Pathology

Pathology. Is the study of structural and functional of the body in diseases

    Eras of pathology
Religion and superstition belief to rational approach antiquity to AD 1500
    Era of gross pathology 1500—1800
    Eras  of technology development and cellular pathology 1800-1950s
    Era of new modern pathology 1950 to 20 century

Subdivision
Human pathology
      General
      Systemic  
Histopathology pathology
     Surgical tissue removal
     Forensic
     Autopsy.  tissue and organ removal
Cytopathology
Study of cell shade off from the lesson
    
Four aspects of diseases
   Aetiology or causes
   Pathogenesis
   Morphological charge.   Structural alteration
   Clinical significance.   all form of cell ,,organ start from molecules or structural alteration of cell
Aetiology or causes
   Intrinsic or genetic
   Acquire or environmental

Environmental causes
  Physical
  Chemical
  Infection and infestation
  Aging
  Psychological defect
  Abnormal immunological
  Nutritional Deficiencies and excess

Genetic
Normal gene
Autoimmune
Group A gastric and anaemia
Abnormal gene
Mutation Rise to Abnormalities of chromosomes
Pathogenesis. Is the steps by step where by disease originate and development

Basing on body response disease can be classified
Congenital
Inflammatory
Degenerative
Neoplastic

Cell death
Types of cell death
    Necrosis
   Apoptosis

Differences Btn necrosis and Apoptosis
-Inflammatory but non
-Die internal Bt external
-No membrane injury intact bt loss membrane Integrity
-
-

Causes of cell death
Physical factor
Chemical
Immunological reaction
Aging
Infectious agents
Nutritional defect
Oxygen deprivation

Blood Duff group  negative affected with plasmodium vivax
Group A gastric ulcer
Group B peptic ulcer

Cell the basic unit of life
Cell death is the continue damage or injury of cell become irreversible and cause the cell can not recover and it die
Physiological of cell death
Necrosis out side or  Apoptosis internal
    Necrosis Membrane injury DNA stimulate Ritic Enzymes from resosome for kill to protein Also affect other part
Apoptosis

CELL DEATH
Morphological charges
Atrophy shrinkage of cell in size or decrease
Infection
Chemicals
Nutritional deficiencies
Trauma
Autoimmune

Effect
Loss workload
Nutritional disorders
Growth retardation

Hypertrophy increase in size
Causes
Infection
Trauma

Hyperplasia cells increase in number
Causes
Infection
Trauma
Cell injury or tissue

Effects

Metaplasia replacement of other cells which is not the normal

Dysplasia disorder of  cell growth
Cause
Cell injury
Nutritional deficiencies

Necrosis pattern
Coagulative -
Liqualitive
Ganglinors- dry,wet, death of the cell in hard or
Fat -
Fibroid -
Ceaseous -

Infarction formation of Infarct
Characteristics
Lead to Occlusion of vein
Tissue č dual circulatory system
Tissue previous č

Proliferative potentialive of different body tissue

INFLAMMATION

Inflammation is the ability of vascularized tissue to respond to injury
Types
Acute and chronic
Is the rapid or early response reaction which followed č repair and recover for short time

Importance inflammation
Tissue repair
Reduce bleeding platelate
Brought WBC

Causes
Chemical injury
Physical
Insects bites
Infection
Immunological reaction

Components of Acute inflammation

Cellular event
Vascular change
  
Vascular change
Transient vasocostriction -borrowing
Arteriolar vasodilatation -enlargement
increase vascular permeability
Exudation -discharge

Cellular event
Cellular requetiment
Cellular activation
Phagocytosis  

Features of Inflammation
Redness
Swelling
Loss of function
Pain and tenderness
Hotness

Morphological partten
Fibrous
Serous
Suppralative /purulent

Chemical mediators
Any soluble substance which act on other the blood vessels inflammatory

Cellular delivered mediators
Histamine
Prostaglandins
Serotonin
Platelets activating factor

Plasma delivered mediators
Kinin
Coagulation protein
Complement protein

Outcomes of acute inflammation
Resolution
Progression
Fibrosis
Spread
Death from septicaemia and involvement of viral organic

Chronic inflammation is the progress of acute inflammation
Take long periods or more than 14days

Causes
Followed from acute
Recurrent attack repeating
Occur due to agents or infection

Features
Mononuclear
Tissue death or necrosis
Proliferative change
Small vessels stimulate resulting formation of granulation tissue

Types of chronic
Chronic Non specific
Chronic granulomatous

Squeals of chronic inflammation

Granulomatous TB, LP, syphilis, schistomiasis,foregn body
Granuloma

Outcome
Scaring formation
Chronic discharge
Pathological Fracture

Systemic features
Fever
Anaemia
Leucocytosis  raise of WBC than the normal
Amyloidosis
Elevated erythrocytes
Non steroidal anti inflammatory drugs 
Bacterial products

Repair regeneration and wound healing

Control of the cell Proliferation
Cell cycle or four sequential phase
Go - phase (gap)
G1 -phase (gap 1)
S1 - synthesis gap (phase)
M - mitotic gap (phase)
Types of tissues according to Prolifilative
Labile
Stable
Permanent 

Roles of extracellular matrix
Control of cell growth
Maintain of cell differentiation
Scaffolding for tissue renewal
Establishment of tissues microenvironments
Storage and presentation of regulatory molecules

4 sequential processes of repair by connective tissue and deposition

Formation of new  blood vessels /angiogenesis
Migration and Proliferation of fibroblast
Scar formation /deposition of ECM
Maturation and reorganization of fibrous tissue /remodelling

Wound healing   complex and dynamic process of restoring cellular structures  and tissue layer
.   Division phase
Inflammatory phase
Proliferative phase
Remodelling phase

Types of wound healing
Primary healing
Delayed primary healing
Secondary healing

Shock
Is clinical syndrome which occurs due to hypoperfusion
Cause
  Poor venous return from any source
Excessive losing of blood or
Failure of the heart to reject enough blood

Sequence of events in wound healing phase
hemostasis/ initial phase
Secondary /inflammation
Third phase /granulation
Fourth phase/remodelling 

Types of shock
Cardiogenic
Hypovolomic /hemorrhage
Septic
Anaplastic
Neurological

Pathophysiology and sequel

Reversible shock is an initial shock
Initial /compensatory mechanism involves
Increase heart rate
Stimulate rennin, angiotensin and aldosteron
Dilation of coronal and cerebral blood vessels
Constriction of peripheral vessels

Irreversible shock

Thrombosis and Embolism

Thrombosis the formation of clotting of either partially or block blood vessel.

Embolism is an obstruction of the blood Vessel due to blood clot or foreign body

Hemostasis prevent excessive blood in the body

Both Hemostasis and thrombosis involves three components
Vascular wall
Platelets
Coagulative cascade
Risk factors for thrombosis
Elderly  age
Obesity
Varicose veins
Immobility
Pregnancy
History of previous DVT
surgical and trauma of the pelvic,lower limb
Heart failure
Recent myocardial infarction
Cigarette smoke

Pathogenesis _both

Types of thrombi
Mural
Arterial
Venous
Post mortem clots
Thrombi on heart valve are vegetations

Fate of thrombi events
Dissolution
Propagation
Embolization
Organization and recanalization

Classification
Systemic thromboembolism
Arterial embolism
Cerebral embolism
Venous embolism
pulmonary embolism
Air/gas embolism
Fat and cholesterol
Amniotic

Thyroid hormone a hormone located at neck or larynx

Diseases associated č thyroid
Hypothyroidism
Hyperthyroidism
Mass lesson of thyroid
Graves disease
Goiter
Hypothyroidism caused by low production of thyroid hormone
(T1&T2)

Crenitism the hypothyroidism develops in infancy or childhood
Causes
Primary causes
Dietary iodine deficiencies
Autoimmune /hashimoto's thyroiditis
Reaction of direct from antibiotic
Generic predisposition to the condition
A genesis /dysgenesis of the thyroid gland
Congenital defect
Secondary causes
Defects of the centre /hypothalamus and pituitary gland
Surgery and radiotherapy to treat pituitary adrenaline can destroy
Lymphocytic hypohhysitis
Pathogenesis
Acute illness of the thyroid č severe pain
Inflammation

Hyperthyroidism excessive production of thyroid gland T3 &T4
causes
Primary
Diffuse toxic Hyperplasia /grave's
Hyperfuctioning (toxic) multinodular goiter
Hyperfuctioning toxic adenoma

Secondary

TSH secreting pituitary adenoma
Sebacute granulomatous thyroiditis
Sebacute Lymphocytic thyroiditis
Struma ovarian
Faction thyrotocosis

Three triad of graves
Thyrotocosis
Infiltrative ophtholmopathy
Infiltrative adermopathy
Types of thyroid tumors
Follicular adenoma
papillary carcinoma
Anaplastic carcinoma
Medullar cancer
Hypoparathyroidism a low production of parathyroid hormone due to hypoperfusion of the parathyroid gland
Causes
Surgical ablation
Congenital absence
Autoimmune hyperthyroidism

Hyperparathyroidism  an excessive production of parathyroid hormone due Hyperplasia of the parathyroid gland

Causes
Primary  caused by  sporadic parathyroid adenoma
Secondary and tertiary Hyperparathyroidism caused by renal failure

Body fluids compartment
ICF total volume adult 25lt
ECF total 15lt,3lt out of plasma,12lt found interstitial space

Electrolytes
ICF
K, mg, PO
ECF
Na,Cl, HCo3

Normal water balance
Body gain and loss both equally
Factors for regulate body fluids
Thirsty
Ability of the kidney to eliminate body's water
Plasma sodium concentration

Daily fluid intake depends on on many factors
External temperature
Physical activities
Type of food taken

Disturbances of water and sodium balance
Pure water deficiencies
Effect of pure water deficiencies
Combined of water and sodium deficiencies

Causes of  sodium and water imbalance
Excessive urination
Excessive sweating
Loss from gastrointestinal tract due to the excessive vomiting and diarrhea
Conditions like diabetes, thiazide ,Addison's disease
Severe burn and heavy hemorrhage

Oedema an increase of fluids in the intestinal tissue space or body cavity
Mechanism of oedema
Increases of hydrostatic pressure
Decrease plasma oncotic pressure
Lymphatic obstruction
Water and sodium rentation
Body pH regulated by keeping the balance Btn acid and bases produced by body cells
Normal body pH 7.35-7.45

Steatosis accumulation of fat droplets č the hepatocytes

Cirrhosis end stage of liver disease
The major mechanism that combines to create cirrhosis
Hepatocullular death
Regeneration
Progressive fibrosis
Vascular change

Major characteristics of cirrhosis
Bridging fibrous septa
Paranchymal nodules
Disruption of the architecture of the inner liver

Major clinical consequences of portal hypertension
Ascites
Formation of portal systemic venous shunt
Hepatic encephalopathy
Congestive splenomegaly

Insulinomas is the tumor of the pancreas which derived direct from the B-cell and secret insulin

Gastrinoma gastric producing tumor

GIT process main phases
Ingestion
Fragmentation
Digestion
Absorption
Elimination of undigested material

Features
bdm pain
GI bleeding
Diarrhoea
Steatorrhea
Constipation
nausea and vomiting
Dysplagia
Odynophagia
Gastroesophangeal reflex
Anorexia
Weight loss

Neoplasm /tumor is an abnormal new growth

Types of tumor
Benign
Malignancy

Components of benign and malignancy
The Paranchymal
Host stroma /supportive tissue

Distinguish
Degree of differentiation malignant are poor differentiated
Rate of growth
Benign tumor grow slowly
Malignant grow much faster

Local invasion
Benign localized at the site of original
Malignant invade /metalized to distant site

Spread

Classes of carcinogenic agents
Chemical
Radiation
Microbes agents - virus

Bronchitis inflammation of bronchi

Bronchiectasis  is the permanent dilatation of bronchi and bronchioles caused by destruction of the muscles and elastic supportive

Two process in intertwined in of Pathogenesis of Bronchiectasis
   Obstruction
    Chronic persistent infection

Emphysema is the presence of air in tissue

Classification
Centriacinar
Panacinar
Distal acinar
Irregular

Atelectasis /collapse is the loss of lung volume by inadequate expansion of airspaces

Infectious diseases can be transmitted by
Faecal oral route
Direct contact
Vertical transmission
Insect /arthropods vector
Blood borne contact
Respiratory droplets

Host factor
Age
Sex
Nutritional status
Co-morbid disease
Body immunity

Host's protective barriers
Skin
GI system
Respiratory system
Urogenital system

pneumonia as any infection in the lung

Acute bacterial pneumonia
Bronchopneumonia
Lobar pneumonia

Pathogenesis of pneumonia
Infective dose
Agents must be airborne
Organism must be remain alive

Era before antibiotic
Congestion
Red hepatization
Gray hepatization
Resolution

Arteriosclerosis is the Harding of the arteries
Two anatomic variants
Hyline
Hyper plastic

Types of Arteriosclerosis
Arteriosclerosis abliterans
Medial calcific  sclerosis

Arteriosclerosis - is most often associated with hypertension and diabetes Mellitus

Atherosclerosis is the condition in which the arterial wall thickens

Complications of advanced atherosclerosis
Chronic
Slowly progressive
Accumulation

Aneurysms
abnormal dilation of a blood vessel or the heart

Classification of aneurysms
Saccular aneurysm
Fusiform aneurysms

Causes of aneurysms
Trauma
Congenital defect
Infection
Arterial aneurysms

Hypertension can cause
Cardiac hypertrophy
Heart failure
Aortic dissection
Renal failure

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