaic acid.

For moderate/severe acne: Consider topical antibiotics (clindamycin, erythromycin),

topical vitamin A derivatives (tretinoin).

For severe inflammatory acne or if failure of topical treatment:

Consider systemic antibiotics (oxytetracycline, minocycline, erythromycin).

For severe acne: Also consider oral vitamin A derivative (isotretinoin) – available only by

specialist prescription.

Side effects: Teratogenic, hyperlipidaemia.

For females: Oral contraceptive pill or cyproterone acetate reduces severity.

Advice: Counsel patients that an improvement may not be seen for a couple of months, use

of non-greasy cosmetics, wash face daily.

COM P L IC A T I ONS

 Facial scarring (atrophic, ‘ice pick’, hypertrophic, keloidal), hyperpigmentation,

secondary infection, psychological morbidity.

PROGNOSIS

 Generally improves spontaneously over months or years

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تابع القراءه

 

♦️ #الصيدلة_السريرية ♦️

اغلب الاسئلة دتوصل بخصوص الصيدلة السريرية فهذا توضيح بسيط عنها اتمنى تستفادون منا 

🔷 اول شي موجودة في جامعة جابر بن حيان بواقع (6 مراحل ) 🔷

✅ الصيدلة السريرية هي فرع من فروع الصيدلة حيث الصيادلة وعلماء الجينات يقومون بتوفير الرعاية الصحية للمريض بأن يحققوا الاستخدام الأمثل للدواء وتعزيز الصحة والعافية، والوقاية من الأمراض. الصيادلة السريرين  يهتمون بالعناية بالمرضى وصحتهم في جميع المرافق الطبية وهم يتعاونون مع الأطباء والمتخصصين لتوفير الرعاية الصحية للمريض.

🔴 الصيادلة السريرين يتم تعليمهم برامج علمية مكثفه تتضمن مجال الطب الحيوي وعلوم الصيدلة السريرية وكيفية التواصل مع المجتمع. والصيادلة السريرين يحوزون على شهادة دكتور في الصيدلة (pharm.D)  أو زمالة بالصيدلة. بعض الصيادلة يختارون بأن يحوزوا على شهادة البورد من خلال هيئة التخصصات الصحية التي نظمت في عام كوكالة مستقلة عن شهادة APhA (نقابة الصيادلة الأمريكية). ويجوز للصيدلي أن يصبح

🔴 (أخصائي في المعالجة الدوائية)، أو 

🔴 (صيدلي أخصائي في علاج الأورام)، أو

🔴 صيدلي اخصائي في الطب النووي)، أو 

🔴 صيدلي اخصائي في علم التغذية) ,أو 

🔴(صيدلي اخصائي في الطب النفسي)

‼️ ويحوز على هذه المجالات من خلال هيئة التخصصات الصحية ‼️

◾️ وأيضا يوجد (مجالات فرعية في المعالجة الدوائية) مثل : 

▪️علم أمراض القلب ووالأمراض المعدية.

🔺 وتضاف هذه المجالات كمؤهل للصيدلي🔺

🔵المكونات الأساسية للصيدلة السريرية

   ((وصف الدواء،،أَخذ الدواء،، مُراجعة السجلات الدوائية.

    ،،مُراجعة تعاطي جرعات الدواء ،،المُحادثة.

    الاستِشارة ،، المُراقبة،، التَشخيص.مُحاولة تَجنب الأخطاء الدوائية.))🔵

اعادة توجيه لازملائكم الصيدلانين ❤️

♦️▪️♦️▪️♦️▪️♦️▪️♦️▪️♦️▪️♦️

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PH.Jafar Jassim 8/13/2020 12:54:00 ص

تابع القراءه

يجب أن يتمتع بالثقافة الطبية حتى وإن لم يكن يكن طبيباً  ، والتي تعتبر الثقافة والمعرفة تعتبر عصباً لحياة الإنسان ، وصحة المجتمع الذي يعيش فيه ، وفي هذا المقال سوف تتذكر مجموعة معلومات عامة تختص في مجال الطب.

 من أهمّ الغدد في جسم الإنسان: الغدة الجنبدرقية ، والنخامية ، والدرقية ، والجنسية ، والمعدة ، والكظرية ، والعرقية ، والبنكرياس ، 

واللعابية. 

ينقل القمل للإنسان مرض اسمه التيفوس. 

الغدد الليمفاوية تعمل على تصفية الدم وتطهيره. يطلق عملية غسيل الكلى. 

يعدّ الكبد العضو الوحيد في جسم الإنسان الذي يعود للنمو بعد اقتطاع جزء منه. 

في العام 1989 م تمتت عملية زراعة الكبد في شيكاغو الأمريكية. 

مرض انفصام الشخصية اسمه مرض الشيزوفرينيا. فصيلة الدم

 o + تسمّى باسم فصيلة الدم الكريمة. 

تعرف الذبحة الصدرية بأنّها عبارة عن ألم حاد وقصير الوقت يحدث في الصدر وذلك بسبب إصابة الشريان التاجي. 

فيتامين الوحيد الذي يكسبه الجسم من أشعة الشمس هو فيتامين د. 

يبلغ وزن مخضر الإنسان البالغ من 3 إلى 2 كغم. 

الغدة التي تصبّ جميع محتوياتها بشكل مباشر في الدم هي الغدد الصماء. 

يؤدي نقص فيتامين أ للإصابة بمرض العشى الليليّ. 

من أعراض مرض البلاجرا: الغثيان ، والاكتئاب ، والصداع ، والإسهال ، والتهاب الجلد. 

يعتبر الطبيب العربي مجدي يعقوب من أشهر جراحي القلب على مستوى العالم ، وفردريك بانتينج مكتشف الإنسولين ، والطبيب العربي ابن زهر مكتشف جرثومة الجرب ، وسالك مكتشف مصل شلل الأطفال. يقصد بمرض السرطان الانقسام غير العادي لخلايا الجسم دون توقّف. 

وظيفة كريات الدم البيضاء هي الدفاع عن الجسم ضد الأمراض والجراثيم. 

تقع الغدة الدرقية في الرقبة. 

مادة الميلانين هي المسؤولة عن تلوين جسم الإنسان. 

تعدّ العضلات أثقل من العظام. 

يبلغ عدد فقرات العمود الفقري ثلاثاً وثلاثين فقرة. 

يعتبر مخ ّالمرأة أقل وزناً من مخّ الرجل. يبلغ عدد عظام الجمجمة اثنتين وعشرين عظمة. 

يبلغ حجم الهواء الذي يستنشقه الإنسان في كل عام خمسة ملايين لتر.

يبلغ عدد ضربات قلب الحوت ضربة واحدة في الدقيقة الواحدة. 

يبلغ عدد خلايا الجسم في الإنسان ستين ترليون خلية. 

يبلغ عدد الخلايا العصبية الذي يملكها الإنسان ثمانية وعشرين بليون خلية. 

المسؤول عن التذوق هي الحليمات الذوقية في اللسان. 

تعتبر عضلة الفخذ أكبر عضلة في الجسم ، وعضلة الركاب في الأذن الوسطى أصغر عضلة ، وعضلة الفكين أقوى عضلة. 

ضم المعدة تتكون من المخاط ، ولو لم تكن كذلك له ضمت نفسها .

1 تعليق

PH.Jafar Jassim 7/29/2020 12:19:00 ص

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