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KeenObsidian2913

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Harvard University

Prof. Dr. A. Kubila KorKut, MD

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pathology gastrointestinal system nervous system renal system

Summary

This document is a summary of lessons on pathology, covering the gastrointestinal system, including esophageal and stomach disorders, and the nervous systems such as meningitis and encephalitis. It also encompasses renal pathology including functions and pathologies of the renal system.

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PATHOLOGY PROF. DR. A. KUBİLAY KORKUT, MD GASTROINTESTINAL SYSTEM PATHOLOGY Muscular Dysfunctions of the Esophagus Achalasia (Cardiospasm) Neuromuscular dysfunction of the cardiac sphincter which fails to relax during swallowing. Muscular Dysfunctions of the Oesophagus Hiatus hernia...

PATHOLOGY PROF. DR. A. KUBİLAY KORKUT, MD GASTROINTESTINAL SYSTEM PATHOLOGY Muscular Dysfunctions of the Esophagus Achalasia (Cardiospasm) Neuromuscular dysfunction of the cardiac sphincter which fails to relax during swallowing. Muscular Dysfunctions of the Oesophagus Hiatus hernia Herniation of part of the stomach through the esophageal hiatus of the diaphragm. Etiology; congenitally short esophagus acquired degeneration of muscle, increased intra-abdominal pressure such as in pregnancy Muscular Dysfunctions of the Oesophagus Esophageal Diverticula Outpouching of esophagus wall at the point of weakness Etiology; congenitally acquired (pulsion or traction) Inflammatory Diseases of Stomach Acute Gastritis Etiopathogenesis ; 1. Diet and personal habits (spiced food, alcohol, malnutrition, smoking) 2. Infections (Helicobacter pylori, staphylococcal food poisoning) 3. Drugs (aspirin, Non-steroidal anti-inflammatory drugs NSAID, cortisone) 4. Chemical and physical agents (intake of corrosive materials) 5. Severe stress (emotional, trauma, surgery) Inflammatory Diseases of Stomach Chronic Gastritis Etiopathogenesis ; 1. All the factors of acute gastritis 2. Infection with Helicobacter pylori (most common) 3. Reflux of duodenal contents into the stomach 4. Associated diseases such as gastric or duodenal ulcer or carcinoma 5. Chronic hypochromic anemia 6. Immunological factors Inflammatory Diseases of Stomach Peptic Ulcers Degeneration and necrosis of gastrointestinal mucosa exposed to hydrochloric acid and pepsin. Location; duodenum, stomach, esophagus Inflammatory Diseases of Stomach Acute Peptic (Stress) Ulcers Multiple, small mucosal erosions located mostly in stomach. Etiology; 1. Psychological stress 2. Physiological stress (shock, severe trauma, septicemia, extensive burns, intracranial lesions, drug intake, local irritants) Pathogenesis; Ischemic hypoxic injury to the mucosal cells cause depleting of the mucus barrier Inflammatory Diseases of Stomach Chronic Peptic Ulcers Duodenal ulcer is four times more common than gastric ulcer. More common in males. Etiology; 1. Helicobacter pylori (15-20% cases infected with H.p.) 2. NSAIDs induced mucosal injury 3. Acid-pepsin secretions 4. Gastritis 5. Local Irritants (alcohol, smoking, aspirin) Inflammatory Diseases of Stomach Chronic Peptic Ulcers Etiology; 6. Dietary factors 7. Psychological factors (psychological stress, anxiety) 8. Genetic factors 9. Hormonal factors 10. Miscellaneous (alcoholic cirrhosis, chronic renal failure) Inflammatory Diseases of Stomach Complications of Peptic Ulcers Acute and subacute peptic ulcers usually heal without leaving scar. Chronic ulcer may result; 1. Obstruction (fibrous scar cause pyloric or duodenal stenosis) 2. Hemorrhage (minor or severe bleeding) 3. Perforation (acute abdominal emergency) 4. Malignant transformation Inflammatory Diseases of Stomach Clinical Features of Peptic Ulcers 1. Age (peak incidence of duodenal ulcer is in 5th decade, gastric ulcer is in 6th decade 2. People with more stress and strain prone to duodenal ulcer, gastric ulcer is more in laboring people. 3. Pain, in gastric ulcer pain occurs within 2 hours after food. In duodenal ulcer, pain is severe and occurs late at night – hunger pain and relieved by food Inflammatory Diseases of Stomach Clinical Features of Peptic Ulcers 4. Vomiting relieves the pain of gastric ulcer. Duodenal ulcer patients have heart-burn-retrosternal pain, but rarely vomiting. 5. Weight loss is common in gastric ulcer, duodenal ulcer patients tend to gain weight 6. Diet, gastric ulcer patients avoid fried and spiced foods, duodenal ulcer patient take all kind of diet. 7. Hematemesis and Melena. Hematemesis occur more in gastric ulcer, while melena occur more in duodenal ulcer patients. Small Intestine Function, digestion and absorption Anatomical 3 Parts ; Duodenum, jejunum, ileum Histologically 4 layers ; 1. Serosa 2. The muscularis propria (2 layers of smooth muscle) 3. The submucosa 4. The mucosa (absorptive surface is increased by the Villi) Intestinal Obstruction 1. Mechanical Obstruction Internal obstructions (inflammatory disease-Crohn, Tumors, Meconium, Gallstones, Foreign body) External compression (Peritoneal adhesions, strangulated hernia, intussusception, volvulus, intraabdominal tumor) Intestinal Obstruction 2. Neurologic Obstruction Paralytic ileus (after abdominal operations or acute peritonitis) 3. Vascular Obstruction Obstruction of the superior mesenteric artery (thrombosis, embolism, accidental ligation) Large Intestine Anatomical 6 parts Cecum, ascending colon, transverse colon, descending colon, sigmoid colon, rectum Histologically 4 layers Mucosa, Submucosa, Muscularis, Serosa Miscellaneous Lesions Hemorrhoids (Piles) Varicosities of the hemorrhoidal veins Internal and External piles Commonly in elderly and pregnant woman Etiology; 1. Chronic constipation 2. Hereditary 3. Venous stasis of pregnancy 4. Portal Hypertension 5. Cardiac failure 6. Rectum tumors THE NERVOUS SYSTEM PATHOLOGY Central Nervous System Neurons Neurons are highly specialized cells which are incapable of dividing after the first week of birth. Thus, neuron damage is irreversible. 3 main parts : The cell body, Axon, Dendrites Neuroglia (glia) 3 types of cells : Astrocytes, Oligodendrocytes, Ependymal cells Microglia Monocyte-macrophage system, they have phagocytic function Central Nervous System Dura mater (fibrous layer attached to the skull) Arachnoid mater (vascular layer) Subarachnoid space contains cerebrospinal fluid Pia mater (closely applied to the brain) Infections Meningitis ; 1. Acute Pyogenic (Purulent) Meningitis : acute infection of pia- arachnoid and CSF (subarachnoid space). Escherichia coli, Hemophilus influenza, Neisseria meningitidis, Streptococcus pneumonia the most common etiologic agents. Clinical features ; fever, severe headache, vomiting, drowsiness, stupor, coma, convulsion, stiffness of the neck Infections Meningitis ; 2. Acute Lymphocytic (Viral, Aseptic) Meningitis : Etiologic agents are enteroviruses, mumps, ECHO viruses, coxsackie virus, Epstein-Barr virus, herpes simplex virus-2, HIV, arthropod-borne virus Clinical features ; fever, severe headache, vomiting, drowsiness, stupor, coma, convulsion, stiffness of the neck Infections Meningitis ; 3. Chronic (Tuberculous and Cryptococcal = fungal) Meningitis : Clinical features ; headache, confusion, malaise, vomiting Infections Encephalitis ; Parenchymal infection of brain 1. Bacterial encephalitis : usually secondary to meningitis, may progress to brain abscess (fever, headache, vomiting, seizures, focal neurological deficits) 2. Viral encephalitis : Herpes simplex, herpes zoster- varicella, enteroviruses, cytomegalovirus, HIV, rabies virus Cerebrovascular Diseases (CVD) CVD ; Pathological processes of the blood vessels of the brain, Etiologies ; thrombosis, embolism, rupture of the vessel, hypoxia, hypertensive arteriolosclerosis, atherosclerosis, arteritis, trauma, aneurysm, developmental malformations CVD results in 2 main types of parenchymal diseases 1. Ischemic brain damage 2. Intracranial hemorrhage Cerebrovascular Diseases (CVD) 1. Ischemic brain damage a. Generalized reduction in blood flow results in global hypoxic- ischemic encephalopathy b. Local vascular obstruction cause cerebral infarcts 2. Intracranial hemorrhage a. Intracerebral hemorrhage b. Subarachnoid hemorrhage Cerebrovascular Diseases (CVD) 1. Ischemic brain damage a. Generalized reduction in blood flow results in global hypoxic- ischemic encephalopathy b. Local vascular obstruction cause cerebral infarcts 2. Intracranial hemorrhage a. Intracerebral hemorrhage b. Subarachnoid hemorrhage Cerebrovascular Diseases (CVD) Clinical Features ; The stroke is the essential feature of CVD, which is used for sudden developing of focal neurologic deficit varying from minor neurologic disorder to hemiplegia and coma. Transient ischemic attacks (TIA) ; temporary period of symptoms of the stroke Degenerative Diseases Alzheimer’s Disease ; Most common cause of dementia in the elderly, Occurs after 5th decade of life and progressively increases with age. The brain is reduced in weight and bilaterally atrophic. Etiology is unknown, family history is important Degenerative Diseases Parkinsonism ; Chronic progressive disorder of motor function, Characterized by tremor apparent at rest and worsen with emotional stress, Rigidity, disordered gait and posture Etiology ; Parkinson’s disease, Trauma Toxic agents and drugs (dopamine antagonist) Peripheral Neuropathy PN is characterized by symmetrical sensory features such as tingling, pricking, burning sensation or dysesthesia in feet and toes. Motor features are muscle weakness and loss of tendon reflexes. Etiology ; Diabetes, Thiamine (B1 Vitamin) deficiency, amyloidosis, autoimmune demyelinating disease (Guillain-Barre syndrome), toxins and chemotherapeutic agents, RENAL PATHOLOGY Structure Kidneys are bean-shaped paired organs, each weighing 150 gr in male, 135 gr in female. The hilum of the kidney has artery, vein and ureter. Each kidney ,s composed of approximately 1.000.000 nephrons. Nephron is the functional unit of the kidney. Structure The major function of glomerulus is filtration from the capillaries to the urinary space. Glomerular filtration rate (GFR) is 125ml/dk Tubules ; reabsorption of sodium, potassium, bicarbonate, calcium, uric acid, water, and secrete hydrogen, potassium, Renal Functions Excretion of waste products resulting from protein metabolism (urea, ammonia, uric acid) Regulation of acid-base balance by excretion of H+ and bicarbonate ions. Regulation of salt-water balance by excretion or reabsorption of Na+ Regulation of blood pressure by formation of renin Regulation of erythropoiesis by erythropoietin Formation of Vit. D Renal Function Tests Urine Analysis ; Microscopic, bacteriologic, chemical (glucose, protein, hemoglobin) Blood chemistry ; urea, blood urea nitrogen (BUN), creatinine Renal clearance test ; creatinine clearance, urea clearance Acute Renal Failure Characterized by ; Rapid onset of renal dysfunction : oliguria and anuria, sudden increase in urea and creatinine in blood (uremia) Clinical features ; 1. Oliguric phase : 7-10 days urinary output less than 400ml/day, uremia, hypervolemia, metabolic acidosis, hyperkalemia, hypernatremia. 2. Diuretic phase : onset of healing of tubules, improvement in urinary output 3. Phase of recovery : full recovery may take up one year and occurs in half of case, while others terminate with death. Chronic Renal Failure Progressive and irreversible deterioration of renal function Etiopathogenesis : Classified in 2 major groups ; glomerular pathology and tubulointerstitial pathology Progressively 4 stages ; Decreased renal reserve : GFR 50% of normal, patients asymptomatic Renal insufficiency : GFR 25% of normal, polyuria and nocturia occur Renal failure : GFR 10%, edema, metabolic acidosis, uremia End-stage kidney : GFR

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