This document provides an overview of shock, including its definition, types, etiology, pathogenesis, stages, and pathophysiological changes. It discusses the classification of shock into types such as hypovolemic, septic, traumatic, neurogenic, and distributive shock. For septic shock specifically, it covers the etiology as severe infection, pathophysiology involving the immune response and release of toxins, and key features including hypotension, tissue hypoperfusion, and high mortality rates. Treatment focuses on fluid resuscitation and source control for hypovolemic and septic shock.
CONTENTS:
GENERAL
NORMAL FLUID CIRCULATION
EDEMA- INTRODUCTION
CAUSES
CLASSIFICATION
MAJOR TYPES
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This document provides an overview of the three phases of wound healing: inflammatory, proliferative, and remodeling. It describes the key cellular and molecular processes that occur in each phase, including hemostasis, inflammation, granulation tissue formation, angiogenesis, epithelialization, and collagen deposition/remodeling. Complications of wound healing like deficient or excessive scarring, dehiscence, and exaggerated contraction are also summarized. The roles of various growth factors like PDGF, EGF, VEGF, and cytokines in stimulating and orchestrating wound repair are highlighted. Factors that can delay or impair healing, such as infection, poor nutrition, diabetes, and large wound size/location are also reviewed.
This document discusses the pathophysiology of edema. It defines edema as swelling caused by excess fluid in the interstitial spaces between tissues. Edema can be classified as transudate or exudate based on protein content, and as localized or generalized based on location. The key mechanisms that can cause edema are increased hydrostatic pressure, reduced plasma oncotic pressure, lymphatic obstruction, and sodium and water retention. The movement of fluid between blood vessels and tissues is normally regulated by the balance of hydrostatic and oncotic pressures according to Starling's forces, but imbalances in these forces can result in excess fluid accumulation in the tissues and cause edema.
Shock is a condition where the cardiovascular system fails to adequately perfuse tissues. It can be caused by an impaired pump (cardiogenic shock), reduced circulating volume (hypovolemic shock), or maldistribution of blood flow (distributive shock). The main effects are cellular hypoxia, impaired metabolism, and organ damage or failure if not treated. Compensatory mechanisms aim to increase perfusion but eventually fail, leading to irreversible cellular damage and death if shock persists.
Gangrene is the death of body tissue due to lack of blood supply and oxygenation. There are two main types - dry gangrene caused by arterial blockages, and wet gangrene caused by both arterial and venous blockages along with infection and putrefaction. Gangrene has many potential causes including diabetes, peripheral vascular disease, trauma, frostbite, and infection. Treatment depends on the type and cause but may include antibiotics, debridement, amputation, or in some cases limb salvaging procedures to restore blood flow.
This document discusses hypovolemic shock, which is characterized by decreased circulating blood volume resulting in reduced tissue perfusion. It can be hemorrhagic, due to blood loss from wounds or internal bleeding, or non-hemorrhagic from digestive, renal, skin or third space losses. The pathophysiology involves a macrocirculatory reaction with centralization of circulation and microcirculatory changes impairing capillary function. Treatment involves stopping losses, aggressive volume resuscitation with isotonic fluids, monitoring for efficacy, and inotropic support if needed to boost cardiac output after volume is restored.
This document defines and describes different types of embolism. It states that an embolism is a detached solid, liquid, or gas mass carried by the bloodstream to a distant site. It then lists and provides details on various types of embolisms including venous (pulmonary), arterial, paradoxical, fat, amniotic fluid, air, and septic embolisms. For pulmonary embolisms, it notes they most commonly arise from deep vein thromboses in the legs and can cause further recurrent embolic episodes. It also provides information on symptoms and causes of fat, air, and amniotic fluid embolisms.
The document provides guidance on the nursing management of shock. It discusses assessing the type and phase of shock, providing emergency nursing care, monitoring the patient closely, making a diagnosis based on history and assessments, treating with fluid resuscitation and blood products, and monitoring the patient's response. It also covers age-related considerations and the three phases of shock: compensated, uncompensated, and irreversible.
Neoplasia refers to new abnormal growth of tissue. A neoplasm is an abnormal mass of tissue that grows in an uncontrolled manner. Neoplasms can be benign (non-cancerous) or malignant (cancerous). The growth of neoplasms is driven by genetic changes that allow the cells to proliferate autonomously. Tumors are monoclonal in origin, arising from a single cell. The hallmarks of neoplasms include persistent and purposeless proliferation, a parasitic nature, progression, and clonal expansion. Tumors are classified based on their tissue of origin and behavior. Malignant tumors can invade surrounding tissues and metastasize to distant sites. The development of neoplasms involves genetic and environmental factors
1. Septic shock is caused by infection which releases cytokines that damage microcirculation and cause vasodilation and capillary leakage, leading to tissue hypoxia and multiple organ failure. Early, aggressive treatment of infection along with cardiovascular and organ system support is needed to prevent high mortality rates.
2. Hypovolaemic shock results from decreased blood volume due to blood loss, fluid loss, or fluid shifts. It progresses from mild to severe as compensation fails, leading to cellular changes, metabolic acidosis, and potentially multiple organ failure without timely fluid resuscitation and hemostasis.
3. Cardiogenic shock stems from heart failure to pump adequately due to causes like myocardial infarction, arrhythmias
This document provides an overview of different types of shock, including hypovolemic, cardiogenic, septic, anaphylactic, and neurogenic shock. It describes the pathophysiology, clinical manifestations, diagnosis, and treatment principles for each type. Hypovolemic shock is the most common and results from reduced circulating volume due to causes like bleeding or dehydration. Septic shock involves systemic inflammation and vasodilation in response to infection. Treatment focuses on fluid resuscitation, vasopressor support, source control, and antibiotics depending on the shock etiology.
This document discusses various types of cellular adaptations: atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia. Atrophy is a reduction in cell size and number. Hypertrophy is an increase in cell size but not number. Hyperplasia is an increase in cell number. Metaplasia is a change from one adult cell type to another. Dysplasia refers to abnormal cell shapes and sizes that can progress to cancer. Cellular adaptations provide clues for pathologists to diagnose disease.
The document discusses factors that can affect wound healing by interfering with the normal phases of wound repair. It describes the four phases of wound healing and notes that interruptions or abnormalities in the phases can lead to delayed or impaired healing. Both local factors, like infection, oxygen levels, and venous insufficiency, as well as systemic factors, such as age, stress, diabetes, obesity, and certain medications, are reviewed as influences on wound healing. Proper wound healing requires coordination of the phases at the right times and intensities, and internal and external factors can disrupt this process.
This document discusses osteomyelitis, an infection and inflammation of bone and bone marrow. It describes the different types of osteomyelitis, including pyogenic (bacterial), tuberculous, and syphilitic osteomyelitis. The stages and morphology of osteomyelitis are outlined from the acute stage of bacterial proliferation to the chronic stage involving bone necrosis, abscess formation, and new bone growth. Clinical manifestations, laboratory diagnosis, and radiological findings are also summarized.
Acute inflammation is characterized by five signs: redness, heat, swelling, pain, and loss of function. The main events of acute inflammation are vascular events like vasodilation and increased permeability, and cellular events involving leukocyte recruitment and activation. This results in an inflammatory cell-rich exudate. Acute inflammation can resolve, repair through regeneration or fibrosis, lead to suppuration or pus formation, or progress to chronic inflammation. Examples include acute appendicitis, meningitis, and pneumonia.
This document provides information on the pathophysiology of shock. It defines shock and describes the main types: primary/initial shock, secondary/true shock. It then discusses the mechanisms and stages of shock, including compensated/non-progressive shock, decompensated progressive shock, and decompensated/irreversible shock. The management of different types of shock such as hypovolaemic shock and septic shock is also summarized.
This document summarizes the key aspects of shock. Shock occurs when there is inadequate oxygen delivery to tissues, which can lead to cellular damage and death if left untreated. The main causes of shock discussed are hypovolaemic, septic, and cardiogenic shock. Signs and symptoms of shock include low blood pressure, fast heart rate, pale skin, confusion, and low urine output. Management involves identifying the type and stage of shock to guide fluid resuscitation and drug therapy aimed at restoring adequate circulation and oxygen delivery to tissues.
This seminar covers different types of shock including definitions, pathophysiology, clinical features, investigations, and treatment. The main types discussed are hypovolaemic shock, traumatic shock, cardiogenic shock, neurogenic shock, septic shock, and crush syndrome. Hypovolaemic shock is the most common and results from sudden loss of blood or fluid volume. Treatment focuses on fluid resuscitation and controlling bleeding. Septic shock has a high mortality and is usually caused by gram-negative bacteria. Crush syndrome occurs after body portions are compressed by heavy weights.
This document discusses different types of shock, including cardiogenic, hypovolemic, and shock associated with inflammation. It covers the pathogenesis and stages of shock, from the non-progressive stage involving vasoconstriction to the irreversible stage involving tissue injury. Various organ dysfunctions that can result from shock are also outlined, such as hypoxia, edema, acute respiratory distress syndrome, and damage to the kidneys, liver, lungs and heart. Clinical consequences of shock include hypotension, tachycardia, tachypnea, and cool clammy cyanotic or warm flush skin depending on the type of shock.
Shock - Pathophysiology, Clinical Features & ManagementAnkit Sharma
1. Hemorrhagic shock is the most common cause of shock in surgical or trauma patients and results from blood loss that exceeds 15% of circulating volume.
2. Initial management of hemorrhagic shock involves identifying the source of bleeding, providing immediate resuscitation with fluids and blood products, and controlling hemorrhage.
3. Damage control resuscitation principles are followed, including permissive hypotension to limit blood loss and balanced use of crystalloids, colloids, platelets, and plasma to prevent coagulopathy.
Shock is a clinical state characterized by inadequate tissue perfusion resulting from insufficient oxygen and substrate delivery to meet metabolic demands. There are several types of shock defined by etiology (hypovolemic, cardiogenic, distributive) and effects on blood pressure (compensated, decompensated). Signs of shock include tachycardia, altered mental status, and decreased urine output. Treatment involves rapid fluid resuscitation and vasoactive drugs like dopamine, epinephrine, and norepinephrine to support cardiac output as needed.
Shock is a state of impaired tissue perfusion that can result from low cardiac output or reduced circulating blood volume. There are several types of shock, including cardiogenic shock from heart failure, hypovolemic shock from fluid loss, and septic shock caused by the body's inflammatory response to infection. Septic shock is characterized by endothelial cell activation, tissue edema, blood clotting abnormalities, and metabolic disturbances that can lead to multiple organ failure and death. The pathogenesis involves an overactive inflammatory response triggered by microbial components that activate immune cells and cause widespread vascular leakage, hypotension, and tissue hypoxia. This can progress to organ dysfunction and failure if not corrected.
The document discusses different types of shock, including hypovolaemic, cardiogenic, septic, traumatic, neurogenic, and hypoadrenal shock. It defines shock as a life-threatening condition characterized by a reduction in circulating blood volume and inadequate tissue perfusion. The pathogenesis of different types of shock is explained, noting how reduced blood supply can lead to cellular injury and anoxia in tissues. Clinical features common to many types of shock include tachycardia, hypotension, oliguria or anuria, and alterations in mental state. Specific causes and effects of hypovolaemic, cardiogenic and septic shock are detailed.
This document discusses the diagnosis and management of shock. It defines shock as impaired tissue oxygenation and perfusion that can lead to organ dysfunction and death if left untreated. The document classifies shock into 4 main categories: hypovolemic, cardiogenic, distributive, and obstructive. It then describes the key clinical features, causes, and goals of treatment for each type of shock. The general principles of shock management are also summarized, which include treating the underlying cause, restoring adequate perfusion and tissue oxygen delivery, and reducing oxygen demand through supportive care.
I. El shock se define como un estado de falla cardiocirculatoria caracterizado por una inadecuada perfusión tisular que resulta en déficit de oxígeno y nutrientes en las células.
II. Existen tres fases del shock: fase compensada, fase descompensada e irreversible.
III. En la fase compensada se activan mecanismos como la vasoconstricción y el aumento de la frecuencia cardíaca para preservar la circulación a órganos vitales.
El documento define el shock como un síndrome de etiología multifactorial caracterizado por un desequilibrio entre la demanda y oferta de oxígeno a los tejidos. Describe cuatro tipos principales de shock: hipovolémico, cardiogénico, obstructivo y distributivo. Explica cada uno en detalle incluyendo sus causas, manifestaciones clínicas y criterios de diagnóstico.
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د/باسم السيد
Management of shocked patient
المحاضرة التي قدمت يوم الثلاثاء 8 ابريل 2014 في دار الحكمة بالقاهرة
من فعاليات مشروع اعداد طبيب حكيم ناجح بالتعاون مع معتمد باتحاد الاطباء العرب
و ضمن موديول الطوارئ و التخدير و العناية المركزة
This document provides an overview of shock, including its definition, types, stages and symptoms, and treatment. Shock is defined as inadequate tissue perfusion resulting from problems with oxygen delivery or utilization at the cellular level. The main types of shock are cardiogenic, distributive, hypovolemic, and obstructive. Shock progresses through initial, compensatory, progressive, and refractory stages associated with specific symptoms at each stage like tachycardia and hypotension. Treatment involves addressing the underlying cause and supporting organ function through measures like fluid resuscitation, vasopressors, antibiotics, and surgery as needed for the shock type.
This document summarizes several modern non-invasive methods for caries diagnosis, including methods based on changes in optical properties between healthy and carious tissue. It describes techniques such as fluorescence, optical coherence tomography, polarized Raman spectroscopy, fiber optic transillumination, and the Midwest Caries I.D. system. The techniques use light, scattering, absorption, and fluorescence to detect differences between sound and carious enamel or dentin in a non-invasive manner to allow for early detection and monitoring of dental caries.
This document provides the results of a race, listing the position, bib number, name, hometown, and time of the top 30 finishers. Charles Ogari of Kenya finished first with a time of 00:51:55. Geoffrey Le Dean of Caen finished second at 00:53:35. Jeremy Legout of Joue les Tours finished third at 00:53:46. The document continues listing positions 4 through 30 with their corresponding bib numbers, names, hometowns and times.
Shock is a state in which diminished cardiac output or reduced circulating blood volume impairs tissue perfusion and leads to cellular hypoxia. There are three main types of shock: hypovolemic, cardiogenic, and distributive. Hypovolemic shock occurs due to loss of intravascular volume from bleeding, burns, vomiting, or diarrhea. Cardiogenic shock results from heart failure that limits the heart's ability to pump blood adequately. Distributive shock involves decreased peripheral vascular resistance from sepsis, neurogenic causes, or anaphylaxis that causes vasodilation and pooling of blood in the veins. The manifestations of shock reflect both the impaired tissue perfusion and the body's compensatory responses to try to maintain
The document discusses the anatomy of the visual pathway and tumors of the optic nerve. It describes the components of the visual pathway including the optic nerve, optic chiasma, optic tracts, lateral geniculate bodies, optic radiations, and visual cortex. It then discusses lesions that can occur along the visual pathway and their effects. Finally, it describes three types of tumors that can affect the optic nerve: optic nerve glioma, optic nerve sheath meningioma, and optic nerve melanocytoma.
- Shock is defined as a condition where the cardiovascular system can no longer meet the body's metabolic and oxygen needs. It is potentially life-threatening and can affect many organs.
- There are four stages of shock: initial, compensatory, progressive, and refractory. In the initial stage, cardiac output and tissue perfusion decrease. In the compensatory stage, the body tries to compensate through neural, hormonal, and chemical responses. In the progressive stage, compensatory mechanisms begin to fail and vital organs become hypoperfused. In the refractory stage, cell destruction occurs and vital organ failure leads to imminent death.
- The main types of shock are hypovolemic, cardiogenic,
Approach to hypovolemic and septic shockAhmed Bahamid
This document discusses approaches to hypovolemic and septic shock in children. It defines shock and describes the pathophysiology, stages, and management. Shock results from inadequate oxygen delivery to tissues. Initially, compensatory mechanisms attempt to maintain blood pressure, but the condition can progress to decompensated then irreversible shock without treatment. Sepsis causes an inflammatory response that can lead to organ dysfunction if uncontrolled. Early intervention is important to improve outcomes from shock.
This document provides an overview of shock, including its classification, causes, pathophysiology, clinical features, and management. It defines shock as a clinical manifestation of inadequate tissue perfusion and cellular hypoxia due to a reduction in effective circulating blood volume. The main types of shock discussed are hypovolemic, cardiogenic, obstructive, distributive, and endocrine shock. The document examines the cellular, microvascular, and systemic pathophysiological changes that occur in shock, as well as compensatory mechanisms and signs of decompensation. Clinical features, diagnosis, and general management principles are also summarized.
This topic contains definition, meaning, classification, pathophysiology, clinical menifestations, metabolic and general changes, management of obstetrical shock
Shock and its management is summarized as follows:
1. Shock is a life-threatening condition characterized by inadequate tissue perfusion due to reduced circulating blood volume or cardiac output.
2. Shock is classified as hypovolemic, cardiogenic, septic, traumatic, neurogenic, or hypoadrenal based on etiology.
3. The pathophysiology involves reduced circulating volume, impaired tissue oxygenation, and release of inflammatory mediators, progressing from compensated to decompensated to irreversible stages if left untreated.
This document provides an overview of shock, including:
1. Definitions of shock and classifications according to etiology and pathophysiology. Shock results from inadequate oxygen delivery to tissues.
2. Descriptions of the pathophysiology of shock at the cellular, microvascular, and systemic levels, including metabolic changes, inflammation, and compensatory responses.
3. Clinical features of shock ranging from mild to severe based on degree of blood or fluid loss. Monitoring includes vital signs, urine output, and invasive monitoring like Swan-Ganz catheter.
4. Treatment principles for different types of shock including fluid resuscitation and management of underlying causes like bleeding control or cardiac dysfunction. Outcomes can include
7&8. SHOCK.pdf new new w new w new w new beSafinRoka
Shock is defined as a state of impaired tissue perfusion that results in cellular hypoxia. There are several types of shock, including cardiogenic, hypovolemic, septic, anaphylactic, and neurogenic shock. The pathogenesis of shock involves an initial compensatory response followed by progressive cellular hypoxia if shock persists. This can lead to irreversible cellular injury and organ failure if not corrected. Septic shock results from an inflammatory response to infection that causes vasodilation, hypotension, and multiple organ dysfunction through the effects of inflammatory mediators on endothelial cells and induction of a procoagulant state. Prolonged shock can cause hypoxic injury to vital organs like the brain, heart, lungs
Shock results from the failure of the cardiovascular system to provide sufficient blood circulation.
To maintain circulatory homeostasis the following mechanisms must be present –
1. a functioning of heart to circulate blood .
A sufficient amount of blood volume .
The capability of the vascular system , accommodating blood flow to the capillaries and returning to the right side of the heart.
This document provides an overview of shock in children, including:
1. It defines shock and describes the pathophysiology involving reduced tissue perfusion and oxygen delivery.
2. It classifies the main types of shock as hypovolemic, cardiogenic, distributive, obstructive, and septic shock and discusses their causes.
3. It describes the stages of shock from compensated to decompensated to irreversible, and the clinical manifestations including vital signs and mental status changes.
4. It outlines the approach to evaluating a child in shock including history, physical exam focusing on appearance, breathing and circulation, vital signs, mental status, and initial investigations.
5.
This document discusses shock, including its definition, pathophysiology, classification, and severity. Shock is defined as a state of inadequate tissue perfusion resulting from reduced cardiac output, blood loss, or vascular dysfunction. The main types are hypovolemic, cardiogenic, obstructive, distributive, and endocrine shock. The pathophysiology involves cellular hypoxia, inflammation, microvascular dysfunction, and ischemia-reperfusion injury. More severe shock is characterized by worsening metabolic acidosis, hypotension, oliguria, and loss of consciousness. Early recognition and treatment of compensated shock is important to prevent multi-organ failure.
Shock is a state of low tissue perfusion that can be fatal if not treated promptly. There are several types of shock based on the underlying pathophysiology, including hypovolaemic shock (from blood or fluid loss), cardiogenic shock (from heart failure), distributive shock (from sepsis or anaphylaxis), and obstructive shock (from embolism or pulmonary hypertension). Early resuscitation is crucial and involves restoring circulating volume through intravenous fluids while also identifying and treating the underlying cause of shock. Outcomes depend on limiting the duration of tissue hypoperfusion to prevent multiple organ failure.
This document discusses shock, specifically endotoxic shock. It begins with definitions of terms like shock, sepsis, and systemic inflammatory response syndrome. It then classifies and describes the different types of shock: hypovolaemic, distributive, obstructive, and cardiogenic. The main focus is on the pathophysiology and management of septic shock. It discusses the circulatory dysfunction that occurs in sepsis and leads to shock. The clinical features, evaluation, and treatment principles including hemodynamic support, fluids, vasopressors, inotropes, antimicrobial therapy, and surgery are covered. Prevention and prognosis of septic shock are also mentioned.
This document discusses shock in children, including:
1. Defining shock as a state of reduced tissue perfusion leading to cellular hypoxia.
2. Classifying the main types of shock as hypovolemic, cardiogenic, distributive, obstructive, and septic shock.
3. Describing the pathophysiology of shock, including compensatory mechanisms in the early stages and end-organ damage in late stages.
This document discusses various factors that can cause disease and discusses disease processes at the cellular, tissue, organ, and whole body levels. It covers several key topics related to disease pathogenesis including genetics, hypoperfusion/shock, and the effects of disease on individuals and populations. Some key points are that many genetic and environmental factors combine to cause disease, shock occurs first at the cellular level due to impaired oxygen use and glucose breakdown, and the body attempts to compensate for changes through mechanisms like hormone secretion but decompensation can occur if these fail.
neonatal shock and hypitension in neonatal unitsFayrouz Essawi
This document discusses shock in neonates. It defines shock and describes the physiology of circulation and factors that influence tissue perfusion. It outlines the epidemiology and types of shock seen in neonates, including distributive, hypovolemic, cardiogenic, and obstructive shock. The document discusses the pathophysiology of shock in neonates in detail, covering circulation, vascular tone, blood properties, and causes of inadequate tissue perfusion. It also covers the clinical manifestations and treatment of neonatal shock.
This document discusses different types of shock including hypovolemic, cardiogenic, septic, anaphylactic, and neurogenic shock. It defines shock as systemic hypoperfusion caused by reduced cardiac output or effective circulatory volume. Key signs are hypotension, tissue hypoperfusion, and end organ dysfunction. The stages of shock are described as initial non-progressive, progressive, and irreversible. Treatment involves restoring blood volume, vasoactive drugs, treating the underlying cause, and intensive care management to prevent multi-organ failure. Prognosis depends on the type and duration of shock.
Circulatory shock occurs when blood volume is displaced in the vasculature, causing hypovolemia and decreased cardiac output. There are three main types: septic shock (caused by infection), neurogenic shock (caused by loss of sympathetic tone), and anaphylactic shock (caused by allergic reaction). Septic shock is the most common and results from an immune response to infection that causes widespread vasodilation and capillary leakage. Treatment involves identifying and treating the infection, restoring intravascular volume, and providing supportive care.
This document defines and describes shock, its causes, clinical features, assessment, pathophysiology, classification, management, complications, SIRS and MODS. Shock is defined as a state of poor perfusion with impaired cellular metabolism due to inadequate end-organ perfusion and tissue oxygenation. The main causes of shock include hypovolemia, cardiogenic, obstructive, distributive, endocrine and septic origins. Management involves resuscitation of airway, breathing and circulation through fluid administration and treatment of the underlying cause. Complications can include multiple organ failure if not treated promptly.
This document discusses saliva as a diagnostic fluid. It defines saliva and describes its general properties, composition, formation, and functions. Methods for collecting saliva are provided for adults, children, and infants. Advantages of saliva analysis include its noninvasive nature, low cost, and applicability for screening large populations. Limitations relate to variability in salivary markers based on collection method and flow rate. The document outlines analysis of saliva for diagnosing conditions like Sjogren's syndrome based on changes in immunoglobulin and protein levels.
The tongue has several parts and functions. It is divided into a root, tip, and body. The root attaches the tongue to bones in the mouth. The tip lies behind the upper teeth. The body has an upper dorsum surface and lower ventral surface. The dorsum has oral and pharyngeal parts divided by the sulcus terminalis. The oral part contains papillae and sits in the mouth floor. The pharyngeal part lacks papillae and forms the mouth's back wall. Muscles like the genioglossus connect the tongue to other structures and allow movement. Arteries supply blood while veins drain it. Nerves provide sensation and control. The tongue develops from arches in the
Central face begins to develop by 4th week, when olfactory placodes appear on both sides of the frontonasal process.
Gradually both placodes develop to form the median and lateral nasal process.
Upper lip is formed by 6th week by fusion of two median nasal processes in midline and the maxilllary process of the 1st branchial arch.
PRE-NATAL GROWTH AND DEVELOPMENT OF PALATEFormation of primary and secondary palate
Elevation of palatal shelves
Fusion of palatal shelves
Introduction
Epidemiology
Etiology
Manifestations
TNM staging
Squamous cell carcinoma is defined as malignant epithelial neoplasm exhibiting squamous differentiation as characterised by the formation of keratin and/or the presence of intercellular bridges.
( Pindborg et al, 1997).
Occipital (2-4)
Superior nuchal line between sternocleidomastoid and trapezius
Occipital part of scalp
Superficial cervical lymph nodes
Accessary lymph nodes
Mastoid (1-3)
Superficial to sternocleidomastoid insertion
Posterior parietal scalp
Skin of ear, posterior external acoustic meatus
Superior deep cervical nodes Accessary lymph nodes
Preauricular (2-3)
Anterior to ear over parotid fascia
Drains areas supplied by superficial temporal artery
Anterior parietal scalp
Anterior surface of ear
Superior deep cervical lymph nodes
Parotid (up to 10 or more)
About parotid gland and under parotid fascia
Deep to parotid gland
External acoustic meatus
Skin of frontal and temporal regions
Eyelids, tympanic cavity
Cheek, nose (posterior palate)
Superior deep cervical lymph nodes
Facial
Superficial(up to 12)
Maxillary
Buccal
Mandibular
Distributed along course of facial artery and vein
Skin and mucous membranes of eyelids, nose, cheek
Submandibular nodes
Deep
Distributed along course of maxillary artery lateral to lateral pterygoid muscle
Temporal and infratemporal fossa
Nasal pharynx
Superior deep cervical lymph nodesSuperficial
Anterior jugular vein between superficial cervical fascia and infrahyoid fascia
Skin, muscles, and viscera of infrahyoid region of neck
Superior deep cervical lymph nodes
Deep
Between viscera of neck and investing layer of deep cervical fascia
Adjoining parts of trachea, larynx, thyroid gland
Superior deep cervical lymph nodes
Anterior cervical/Superficial
Submental (2-3)
Submental triangle
Chin
Medial part of lower lip
Lower incisor teeth and gingiva
Tip of tongue
Cheeks
Submandibular lymph node to jugulo-omohyoid lymph node and superior deep cervical lymph nodes
Is a phenomenon of reflex sequence of muscle contractions that propels the ingested materials and pooled saliva from the mouth to the stomach.
PATTERNS
Infantile (visceral) swallow
Adult/mature swallow
ADULT SWALLOWING
Is composed of 4 stages
Voluntary
Preparatory phase
Oral or buccal
Involuntary: Controlled By Medulla and Lower Pons
Pharyngeal
b. Oesophageal
• Function
• External features
• Papillae of tongue
• Muscles of the tongue
• Arterial supply
• Venous drainage
• Lymphatic drainage
• Nerve supply
• Histology
• Development of tongue -
Intrinsic muscles
Superior longitudinal
Inferior longitudinal
Transverse
Vertical
- Extrinsic muscles
Genioglossus
Hyoglossus
Styloglossus
Palatoglossus
1. Vallate or circumvallate papillae
These are large in size 1-2mm in diameter and are 8-12 in number.
They are situated immediately in front of the sulcus terminalis.
Each papillae are cylindrical projection surrounded by a circular sulcus.
The walls of the papilla are raised above the surface.
2. Fungiform papillae
Are numerous
Near the tip and margins of the tongue, but some of them are scattered over the dorsum.
These are smaller than the vallate papillae but larger than the filliform papillae.
Each papilla consists of a narrow pedicle and a large rounded head.
They are distinguished by their bright red colour.
3. Filliform papillae
Conical papilla
Cover the presulcal area of the dorsum of the tongue and gives it a characteristic velvety appearance.
They are the smallest and most numerous of the lingual papillae.
Each are pointed and covered with keratin
The apex is often split into filamentous processes.
Fifth cranial nerve
Have a large sensory root and a small motor root.
Motor root arises – arises from the lateral aspect of lower pons (cranially) the motor root cross the apex of the petrous temporal bone beneath the superior petrosal sinus, to enter the middle cranial fossa.
Sensory root – arises from the lateral aspect of lower pons (caudally).
RELATIONS
Medially
(a) internal carotid artery
(b) posterior part of cavernous sinus
Laterally - middle meningeal artery
Superiorly - parahippocampal gyrus
Inferiorly
motor root of trigeminal nerve
(b) greater petrosal nerve
(c) apex of the petrous temporal bone
(d) foramen lacerum.OPTHALIMIC DIVISION
Terminal branches of Ophthalmic division of trigeminal nerve, are
1. Frontal
Supratrochlear
Supraorbital
2. Nasociliary
Branch of ciliray ganglion
2-3 long ciliary nerves
Posterior ethmoidal
Infratrochlear
Anterior ethmoidal
3. Lacrimal
Branches
From main trunk
Meningeal branch
Nerve to medial pterygoid
From the anterior trunk
Sensory branch
Buccal nerve
Motor branch
Masseteric
Deep temporal nerve
Nerve to lateral pterygoid
From the posterior trunk
Auriculotemporal
Lingual
Inferior alveolar nerves
COTTON-WOOL APPEARANCE
Active phase showing disorganised bone architecture with numerous, large, multinucleated osteoclasts. The stroma is vascular and fibrous
The late phase features thick trabeculae with a prominent mosaic pattern of prominent, hematoxyphilic, cement lines at the interfaces of episodes of resorption followed by deposition.
Paget disease showing very prominent blue cement lines. The lamellae are arranged haphazardly giving an overall effect of a jigsaw puzzle.
Hume- “caries is essentially a progressive loss by acid dissolution of the apatite component of the enamel then the dentin or of the cementum then dentin.”
According to location:
Pit or Fissure caries
Smooth Surface caries
According to rapidity:
Acute
Chronic
Arrested
According to occurrence:
Primary (Virgin) caries
Secondary (Recurrent) caries
According to the site of occurrence:
Enamel caries
Cemental caries.
Acidogenic [ Miller’s Chemico-parasitic] theory.
Proteolytic theory.
Proteolysis- chelation theory.
The lymphatic system has three functions:
Fluid recovery.
Immunity
Lipid absorption
The lymphatic vessels of the small intestine receive the special designation of lacteals or chyliferous vessels.
The components of the lymphatic system are :-
lymph, the recovered fluid;
Lymphatic vessels, which transport the lymph;
Lymphatic tissue, composed of aggregates of lymphocytes and macrophages that populate many organs of the body; and
Lymphatic organs, in which these cells are especially concentrated and which are set off from surrounding organs by connective tissue capsules.
A Magnified Microscopic Image Is Worth More Than A Thousand Words.
DARK FIELD MICROSCOPE
PHASE CONTRAST MICROSCOPY
POLARIZED LIGHT MICROSCOPY
FLUORESCENT MICROSCOPY
STEREO MICROSCOPE
ELECTRON MICROSCOPY
Maxillary Second Premolar
the maxillary first premolar in function
Less angular ,rounded crown in all aspects.
Single root
Smaller crown cervico occlusally
Root length is as great or greater
BUCCAL ASPECT
Not as long as that of the first premolar
Less pointed
Mesial slope is
shorter than the distal slope
Buccal ridge of the crown may not be so prominent whencompared with the first premolarLINGUAL ASPECT
Lingual cusp is longer making the crown longer on the lingual sideMESIAL ASPECT
Cusps of second premolar are shorter with the buccal and lingual cusps more nearly the same length
Greater distance between cusp tips-that widens the occlusal surface buccolingually
No developmental depression on the mesial surface of the crown as on the first premolar
Crown surface is convex instead
No deep dev. Groove crossing the mesial marginal ridgeOCCLUSAL ASPECT
Outline of the crown is more rounded or oval rather than angular
Central dev. groove is shorter and more irregular
Tendency toward multiple supplementary grooves radiating from the central groove that may extend out to the cusp ridges
Makes for an irregular occlusal surface and gives a very wrinkled appearance
Centered in the maxilla, one on either side of median line, with mesial surface of each in contact with mesial surface of other
Two in number
Larger than the lateral incisor
These teeth supplement each other in function, and they are similar anatomically
Shearing or cutting teeth
Major function is to punch and cut food material during the process of mastication
These teeth have incisal ridges or edges rather than
cusps such as are found on canines & posterior teeth
First evidence of calcification
Crown completion
Eruption
Root completion
3-4 months
4-5 years
7-8 years
10-11 years
PHYSICAL PROPERTIES
CHEMICAL PROPERTIES
STRUCTURE OF ENAMEL
DEVELOPMENT OF ENAMEL
EPITHELIAL ENAMEL ORGAN
AMELOGENESIS
LIFE CYCLE OF AMELOBLASTS
AGE CHANGES IN ENAMEL
DEFECTS OF AMELOGENESIS
CLINICAL IMPLICATIONS
PRENATAL GROWTH OF MANDIBLE
Occurs between the 4th and 7th week of intrauterine life.
4th week of intrauterine life
Formation of the head fold
Following which the developing brain and the pericardium form 2 prominent bulges on the ventral aspect of the embryo.
The 2 bulges are separated from each other by a shallow depression called stomatoedum (corresponding to the primitive mouth).
Floor of the stomatodeum is formed by the Buccopharyngeal membrane, which separates the stomatodeum from the foregut.Soon, mesoderm covering the developing forebrain proliferates, and forms a downward projection that overlaps the upper part of the stomatodeum – this downward projection is called frontonasal process.
Since the formation of various parts of the face involves fusion of diverse components.
Occasionally this fusion can be incomplete give rise to various anomalies
MANDIBULOFACIAL DYSOSTOSIS OR FIRST ARCH SYNDROME
- Entire first arch may remain underdeveloped on one or both sides, affecting
Lower eyelid
Maxilla
Mandible
External ear.
- Prominence of the cheek is absent
- Ear is displaced ventrally and caudally
Face develops in humans between 4th – 10th week of intrauterine life.
prenatal growth of the maxilla
DEVELOPMENT OF UPPER LIP
Development of lower lip
Development of nose
hare lip
OBLIQUE FACIAL CLEFT
macrostomia
lateral facial cleft
microstomia
PART 1 The New Natural Principles of Electromagnetism and Electromagnetic Fie...Thane Heins
Document Summary and the History of Perpetual Motion
Every single Faraday Generator coil since 1834 has been and is currently performing Negative Work at infinite efficiency with created Electromagnetic Field Energy during electricity generation and its physical Kinetic Energy reduction or Electromagnetic Resistance of the changing magnetic field which is initially inducing Electric Current in the generator coil according to Faraday's Law of Induction.
The Work-Energy Principle confirms mathematically that the magnitude of the changing magnetic field's Kinetic Energy reduction is equal to the magnitude of Negative Work performed at infinite efficiency, which is equal to the magnitude of Energy (Electromagnetic Field Energy which is created according to Oersted's Law of Creation of Energy of 1820). Created Electromagnetic Field Energy is required in order to perform the Negative Work – because Work cannot be performed in the absence of Energy.
In 2007 Thane Heins of Almonte Ontario, Canada discovered that unlimited amounts of Positive Electromechanical Work could be performed at infinite efficiency with created and TIME DELAYED Electromagnetic Field Energy.
Every single ReGenX Generator coil since 2007 has been and is currently performing Positive Work at infinite efficiency with created Electromagnetic Field Energy during electricity generation and during its physical Kinetic Energy increase or Electromagnetic Assistance of the changing magnetic field which is initially inducing Electric Current in the generator coil according to Heins' Law of Induction.
Faraday Electric Generators all harness internally Created Electromagnetic Field Energy in order to perform Negative Work (system Kinetic Energy reduction) at infinite efficiency and ReGenX Electric Generators harness internally created and Time Delayed Electromagnetic Field Energy in order to perform Positive Work (system Kinetic Energy increase) at infinite efficiency.
Both Faraday Generators and ReGenX Generators operate as Perpetual Motion Machines of the First Kind because they both have the ability to perform both Negative or Positive Work indefinitely and at infinite efficiency without requiring any External Energy input. The unlimited Energy required to perform either the Negative or Positive Work is created at the Sub-Atomic Quantum Electron level inside the generators' Current Bearing Wires according to the Law of Creation of Energy.
Hans Christian Oersted discovered the Law of Creation of Energy in 1820 when he demonstrated the world's first Perpetual Motion Machine of the First Kind at the University of Copenhagen when he also simultaneously violated Newton's 1st, 2nd and 3rd Laws of Motion.
Michael Faraday built and demonstrated the world's second Perpetual Motion Machine of the First Kind in 1822 when he demonstrated his Electric Motor invention which harnessed created Electromagnetic Field Energy in order to perform Positive Electromechanical Work at infinite efficienc
Dalghren, Thorne and Stebbins System of Classification of AngiospermsGurjant Singh
The Dahlgren, Thorne, and Stebbins system of classification is a modern method for categorizing angiosperms (flowering plants) based on phylogenetic relationships. Developed by botanists Rolf Dahlgren, Robert Thorne, and G. Ledyard Stebbins, this system emphasizes evolutionary relationships and incorporates extensive morphological and molecular data. It aims to provide a more accurate reflection of the genetic and evolutionary connections among angiosperm families and orders, facilitating a better understanding of plant diversity and evolution. This classification system is a valuable tool for botanists, researchers, and horticulturists in studying and organizing the vast diversity of flowering plants.
Keys of Identification for Indian Wood: A Seminar ReportGurjant Singh
Identifying Indian wood involves recognizing key characteristics such as grain patterns, color, texture, hardness, and specific anatomical features. These identification keys include observing the wood's pores, growth rings, and resin canals, as well as its scent and weight. Understanding these features is essential for accurate wood identification, which is crucial for various applications in carpentry, furniture making, and conservation.
Additionally, the application of Convolutional Neural Networks (CNN) in wood identification has revolutionized this field. CNNs can analyze images of wood samples to identify species with high accuracy by learning and recognizing intricate patterns and features. This technological advancement not only enhances the precision of wood identification but also accelerates the process, making it more efficient for industry professionals and researchers alike.
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ScieNCE grade 08 Lesson 1 and 2 NLC.pptxJoanaBanasen1
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Cause and solution of Water hyacinth (Terror of Bengal)saloniswain225
Water hyacinth is a buoyant plant that has a clump of leaves with squishy stalks arising from the lower feathery roots and it is an invasive species came from South America
ALTERNATIVE ANIMAL TOXICITY STUDY .pptxSAMIR PANDA
Alternatives animal testing are development and implementation of test methods that avoid the use of live animals.
Human biochemistry, physiology, pharmacology, and endocrinology and toxicology has been derived from animal models.10-100 millions of animals are using for experimentation in a year.
Animals used experimentation distributed among zebra- fish to primates.
Vast majority of animals are sacrificed at end of research programme.The use of animals can be further subdivided according to the degree of suffering
Minor animal suffering:- observing animals in behavioral studies, single blood sampling, Immunization without adjutants, etc.
Moderate animal suffering:- repeated blood sampling, recovery from general anesthesia, etc.
2. WHAT IS SHOCK
TYPES OF SHOCK
ETIOLOGY AND PATHOGENESIS OF SHOCK
STAGES OF SHOCK
PATHOPHYSIOLOGIC CHANGES
CLASSIFICATION OF SHOCK
HYPOVOLEMIC SHOCK
SEPTIC SHOCK
TRAUMATIC SHOCK
NEUROGENIC SHOCK
DISTRIBUTIVE SHOCK
ANAPHYLATIC SHOCK
BURN SHOCK
TREATMENT OF SHOCK.
CONTENTS
3. Shock or Cardiovascular
collapse
Shock may be defined as a condition in which
circulation fails to meet the nutritional needs of
the cells and at the same time fails to remove the
metabolic waste products.
A final common pathway for many potentially
lethal clinical events (hemorrhage,trauma, burns,
large MI, massive pulmonary embolism microbial
sepsis)
4. Shock is also defined as a clinical state of cardiovascular
collapse characterised by:
An acute reduction of effective circulating blood
volume
An adequate perfusion of cells and tissues.
The end result is hypotension and cellular hypoxia and
if uncompensated may lead to impaired cellular
metabolism and death.
5. 1)Primary or Initial shock
Is a transient and usually benign vasovagal attack resulting from sudden
reduction of venous return to the heart caused by neurogenic
vasodilatation and consequent peripheral pooling of the blood.
It can occur immediately following
Trauma
Severe pain
Emotional overreaction due to
a) Fear
b) Sorrow and surprise
c) Sight of blood
6. Clinically Patient develops,signs and
symptoms similar to that of syncope
Unconsciousness
Weakness
Sinking Sensation
Pale and Clammy limbs
Weak and rapid pulse and
Low Blood Pressure
……Primary shock can be labelled as a severe form of syncope….Lasting few
seconds to minutes.
7. 2) Secondary (or) True shock
……occurs due to haemodynomic derangements with hypoperfusion of the
cells, this type of shock is the ‘true shock’.
10. Stages of shock
Deteriotion of the circulation in shock is a progressive
phenomenon and can be devided arbitarily into 3 stages:
1. Non – progressive (initial. Compensated reversible)shock
2. Progressive decompensated shock
3. Decompensated (irreversible) shock.
11. Widespread vasoconstriction: In resaponse to
reduced blood flow(hypotension) and tissue anoxia,
the neural and hormonal factors(e.g.
Baroreceptors,chemoreceptors, catecholamines,
renin VEM or Vasoexitor material from hypoxic
kidney). Are activated. All these bring about
vasoconstriction , partiularly in the vessels of the skin
and abdominal viscera. It is a protective mechanism
as it causes increased peripheral reasistance,
increased heart rate(tacchycadia). And incresesd
blood pressure.
12. IRREVERSIBLE STAGE
It is the progression of shock to a stage where therapy does not help.
The Brain fails to function due to cerebral ischemia
Even infusion of blood fails to restore blood pressure
Multiple organ failure occurs.
Depression of cellular high energy phosphates
Finally, cardiac failure occurs due to decreased myocardial activity and
decreased arterial tone.
If Low Perfusion States persists:
IRREVERSIBLE DEATH IMMINENT!!
13. In the early stage of shock, an attempt to maintain adequate
cerebral and coronary blood supply by redistribution of blood
so that the vital organs(brain and heart) are adequately
perfused and oxygeneted. This is achieved by activation of
various neurohormonal mechanism causing WIDESPREAD
VASOCONSTRICTION and by FLUID CONSERVATION BY THE
KIDNEY.
Non – progressive (initial. Compensated
reversible)shock
14. Hypotension
Oliguria
Tachypnea, due to pulmonary hypoperfusion
Acute Respiratory Distress Syndrome (ARDS) …….. due to pulmonary
hypoperfusion.
Acidosis due to anoxia of liver causing reduced clearance of lactate.
Clinically in progressive shock…….
15. Fluid conservation by the kidney: the following factors
may assist in restoring the blood volume and improve
vennous return to the heart :
release of aldosterone from hypoxic kidney.
Release of ADH due to to decreased effective
circulayting blood volume.
Reduced glomerular filtration tate
Shifting of tissue fluid into plasma due to lawered
capillary hydrostatic pressure.
16. PROGRESSIVE DECOMPENSATED SHOCK:
This is a stage when the patients suffer from some
stress or risk factors besides persistance of of the shock
so that there is progressive deterioration.
DECOMPENSATED (IRREVERIBLE) SH0CK At this stage
patient has features like coma, worsened heart function
and progressive renal failure and it is characterised by
irrreversibility of shock with tissue anoxia occupying
central role an dthese are under
1.PERSISTANCE OF WIDESPREAD VASOCONSTRICTION
2.VASODILATION AND INCREASED VASCULAR
PERMEABILITY
3.MYOCARDIAL ISCHAEMIA
4.CEREBRAL ISCHAEMIA
5.VASODEPPRESOR MATERIAL(VDM)
6.TUMOR NECROSIS FACTORS(TNF)
7.INTESTINAL FACTORS
8.BACTERIAL FACTORS
9.HYPERCOAGULABILITY OF BLOOD
18. PATHOPHYSIOLOGIC CHANGES
When cardiac output fall…..Cardiogenic, Hypovolaemic or obstructive
shock….BP remain stable as long as a compensatory increase in the
peripheral vascular resistance occurs.
Low B.P.
Baroreceptors
Hypothalmous impulse
Adrenal Medulla
Catcholamines
Increased peripheral vascular
resistance
Chronotropic and
inotropic effect
Incresaed blood flow to
heart & brain
Decreased blood flow to
the extremities
19. ULTIMATE EFFECTS OF ANAEROBIC METABOLISM
Inadequate
Energy
Production
Metabolic
Failure
Lactic
Acid
Production
Metabolic
Acidosis
CELL
DEATH
Inadequate
Cellular
Oxygen
Delivery
Anaerobic
Metabolism
22. Hypovolaemic shock
Results from loss of blood or plasma volume.
This may be caused by hemorrhage, fluid loss
from severe burns, or trauma.
Hemorrhage usually occurs from the small veins
and systemic venules.
23. Clinical features
Mild shock Moderate shock Severe shock
<20% loss of
volume
20-40% loss of
blood volume
>40% loss of
volume
Collapse of
subcutaneous
of extremities,
– pale & cool
Features of mild
shock + oliguria
Pallor, low urinary
output
Sweat – forehead,
palms, feet
Pulse rate
increased (but
<100). BP remains
normal initially,
fall in later stages
Rapid pulse, low
Urinary output,
pulse rate, BP
normal
24. Treatment
Resuscitation
Control of bleeding
Extracellular fluid replacement
If there is blood loss, it is best replaced by blood.
Blood substitutes cannot replace blood
25. Septic shock
Septic shock is caused by systemic response to a
severe infection.
Occurs most frequently in elderly or
immunocompromised patients or those who have
undergone invasive procedure in which bacterial
contamination has occurred.
26. Septic shock is the most common cause of mortality in the intensive care
unit.
It is the 13th leading cause of death overall
mortality ranges from 15% in patients with sepsis to 40-60% in patients
with septic shock.
There is a continuum of clinical manifestations from SIRS ----sepsis ----
severe sepsis ---septic shock to Multiple Organ Dysfunction Syndrome
(MODS).
Overview of septic shock
27. In these instances, widespread vasodilation causes a sudden
increase in the vascular bed capacitance, which is not adequately
filled by the normal circulating blood volume
hypotension, tissue hypoperfusion, and cellular anoxia result
Patients go into shock and even die within the hour
The risk of anaphylaxis must be borne in mind when certain
therapeutic agents are administered. Although patients at
risk can generally be identified by a previous history of some
form of allergy, the absence of such a history does not
preclude the possibility of an anaphylactic reaction.
28. Etiology
Most commonly, this occurs in the setting of gram-negative and
gram positive infections, though any agent that is capable of
producing infection (viruses, fungi, parasites).
The most common organisms which cause septic shock are E.coli,
Klebsiella, Proteus, Pseudomonas, Bacteroids in decreasing
frequency.
29. Pathophysiology
Sepsis is triggered by bacteria or fungi that ordinarily do not cause
systemic disease in immunocompetent hosts.
Microbes exploit deficiency in the host defenses to survive in the
body.
Pathogens in turn overcome the defenses by elaborating toxins or
other virulence factors.
Body fails to kill the invaders and mount a severe sepsis.
30. Animals have exquisite mechanisms for recognizing and
responding to conserved microbial molecules.
The endotoxins of a gram negative bacterial cell wall is the best
example.
The lipopolysaccharides (LPS) present on the cell wall account for
their endotoxic activity.
LPS consists of 3 regions
Region I – polysaccharide portion
Region II – core polysaccharide.
Region III – glycolipid (lipid A) = responsible for
endotoxic activity.
31. Engagement of TLR on endothelial cells can lead directly to down-
regulation of natural anticoagulation mechanisms.
Profound mononuclear cell activation
Presumably, this series of responses helps to isolate organisms and
to trigger elements of the immune system to efficiently eradicate
invading microbes.
Unfortunately, depending on the dosage and numbers of
macrophages that are activated, the secondary effects of LPS
release can also cause severe pathologic changes, including fatal
shock.
32. At low doses, LPS predominantly serves to activate monocytes and
macrophages, with effects intended to enhance their ability to
eliminate invading bacteria
With moderately severe infections, and therefore with higher levels of
LPS, cytokine-induced secondary effectors become significant.
Systemic effects of the cytokines such as TNF and IL-1 may begin
to be seen - fever and increased synthesis of acute phase reactants
33. At still higher levels of LPS, the syndrome of septic shock supervenes
the same cytokines and secondary mediators, now at high levels,
result in:
Systemic vasodilation (hypotension)
Diminished myocardial contractility
Widespread endothelial injury and activation, causing systemic
leukocyte adhesion and pulmonary alveolar capillary damage
Activation of the coagulation system, culminating in DIC
34. Skin remains warm, pink well perfused
Cutaneous veins remains full
Pulse rate is high
Intermittent spikes of fever with bouts of chills.
35. Treatment
Treatment of infection by early surgical debridement
or drainage , appropriate antibiotics
Treatment of shock- fluid replacement, steroids
36. Traumatic shock
Caused by major fractures, crush injuries, burns,
extensive soft tissue injuries.
Hypovolemia due to bleeding externally and
internally and due to toxic factors resulting
fragments of tissue entering blood stream.
The traumatized tissue activate coagulation
cascade and release microthrombi into circulation.
37. They occlude pulmonary vasculature.
Microthrombi induce a generalized increase in
capillary permeability.
Loss of plasma into interstitial tissue throughout the
body.
Depletes the vascular volume to great extent
38. Clinical features
Similar to those of hypovolemic shock.
2 differentiating features
- Presence of peripheral and pulmonary edema in
traumatic shock.
- Infusion of large volumes of fluid may be adequate
for pure hypovolemic shock, is usually inadequate
for traumatic shock.
39. Treatment
Resuscitation
Local treatment of trauma and control of bleeding.
Fluid replacement
Full body anticoagulation (1 IV dose of 10,000 U of
heparin)
40. Cardiogenic shock
Caused by injury to heart, MI, cardiac arrythmias
Compressive cardiac shock
When the heart is compressed enough from outside to decrease
cardiac output due to pneumothorax, pericardial tamponade etc
Due to right ventricle dysfunction Due to left ventricle dysfunction
Right heart is unable to pump blood
into lungs in adequate amounts.
Filling of left heart decreases.
Left ventricular output decreases
Unable to maintain adequate stroke
volume
Engorgement of pulmonary
vasculature due to normal right
ventricular output, but failure of left
heart.
41. Clinical features
Initially skin is pale and cool
Urine output is low
Pulse becomes rapid, arterial BP is low
Right ventricular dysfunction – neck veins
distended, liver enlarged
Left ventricular dysfunction – bronchial rales
heard. Gradually heart is enlarged, later neck
veins are also distended.
42. Treatment
Airway is cleared with adequate oxygenation
Large doses of heparin IV (if shock is due to
massive pulmonary embolism)
For pain – morphine
43. Neurogenic shock
Caused by paraplegia, quadriplegia, trauma to
spinal cord or spinal anesthesia.
Loss of arterial and venous tone with pooling of
blood in dilated peripheral venous system.
heart does not fill normally = CO falls
44. Clinical features
Skin is warm ,pink & well perfused
Urine output may be normal
Heart rate is rapid, BP is low
Treatment
Elevation of legs
Fluids
Vasoconstrictor drugs
45. DISTRIBUTIVE SHOCK
This occurs when the blood volume is normal but the capacity of the circulation
is increased by marked vasodilatation
Also called as “Warm shock as the skin is not cold and clammy, as it is in
Hypovolemia shock
Eg: Anaphylactic shock and neurogenic shock
46. ANAPHYLACTIC SHOCK
It is an allergic condition in which the cardiac output and arterial pressure
often fall dramatically.
A rapidly developing, severe allergic relation that sometimes occur when an
individual who has previously been sensitized to an antigen is exposed to it.
47. CLINICAL FEATURES
Signs of profound vasodilatation
a) Warm peripheries
b) Low blood pressure
Erythema, Urticaria Angioedema, Pallor, Cyanosis
Bronchospasm, Rhinitis
Odema of the Face, Pharynx and Larynx
Pulmonary odema
Hypovolaemia due to capillary leak
Nausea, vomiting, abdominal cramps.
48. Anaphylactic shock
In humans, systemic anaphylaxis may occur after administration
of foreign proteins (e.g., antisera), hormones, enzymes,
polysaccharides, and drugs (such as the antibiotic penicillin).
Initiated by a generalized IgE-mediated hypersensitivity
response
Said to be due to increased histamine release by combination of
antigen with IgE on mast cell and basophils
49. The severity of the disorder varies with the level of sensitization.
Extremely small doses of antigen may trigger anaphylaxis,
Within minutes after exposure, itching, hives, and skin erythema
appear, followed shortly thereafter by a striking contraction of
respiratory bronchioles and respiratory distress
Laryngeal edema results in hoarseness.
Vomiting, abdominal cramps, diarrhea, and laryngeal obstruction
follow, systemic vasodilation and increased vascular permeability
50. BURN SHOCK
The most apparent abnormality in this is loss of plasma as exudates from
burned surface
• So there is increased – Hematocrit and Hemoconcentration found.
• Complex metabolic changes seen in such patients.
51. Biochemical Changes Seen In Such
Patients
Electrolyte imbalance:.
Hypoproteinaemia:
Hyperglycemia
Increased blood urea creatinene levels due to kidney
damage in extensive burns.
52. CHANGES IN BLOOD
Hemoconcentration due to outpouring of serum
Increased number of RBC due to outpouring of serum
Sludging of blood – intravascular agglutination
An abrupt fall in eosinophil count during the first 12 hour
which slowly begun to increase
Increased blood viscosity.
53. HYPOADRENAL SHOCK
The normal host response to the stress of illness,
operation, or trauma requires that the adrenals glands
hyper secrete cortisol in excess of that normally required.
Hypoadrenal shock occurs in settings in which the
unrecognized adrenal insufficiency complicates the host
response to the stress induced by acute illness or major
surgery.
54. Treatment for shock
BLOOD TRANSFUSION
PLASMA TRANSFUSION
ADMINISTATION OF PLASMA SUBSTITUTES
ADMINISTRATION OF YMPATHOMIMITIC DRUGS
LIKE EPINEPHRINE AND NOREPINEPHRINE.
ADMINISTATION OF GLUCOCORTICOIDS
OXYGEN THERAPHY
BY CHANGING THE POSTURE