Splenic infarcts – gross Coagulative necrosis Two large infarctions (areas of coagulative necrosis) are seen in this sectioned spleen. Since the etiology.

Slides:



Advertisements
Similar presentations
Cellular lesions I.
Advertisements

Necrosis Definition: Causes:. Development of Necrosis (2 mechanisms) irreversible damage to mitochondria (failure of ATP generation) ↓ anaerobic respiration.
Chapter 2 Cellular Responses to Stress, Injury, and Aging
Intracellular Accumulations Fatty Change (Steatosis): Fatty Change (Steatosis): Abnormal accumulation of triglycerides within parenchymal cells seen in.
Cell Injury and Cell Death
Cell injury is defined as A set of biochemical and morphological changes that occur when the state of homeostasis is disturbed by adverse influence.
Cell Injury, Cell Death, and Adaptations
Week 2 Cell Injury and Cell Death Dr.İ.Taci Cangül Bursa-2008.
Cell Death Dr. Raid Jastania. Case During your clinical year rotation, you work with the transplant team. You see this lady who had kidney transplant.
Detection of Cellular Changes After Injury By: Light microscopy or gross examination  detect changes hours to days after injury Histochemical or ultrastructural.
Inflammation. Acute inflammation The cardinal signs of inflammation are rubor (redness), calor (heat), tumor (swelling), dolor (pain), and loss of function.
بسم الله الرحمن الرحيم.
Cell injury, adaptation and cell death (2). Causes of cell injury Hypoxia (oxygen deprivation) Occurs due to Loss of blood supply - Ischaemia Inadequate.
INFLAMMATION Acute And Chronic. The cardinal signs of inflammation.
Cell injury By Dr. Abdelaty Shawky Dr. Gehan Mohamed.
Cellular Responses To Stress
Cell injury-3.
Cell Injury Cell and Tissue Adaptation Necrosis and Apoptosis Dr. Raid Jastania.
Necrosis and apoptosis
Infarct: Definition: An infarct is a localized area of ischemic necrosis resulting from sudden and complete occlusion of its arterial blood supply without.
Cell injury-1.  Cells are constantly exposed to a variety of stresses.  At first cells try to adapt themselves to overcome this stressful condition,
Infarction Yiran Ni M.D Department of pathology CTGU Mail: Tel: Office room: S-2623.
General Principles of Cell Injury
ปฏิบัติการ วิชา พยาธิ วิทยา ครั้งที่ 1 ภาควิชาพยาธิวิทยาและ นิติเวชศาสตร์ คณะแพทยศาสตร์ มหาวิทยาลัยนเรศวร.
Cell Biology Review and Altered Functions. Embryonic Stem Cells.
Objectives  Define necrosis and apoptosis  List the different types of necrosis, examples of each and its features  List the different conditions associated.
What is Pathology? “Scientific study of disease" or the alterations that occur when abnormal influences (bacteria, viruses, etc.) affect cells, tissues,
Necrosis Apoptosis. Different Types of Cell Death TermDefinition Necrosis Antemortem pathologic cell death Apoptosis Antemortem programmed cell death.
Cell Injury Robert Low MD PhD. sites within cells that are easily injured reversibility of injury and complete recover adaptation to chronic injury cell.
Lecture on pathological anatomy for the 3-rd year students T.Filonenko
Irreversible cell injury Dr Heyam Awad FRCPath. Irreversible injury Necrosis Apoptosis.
1- Introduction of Pathology
Cell Injury 1 & 2. Slide 11: Vacuolar Degeneration Kidney Renal tubules –Note tiny small vacuoles –Displaced nucleus to the side Glomerulus.
Pathology 11/25/20151 SECTION 2 CELL INJURY. Pathology 11/25/20152  Reversible  Irreversible Cellular Swelling Fatty Change Hyaline Change Amyloid Change.
Cell injury Dr Heyam Awad FRCPath.
Robbins’ Basic Pathology th Ed. Histology of Chronic Inflammation.
Reversible cell injury  cellular swelling (Hydropic changes)  Fatty changes Irreversible cell injury  Necrosis  Apoptosis Cell Injury.
But to those who believe and do deeds of righteousness, He will give their (due) rewards, and more, out of His bounty: But those who are disdainful and.
 Definition ◦ It is combination of two Latin words ◦ Pathos meaning disease ◦ Logos meaning study Pathology is a branch of medicine that deals with the.
Chapter 4 Injury, Inflammation, and Repair. Review of Structure and Function The body is capable of undergoing dynamic changes to carry out body functions.
Inflammation 5 Dr Heyam Awad FRCPath. topics to be covered in this lecture Outcome of acute inflammation. Morphology of acute inflammation. Chronic inflammation.
Cellular injury & adaptation.
MYOCARDIAL INFARCTION
Cell injury By Dr. Abdelaty Shawky Dr. Gehan Mohamed.
Cell Injury, Cell Death, and Adaptations. Cell adaptation Hypertrophy Hyperplasia Atrophy Metaplasia.
Practical of Cell Injury Third Year 5th October 2015
Cellular Pathology Outline
Copyright © 2012, 2006, 2000, 1996 by Saunders, an imprint of Elsevier Inc. Chapter 1 Cell Pathology Part 2.
Cell injury By Dr. Abdelaty Shawky Dr. Gehan Mohamed.
Lecture # 20 CELL INJURY & RESPONSE-3 Dr. Iram Sohail Assistant Professor Pathology.
Introduction to Basic Pathology; Cellular Reaction to Injuries`
Adaptation and Injury of Cell and Tissue
NECROSIS -Dr Sowmya Srinivas. DEFINITION NECROSIS Its an irriversible injury produced by enzymatic digestion of dead cellular elements APOPTOSIS.
Cell injury, adaptation and death Unite one Lab..
Cell injury.
Cell Injury, Adaptation, & Death
2- Cell Death Apoptosis Necrosis.
Cell injury, adaptation and death
Cell injury Dr H Awad.
CLS 223.
NECROSIS “Necrosis is the morphological changes that follow cell death in a living tissue or organ, Resulting from the progressive degenerative action.
Death and Necrosis LECTURE FIVE DR.ABDIAZIZ ABDI MOHAMED ABDI
Cell Injury I – Cell Injury and Cell Death
The cardinal signs of inflammation are rubor (redness), calor (heat), tumor (swelling), dolor (pain), and loss of function. Seen here is skin with erythema,
Cell Injury, Cell Death, and Adaptations
Overview of Cell Injury and Cell Death
Cell Injury Lab Dr Mamlook Elmagraby
WHAT IS THE COMMON CAUSE OF THIS LESION
Presentation transcript:

Splenic infarcts – gross Coagulative necrosis Two large infarctions (areas of coagulative necrosis) are seen in this sectioned spleen. Since the etiology of coagulative necrosis is usually vascular with loss of blood supply, the infarct occurs in a vascular distribution. Thus, infarcts are often wedge-shaped with a base on the organ capsule.

Infarcted bowel – gross wet gangrene The small intestine is infarcted. The dark red to grey infarcted bowel contrasts with the pale pink normal bowel at the bottom

Myocardium photomic

Adrenal infarct -- Micro

3 stages of coagulative necrosis (L to R) -- micro Microscopically, the renal cortex has undergone anoxic injury at the left so that the cells appear pale and ghost-like. There is a hemorrhagic zone in the middle where the cells are dying or have not quite died, and then normal renal parenchyma at the far right. This is an example of coagulative necrosis

Lung abscesses (liquefactive necrosis) -- gross Extensive acute inflammation may lead to abscess formation, as seen here with rounded abscesses (the purulent material has drained out after sectioning to leave a cavity) in upper lobe and lower lobe

Liver abscess – micro liquefactive necrosis The liver shows a small abscess here filled with many neutrophils. This abscess is an example of localized liquefactive necrosis

Liquefactive necrosis -- gross Grossly, the cerebral infarction at the upper left here demonstrates liquefactive necrosis. Eventually, the removal of the dead tissue leaves behind a cavity

Liquefactive necrosis of brain -- micro This is liquefactive necrosis in the brain in a patient who suffered a "stroke" with focal loss of blood supply to a portion of cerebrum.

Organizing liquefactive necrosis with cysts -- gross As this infarct in the brain is organizing and being resolved, the liquefactive necrosis leads to resolution with cystic spaces

Macrophages cleaning liquefactive necrosis -- micro At high magnification, liquefactive necrosis of the brain demonstrates many macrophages at the right which are cleaning up the necrotic cellular debris

Caseous necrosis -- gross

Caseous -- gross

Extensive caseous necrosis -- gross

Caseous necrosis lungs -- micro Microscopically, caseous necrosis is characterized by acellular pink areas of necrosis, as seen here at the upper right, surrounded by a granulomatous inflammatory process

Fat necrosis -- gross

Fat necrosis pancreas -- micro Microscopically, fat necrosis adjacent to pancreas is seen here. There are some remaining steatocytes at the left which are not necrotic. The necrotic fat cells at the right have vague cellular outlines, have lost their peripheral nuclei, and their cytoplasm has become a pink amorphous mass of necrotic material

Gangrene -- gross

Wet gangrene -- gross

Gangrenous necrosis -- micro

Myocyte adaptation Ch. 1, p. 2, Fig. 1-2

Physiologic hypertrophy See Ch. 1, p. 3. Fig. 1-3

Left ventricular hypertrophy -- gross

Muscle atrophy -- micro There are some muscle fibers here that show atrophy. The number of cells is the same as before the atrophy occurred, but the size of some fibers is reduced. This is a response to injury by "downsizing" to conserve the cell

Physiologic atrophy See also Ch. 1, p. 5, Fig. 1-4

Atrophic testis -- gross The testis at the right has undergone atrophy and is much smaller than the normal testis at the left

Squamous metaplasia See Ch. 1, p. 5, Fig. 1-5

Gastric metaplasia in esophagus -- micro

Slide – Fatty liver

Leiomyoma

–Ischemia causes cell injury by a.Activation of lipases b.Activation of proteases c.generation of free radicals d.initiating inflammation e.reducing cellular oxygen

reducing cellular oxygen

–The structures of the cell first affected by hypoxia are a.cell membranes b.cell nuclei c.endoplasmic reticula d.Golgi apparatus e.Mitochondria

–Mitochondria

–the first manifestation of decreased oxidative phophorylation is characterized by a.Cell shrinkage b.Decrease glycolysis c.Decrease Na+ pump d.Increased pH e.Increased protein synthesis

Decrease Na+ pump

–Increased cytosolic Ca++ in the cell leads to the activation of proteases, which in turn leads to a.Accumulation of lactic acid b.Cytoskeletal damage c.Decreased ATP production d.Decreased phospholipids e.Increased protein synthesis

a.Cytoskeletal damage

–Which of the following is the feature of reversible hypoxic cell injury? a.Acute cellular swelling b.Apoptotic bodies formation c.Denaturation of cellular proteins d.Mitochondrial vacuolization e.Structural defects of cell membrane

a.Acute cellular swelling

–An irreversible injury to the myocardium will have occurred when a.Blebs form on cell membrane b.Cytoplasmic sodium increases c.Glycogen stores are depleted d.Intracellular pH diminishes e.Nuclei undergo karyorrhexis

a.Nuclei undergo karyorrhexis

–A 5 cm cystic area in left parietal lobe of cortex is found at autopsy. This finding is result of? a.Caseous necrosis b.Coagulative necrosis c.Fat necrosis d.Fibrinoid necrosis e.Liquefactive necrosis

Liquefactive necrosis

Which of the following is typical pathway for the disseminations of sarcomas? a.Direct tumor extension b.Hematogenous spread c.Lymphatic spread d.Seeding of body cavities e.Venous spread

a.Venous spread

Pleomorphism, abnormal nuclear morphology, abnormal mitosis and loss of polarity, are considered hallmarks of a.Anaplastic tumors b.Benign tumors c.Intermediate tumors d.Moderately differentiated tumors e.Well differentiated tumors

Anaplastic tumors

Aberrant differentiation produces a mass of disorganized but mature specialized tissue indigenous to particular site, referred to as: a.Acanthoma b.Adenoma c.Hamartoma d.Lymphoma e.Teratoma a.

Hamartoma

The benign cartilaginous tumors are called a.Chondroma b.Fibroma c.Leiomyoma d.Lymphoma e.Osteoma f.

Chondroma

Which of the following mediators of inflammation is synthesized at the site of inflammation a.Compliment proteins b.Immunoglobulins c.Kinins d.Lysosomal enzymes e.Prostaglandins

Prostaglandins

Which of the following mediators of inflammation facilitates chemotaxis, cytolysis and opsonization at the site of inflammation a.Compliment proteins b.Cytokines c.Immunoglobulins d.Leukotriens e.Prostaglandins

Compliment proteins

Following phagocytosis, micro- organisms are mainly killed by: a.Immunoglobin b.Hydrogen peroxide c.Lactoferrin d.Lymphokines e.Lysozyme

Hydrogen peroxide