Disorders of growth. General Pathology
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Disorders of growth. General Pathology

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Disorders of growth. General Pathology Disorders of growth. General Pathology Presentation Transcript

  • By: Dr/ Walid Zedan Dr/ Basant Hamdy 1433 ،‫الثالثاء، 71 ذو القعدة‬
  • By the end of this lecture students should be able to:  Describe & enumerate the causes of atrophy.  Define hyperplasia, hypertrophy & metaplasia.  Differentiate physiologic from pathologic hyperplasia.  Differentiate physiologic from pathologic hypertrophy.  To get some knowledge about the developmental disorders
  •  Definition: Reversible changes in size, number, phenotype, metabolic activity, or functions of cells in response to changes in their environment  Types: 1- physiologic (response to normal stimulation by hormones or endogenous chemical mediators) 2- pathologic (response to stresses to escape injury)  Forms: hypertrophy, metaplasia hyperplasia, atrophy,
  • Stimulus or stress Adaptation Normal cell Hypertrophy Hyperplasia Atrophy Metaplasia Cell death Apoptosis Necrosis Injury Reversible Irreversible
  • Definition: increase in the size of cells  increase in the size of the organ (with increased functional capacity)  No new cells, just larger cells  Hyperplasia (will be discussed later), entails increase in the cell number 
  • Types & causes: 1- physiologic:  Increased functional demand Skeletal muscles heart (within limit)  Specific hormonal stimulation Pregnant uterus (estrogen stimulates s.m. hypertrophy & hyperplasia)
  • 2- pathologic: a) Adaptive hypertrophy (wall of hollow muscular organs) Stomach in case of pyloric obstruction Left ventricle in case of aortic valve disease or hypertension Urinary bladder in case of urethral stricture
  • b) Compensatory hypertrophy: In paired organs as in kidney: when one kidney is absent or removed surgically, the other kidney is enlarged in size c) Hormonal hypertrophy: eg: excessive growth hormone leads to gigantism or acromegaly * Selective hypertrophy (eg: smooth ER in hepatocytes of patients treated with barbiturates)
  •    Definition: increase in the number of cells  increase in the size of the organ. It may occur with hypertrophy & often in response to the same stimuli. Types: physiologic & pathologic 1- physiologic hyperplasia a) Hormonal (glandular epithelium of female breast at puberty & pregnancy) a) Compensatory (when a portion of tissue is resected or diseased, eg. Liver)
  • 2- Pathologic hyperplasia a) Excessive hormonal or growth factor stimulation • Endometrial hyperplasia: due to loss of balance between estrogen & progesterone hormones. This results in abnormal menstrual bleeding
  • • Thyroid gland: • Adrenal gland: due to increased thyroid stimulating hormone (TSH) in thyrotoxicosis. due adreno-corticotropic hormone (ACTH) Cushing’s syndrome. to in b) Hyperplasia is an important response of CT cells in wound healing. Growth factors are produced by WBCs responding to injury & by cells in ECM.
  • c) Hyperplasia due to viral infection. e.g.: HPV that causes skin warts & squamous cell papilloma of m.m. Here, growth factors may be produced by virus or by infected cells.
  • Sebaceous hyperplasia Papillary hyperplasia of the palate
  • Gingival hyperplasia
  • Hyperplasia & CANCER !! Pathologic hyperplasia constitutes a fertile soil in which cancerous proliferation may eventually arise. • • Endometrial hyperplasia  increased risk of endometrial cancer Certain HPV infections  predisposes to cervical cancers
  •  Definition: shrinkage in the size of cell by loss of cell substance. When a sufficient number of cells involved, the entire tissue/organ diminishes in size.  Mechanism: Reduction in structural components of cell Protein synthesis Mitochondria & myofilaments Atrophy Protein catabolism Endoplasmic reticulum The cells retreats to a smaller size at which survival is still possible. New equilibrium is achieved between cell size & diminished blood supply or trophic stimulation.
  •  Types & causes: 1) Physiological - Atrophy of thymus gland atrophy after puberty & thyroglossal duct after birth (involution) - Decreased workload “disuse”: immobilized limb to permit healing of fracture Loss of hormone stimulation: atrophy of ovaries & uterus after menopause -
  • 2) Pathological 1. Loss of innervation. Starvation (lack of food & its absorption) & malnutrition. 2. Unilateral tongue atrophy following hypoglossal nerve damage
  • 3. Senile atrophy: in old age “brown atrophy of the heart” 4. Pressure atrophy: surrounding tissue. - In many situations, atrophy is accompanied by increased autophagy “self-eating”: a process in which starved cell eats its own components in an attempt to find nutrients & survive. as tumor pressure on
  •  Definition: transformation of one type of tissue into another type of the same differentiation.  Cells sensitive to a particular stress are replaced by other cell types better able to withstand the adverse environment.  Mechanism: it seems to be induced by altered differentiation pathway of tissue stem cells (genetic reprogramming of stem cells rather than transdifferentiation of already differentiated cells)
  •  1) 2) Types: Epithelial metaplasia Connective tissue metaplasia 1- Epithelial metaplasia Squamous metaplasia - In the respiratory epithelium of habitual cigarette smokers & in vitamin A deficiency
  • Squamous metaplasia - Transitional epithelium of urinary bladder to stratified squamous epithelium in urinary bilharziasis a)
  • Odontogenic epithelial metaplasia c) Glandular metaplasia - In chronic gastric reflux, normal st. sq. epith. of the lower esophagus may undergo metaplastic transformation into gastric or intestinal type “Barrett’s” b)
  •  1) 2) Types: Epithelial metaplasia Connective tissue metaplasia 1- cartilage to bone in old age 2- bone occasionally forms at foci of injury 3- muscle tissue to bone “ in traumatic myositis ossificans “
  • Difference Between Congenital & Hereditary Conditions Congenital defects/anomalies: Structural defects that are present at, before, or after birth but not necessarily inherited “transmitted by genes”. They have either cosmetic or functional significance. They may be a significant cause of infant illness, disability & death.   Hereditary defects/Anomalies: Diseases or conditions transmitted by genes, some become apparent at birth & others years after birth.
  • Known causes can be grouped into the following categories: 1. Genetic factors: All chromosomal syndromes are associated with congenital malformations (10-15%). e.g. Down syndrome & Turner syndrome. 2. Environmental influences • Infections: Viral, Rubella, Toxoplasmosis, Syphilis, CMV, HIV to which the mother was exposed (2- 3% ). • Drugs: alcohol, Androgens, Phenytoin , Thalidomide & Warfarin (1%) • Maternal disease states: Diabetes, Phenylketonuria & Endocrinopathies (6-8%). • Pregnant smokers • Irradiation 3. Multifactorial inheritance : which implies the interaction of environmental influences with two or more genes of small effect, is the most common genetic cause of congenital malformation representing 20-25%. 4. Unknown: comprises 40-60%
  • Organ–specific malformations Agenesis : refers to the complete absence of an organ or its primordium Aplasia : indicates incomplete development of an organ Hypoplasia : means underdevelopment of an organ Atresia : describes the absence of an opening of a hollow visceral organ or duct such as that of salivary glands, of intestines or of bile ducts
  • Hemifacial - atrophy Progressive atrophy of tissues on one side of the face Causes: 1. Atrophic malformation of cervical sympathetic nervous system 2. Hereditary 3. Trauma or infection 4. Peripheral trigeminal neuritis 5. A form of localized scleroderma
  • Clinically  Noticed at 1st or 2nd decades of life  Noticed first as a white line or furrow on one side of the face near midline  Lesion extends progressively to include atrophy of all tissues on one side of the face  Eye appears depressed in the orbit  Epilepsy & trigeminal neuralgia might occur  Skin on the affected side would look dark & pigmented with loss of hair on that side
  • Oral Manifestations  Atrophy of tongue & lips on the affected side  Underdevelopment of the roots  Retarded eruption of the teeth  Reduced growth of the jaw on the affected side
  • * Mild form of facial asymmetry is more common * Hemihypertrophy might involve: - entire half of the body - one or both limbs - The face & head Causes: a) b) c) d) e) Chromosomal abnormalities Localized chronic infection Lymphatic & vascular problems Neurogenic abnormalities Unknown
  •  a) b) c) d) e) f) Clinical Features Mental disturbances Skin abnormalities such as nevi Varicosed veins Umbilical hernia Hemangioma Thick & coarse hair on the involved side
  • Oral Manifestations a) b) c) Large permanent teeth in the affected side Premature eruption of the permanent teeth Premature shedding of deciduous teeth on the affected side Differential Diagnosis: Neurofibromatosis, Fibrous Dysplasia
  • 1. Agnathia Extremely rare Total absence of the jaw partial absence of the jaw might be seen In the maxilla: one of the maxillary processes or premaxilla  In the mandible: one side of the mandible, the condyle or ramus    
  • 2. Micrognathia  Either true or relative  True when the actual jaw is small relative to normal size  Relative when jaw size is normal & teeth are large “macrodontia”. It might be due to: 1. posterior positioning of the mandible relative to maxilla or 2. agenesis of condyle  Agenesis of the TMJ or ankylosis of the joint might lead to acquired micognathia
  • 3. Macrognathia  Abnormally large jaw  In both mandible & maxilla in hyper-pituitary gigantism  Mandibular prognathism is considered as a form of Macrognathia  Macrognathia can be true with actual large jaw or relative when the jaw size is normal whereas the size of teeth is smaller ” Microdontia”
  • Causes: 1. increase size of the ramus 2. increase Mandibular length 3. increase the gonial angle 4. anterior position of the glenoid fossa 5. decreased maxillary length 6. posterior positioning of the maxilla 7. prominent chin button 8. Varying soft tissue contour