Complete Pathology for Medical Students - PowerPoint PPT Presentation

Loading...

PPT – Complete Pathology for Medical Students PowerPoint presentation | free to download - id: 7ec138-ZWE3M



Loading


The Adobe Flash plugin is needed to view this content

Get the plugin now

View by Category
About This Presentation
Title:

Complete Pathology for Medical Students

Description:

(PRICE LOWERED)WHAT YOU NEED FOR THE USMLE – PowerPoint PPT presentation

Number of Views:899
Updated: 17 December 2015
Slides: 389
Provided by: drstingrae
Why and how: Dr. Raepsaet and the IMEC staff are attempting to give the best and most proven methods of covering the topics for the USMLE

less

Write a Comment
User Comments (0)
Transcript and Presenter's Notes

Title: Complete Pathology for Medical Students


1
PATHOLOGY
  • IMEC INC.
  • Quick Learning
  • Technique

2
PATHOLOGY
  • Pathology is literally the study of suffering,
  • Pathology actually studies the Etiology or Cause
    of disease.

3
Cellular Response to Injury
  • Acute Cell Injury
  • Reversible Injury
  • Cell Death
  • Necrosis
  • Apoptosis
  • Subcellular Alterations and Cell Inclusions
  • Intracellular Accumulation
  • Pathologic Calcification
  • Cellular Adaptations
  • Atrophy, hypertrophy, hyperplasia, metaplasia

4
Causes of Cell Injury
  • Hypoxia
  • Physical Agents
  • Chemical Agents Drugs
  • Infectious Agents
  • Immunological Reactions
  • Genetic Derangements
  • Nutritional Imbalances

5
Cell Injury Necrosis
  • The molecular mechanism responsible for cell
    injury leading to necrosis are complex
  • The morphological changes that take place only
    become apparent after some critical biochemical
    system within the cell has been deranged.
  • The type, state, and adaptability of the injured
    cell also determine the consequences of cell
    injury.

6
Four Biochemical Schemes
  • Oxygen and Oxygen deprived free radical
  • Intracellular Calcium and loss calcium
    homeostasis
  • ATP Depletion
  • Defects in Membrane Permeability

7
Ischemic and Hypoxic Change
  • Reversible cell injury
  • The first point of attack is the cells aerobic
    respiration, that is the oxidative
    phosphorylation by the mitochondria.
  • As the oxygen tension decrease, there is a loss
    of oxidative phosphorylation, and the generation
    of ATP slows or ceases
  • This can cause a net gain of solute because
    ATPase activity changes, and a iso-osmotic
    swelling of the endoplasmic reticulum, can cause
    detachment of ribosomes

8
(No Transcript)
9
(No Transcript)
10
MITOCHONDRIAL INJURY
11
Mechanism of Irreversible injury
  • Progressive loss of phospholipids
  • Cell Cytoskeletal Abnormalities
  • Reactive Oxygen Species
  • Lipid Breakdown Products
  • Loss of Intracellular amino acids

12
Chemical Injury
  • Mercuric Chloride
  • Binds to sulfhydryl groups
  • Cyanide
  • Directly poisons mitochondria
  • Carbon Tetrachloride
  • Highly reactive, converts to CCL3, INITIATING
    LIPID PEROXIFICATION
  • Acetaminophen
  • Covalently bonds, causing massive liver necrosis
    after about 3-5 days, if taken in large doses

13
NECROSIS
  • Necrosis is one of two morphological expressions
    of cell death (the 2nd being apoptosis), refers
    to a spectrum of changes that follow in the
    beginning of cell death in living tissue
  • Enzymatic digestion of the cell
  • Denaturing of proteins

14
Types of Necrosis
  • Coagulative Necrosis
  • Myocardial tissue
  • Liquifactive Necrosis
  • CNS
  • Gangrenous Necrosis
  • Bacterial induced
  • Caseous Necrosis
  • Tuberculosis
  • Enzymatic Fat Necrosis
  • Pancreatic

15
Apoptosis
  • Apoptosis is thought to be responsible for
    numerous physiological and pathological events.
    (Essentially Programmed Cell Death)
  • The destruction of cell during emryogenesis
  • Hormone dependent involution in adults
  • Cell death in tumors
  • Destruction of immune cells
  • Cell injury during viral disease

16
Apoptosis Morphology
  • Cell Shrinkage
  • Chromatin Condensation-
  • The most characteristic feature
  • Formation of cytoplasmic blebs
  • Phagocytosis of apoptotic cell bodies

17
General Apoptosis
18
Apoptosis
19
Apoptosis in Cancer
20
Genetic Apoptosis
21
Stress (HSP) and Cell Injury
  • Heat shock proteins, Hsp70 Hsp60
  • ( also called chaperones) are intimately
    involved in intracellular protein folding.
  • Another smaller HSP is UBIQUITIN, which is
    involved in protein degradation
  • Thus stress can be induced beyond repair of these
    mechanisms, via various insults

22
INTRACELLULAR Accumulations
  • Fall into 3 categories
  • A normal intracellular constituent, I.e water,
    lipids, proteins and carbohydrates
  • An abnormal substance, either exogenous, such as
    a mineral, or a product or abnormal metabolism
  • A pigment

23
Steatosis (Fatty Change)
  • The term Steatosis and Fatty Change describes
    abnormal accumulation of triglycerides within the
    parenchymal cells.
  • Fatty change is often seem in the liver due to it
    is the major organ involved in fat metabolism
  • In industrialized nations, by far the most common
    significant fatty change in liver is alcohol abuse

24
Liver Disease Spectrum
25
Alcoholic Steatosis
26
Cholesterol and its Esters
  • Atherosclerosis plaques, accumulate in the intima
    layer of the aorta and large arteries smooth
    muscle cells and macrophages become filled with
    lipid laden foamy cholesterol and lipids
  • Xanthomas are an extra-cellular accumulation of
    tryglycerides
  • Foamy macrophages are found at sites of cell
    injury. The myelin is the PNS is very susceptible
  • Cholesterolosis refers to a focal accumulation in
    the lamina propia of the gall bladder

27
Proteins
  • Excesses of protein sufficient to cause
    morphological changes are less common than lipid
    disorders.
  • Examples include
  • Reabsorption droplets in Proximal Renal Tubules
  • Immunoglobulin in plasma cells
  • Alpha-1 Antitrypsin (AAT) in liver cells

28
Glycogen
  • Excessive intra-cellular deposits of glycogen are
    seen in patients with an abnormality in either
    glucose or glycogen metabolism
  • Examples
  • Diabetes
  • Glycogen Storage Disease

29
Hyaline Changes
  • The term Hyaline is widely used as a
    Histological marker rather than a specific marker
    for cell injury
  • Usually gives a glassy pink appearance in
    histological sections
  • Mallory bodies in the liver are considered
    hyaline deposits.
  • The protein AMYLOID also has a hyaline
    appearance.

30
MALLORY BODIES
31
(No Transcript)
32
Pigments
  • Bilirubin
  • The normal pigment found in Bile
  • Lipofuscin
  • Normal where and tear pigment with age
  • Melanin
  • Endogenous Brown black pigment associated
    oxidation of tyrosine. And a black pigment with
    alkaptonuria
  • Hemosiderin
  • This pigment represents the aggregates of IRON
    FERRITIN micelles. Whenever there is an excess
    overload it can be deposited in organs and
    tissues.

33
Pathologic Calcification
  • Dystrophic Calcification
  • This is almost inevitable in atheromas and
    atheroscerosis
  • It commonly develops in aging on the damaged
    heart valves
  • Metastatic Calcification
  • The can happen in many disorders
  • It principally effects kidney, interstitial
    tissue in vessels, the lungs, and gastric mucosa

34
Cellular Growth and Differentiation
35
Repair of Tissue
  • This all to control the influences of the cell
    population , whether is be stimulated or
    inhibited
  • Repair of tissue involves 2 distinct processes
  • Regeneration
  • Replacement of connective tissue

36
Control of Cell Growth
  • Injury, cell death and mechanical deformation of
    tissues all can stimulate the proliferation
    however it is now clear that cell replication is
    controlled largely by the micro-environment,
    which either stimulates or inhibit proliferation.

37
Cell Cycle and Types of Cells
  • There are mainly three(3) groups on the basis of
    proliferation capacity
  • Continuously dividing cells
  • Quiescent (stable cells) that show a low level of
    replication
  • Non-dividing cells

38
(No Transcript)
39
Molecular Events and Growth
  • Some of these substances only keep the cell cycle
    in tact, whereas others ate actual progression
    molecules
  • Ligand Receptor Binding
  • Growth Factor Receptor Activation
  • Signal Transduction and 2nd Messengers
  • Transcription Factors

40
Ligand-Receptor Binding
  • Cell growth is initiated by the binding of growth
    factors to specific receptors on the cell surface

41
Importance of Receptor Ligand
42
Growth Factor Receptor
  • Most growth factors are equipped with intrinsic
    protein Tyrosine Kinase Activity which is
    activated after ligand binding

43
Second Messenger Signals
  • PIP2
  • IP3
  • DAG
  • BOTH ACTIVATE PROTEIN KINASES
  • GTP Binding Proteins
  • Activate MAPK
  • Raf 1
  • Activates the rest of MAPK

44
Signal Transduction
45
Transcription Factors
  • MAP kinase Cascade
  • c-jun
  • c-myc
  • c-fos
  • For protein synthesis between G1-Gs of the cell
    cycle
  • Activated ras, in turn, phosphorylates a cascade
    of enzymes that active MAPK (mitogen activated
    protein kinases)

46
Cell Cycle Cyclins
  • The cycle kinase complexes phosphorylate a number
    of proteins involved in DNA replication,
    formation of the mitotic spindle and other events
    in the cell cycle

47
Oncogenes
  • Some of the oncogenes such as bcl1, and
    antioncogenes, such as Rb gene and p53, act in
    the cyclin pathway to control cell growth

48
Growth Inhibition
  • The other side of growth is cellular inhibition.
  • The recent discovery that loss of tumor
    suppressor genes occur in certain cancers suggest
    that genes encode components of some cellular
    pathways.
  • Polypeptides factors that act as growth
    inhibitors are (TNF) and (TGF-B) transforming
    growth factor -beta

49
Growth Factors
  • There are many growth factors, examples are
  • Epidermal Growth Factor
  • Platelet Derived Growth Factor
  • Fibroblast Growth Factor
  • Insulin Like Growth Factor
  • Transforming Growth Factor- Beta
  • Cytokines
  • Interleukins, Tumor Necrosis Factor, Interferons

50
Epidermal Growth Factor
  • EGF was first discovered in precocious tooth
    eruption.
  • EGF is Mitogenic for a variety of epithelial
    cells and fibroblast cause cell division,
    specifically hepatic.

51
Platelet Derived Growth Factor
  • Is released in platelet activation.
  • It is produced by activated macrophages,
    endothelial cell, and smooth muscle cells.
  • PDGF causes both migration and proliferation of
    fibroblasts, and other pro-inflammatory
    properties as well

52
Fibroblast Growth Factor
  • Basically, FGF, in patricular has the ability to
    create (angiogenesis) blood cell formation

53
Insulin Like Growth Factor
  • The insulin-like growth factors (IGFs) are
    polypeptides with high sequence similarity to
    insulin.
  • IGFs are part of a complex system that cells use
    to communicate with their physiologic
    environment. This complex system (often referred
    to as the IGF "axis") consists of two
    cell-surface receptors (IGF1R and IGF2R), two
    ligands (IGF-I and IGF-II), a family of six
    high-affinity IGF binding proteins (IGFBP 1-6),
    as well as associated IGFBP degrading enzymes,
    referred to collectively as proteases.

54
Transforming Growth Factor- Beta
  • All of these favor fibrinogenesis

55
Cell Matrix Interactions
  • Cells grow, move, and differentiate in intimate
    contact with the extra-cellular matrix, and there
    is overwhelming evidence that the matrix
    critically influences these cell functions

56
Collagen Matrix
57
Laminin Matrix
58
(No Transcript)
59
Basal Lamina
60
Proteoglycans

61
Joint Function
62
Cellular Adaptation
63
Hyperplasia
  • Hyperplasia constitutes an increase in the number
    of cells in an organ or tissue, which may have
    increase volume.
  • Physiological Hyperplasia is divided
  • Hormonal Hyperplasia
  • Puberty
  • Compensatory
  • Liver

64
Ductal Hyperplasia
65
BPH
66
BPH
67
Hypertrophy
  • Hypertrophy refers to an increase in size of the
    cells, and with it the increased size of an organ
  • It is either physiological or pathological.

68
Muscle Hypertrophy
69
Muscle Hypertrophy
70
Cardiac Hypertophy
71
Atrophy
  • Causes of Atrophy
  • Decreased Workload
  • Loss of Innervation
  • Diminished Blood Supply
  • Inadequate Nutrition
  • Loss of Endocrine Stimulation
  • Aging

72
Inflammation Repair
73
Inflammation
  • Inflammation is fundamentally a protective
    response whose ultimate goal is to rid the
    organism of both the initial cause of cell injury
    (I.e. Microbes, Toxins) and the consequences of
    cell injury

74
Inflammation Response
  • Inflammation response occurs in vascularized
    connective tissue, including plasma, circulating
    cells, and blood vessels.
  • The vascular and cellular response of both acute
    chronic inflammation are mediated by
    chemotactic factors derived from plasma cells,
    and other cells stimulated by histamine,
    leukotrienes, kinins etc.
  • The circulating cells include neutrophils,
    eosinophils, lymphocytes, basophils, and
    platelets.

75
(No Transcript)
76
Signs Symptoms
  • Rubor---- Red
  • Tumor----Swelling
  • Calor----Heat
  • Dolar----Pain

77
Acute Inflammation
78
Keys to Acute Inflammation
  1. Alteration in Vascular caliber that leads to an
    increase in blood flow
  2. Structural changes in micro-vasculature that
    permit the plasma proteins and leukocytes from
    the micro-circulation
  3. Emigration of leukocytes from microcirculation
    and their accumulation and accumulation in focus
    of injury

79
Vascular Changes
  1. Following a inconstant vasoconstriction of the
    arterioles, lasting a few seconds Vasodilatation
    occurs
  2. Slowing of circulation. This is brought on from
    protein rich leakage during the increase in
    micro-vascular membrane permeability
  3. Stasis begin in periphery, principally beginning
    with neutrophils, along the vascular epithelium.
  4. Leukocyte margination
  5. Rolling

80
(No Transcript)
81
Margination
82
(No Transcript)
83
Diapedisis
  • Diapedesis is the movement of leukocytes across
    the endothelial lining of blood vessels
  • Chemo-tactic factors (V-Cams, I-Cams, E-selectin)
    etc alter the expression of regulation of
    adhesion of leukocytes adjacent to site of
    infection.
  • This causes leukocytes to slow down and cause
    integrin molecules to switch from low affinity to
    high affinity state.

84
(No Transcript)
85
Vaso-active amines
  • Histamine------ Mast Cells, Platelets
  • Serotonin------ Platelets, Mast Cells
  • Lysosomal Enzymes------Neutrophils
  • Prostaglandins----Leukocytes, platelets
    endothelium
  • Leukotrienes-----Leukocytes
  • Platelet Activating Factor-----Leukocytes,
    endothelium
  • Cytokines-----Macrophages, endothelium
  • Nitric Oxide-----Macrophages, endothelium

86
Plasma Proteases
  • A variety of phenomena in the inflammatory
    response system are mediated by three
    inter-related plasma derived factors The
    Complement, Kinin, and the Clotting System

87
Complement System
  • The complement system consists 20 component
    proteins which are found in greatest
    concentration in the plasma
  • Complement components are present as inactive
    components found in plasma numbers C1 through C9
  • They are responsible for
  • Vascular phenomena( I.e Histamine Vasodilation)
  • Leukocyte adhesion, chemotaxis activation
  • Phagocytosis

88
(No Transcript)
89
(No Transcript)
90
(No Transcript)
91
Kinin System
  • The kinin system is directly triggered by contact
    with surface activation of Hageman Factor (
    factor XII) of the intrinsic clotting pathway
  • Bradykinin is ultimately released causing
    vasodilation and INCREASED VASCULAR PERMEABILITY.

92
Hageman Factor
93
(No Transcript)
94
(No Transcript)
95
(No Transcript)
96
The Clotting System

97
(No Transcript)
98
  • The Intrinsic Clotting Cascade
  • The intrinsic pathway is much less significant to
    hemostasis under normal physiological conditions
    than is the extrinsic pathway. However, abnormal
    physiology such as hyperlipidemic states or
    bacterial infiltration can lead to activation of
    thrombosis via the intrinsic clotting cascade.
  • The intrinsic pathway requires the clotting
    factors VIII, IX, X, XI, and XII. Also required
    are the proteins prekallikrein (PK) and
    high-molecular-weight kininogen (HK or HMWK), as
    well as calcium ions and phospholipids secreted
    from platelets. Each of these pathway
    constituents leads to the conversion of factor X
    (inactive) to factor Xa (a signifies active).
    Initiation of the intrinsic pathway occurs when
    prekallikrein, high-molecular-weight kininogen,
    factor XI and factor XII are exposed to a
    negatively charged surface

99
(No Transcript)
100
  • Extrinsic Clotting Cascade
  • Activated factor Xa is the site at which the
    intrinsic and extrinsic coagulation cascades
    converge. The extrinsic pathway is initiated at
    the site of injury in response to the release of
    tissue factor (factor III). Tissue factor is a
    cofactor in the factor VIIa-catalyzed activation
    of factor X. Factor VIIa, a gla residue
    containing serine protease, cleaves factor X to
    factor Xa in a manner identical to that of factor
    IXa of the intrinsic pathway. The activation of
    factor VII occurs through the action of thrombin
    or factor Xa. The ability of factor Xa to
    activate factor VII creates a link between the
    intrinsic and extrinsic pathways. An additional
    link between the two pathways exists through the
    ability of tissue factor and factor VIIa to
    activate factor IX. The formation of complex
    between factor VIIa and tissue factor is believed
    to be a principal step in the overall clotting
    cascade. Evidence for this stems from the fact
    that persons with hereditary deficiencies in the
    components of the contact phase of the intrinsic
    pathway do not exhibit clotting problems.

101
Arachidonic Acid
102
(No Transcript)
103
PIP2 IP3, DAG
104
CYTOKINE FUNCTION
105
Outcomes of Acute
Inflammation
  • COMPLETE RESOLUTION
  • HEALING BY CONNECTIVE TISSUE REPLACEMENT
  • ABSCESS FORMATION
  • PRGRESSION TO A CHRONIC INFLAMMATORY STATE

106
CHRONIC INFLAMMATION
107
Chronic Inflammation
  • Persistent Inflammation and tissue destruction
    despite the bodies attempt to heal
  • Organisms that cause delayed hypersensitivity
  • Prolonged exposure to potentially endogenous or
    exogenous agent
  • An auto-immune disorder that can self perpetuate
    a chronic inflammatory state

108
Mononuclear Infiltration
  • Macrophages are just one part of the mono-nuclear
    inflammatory system, previously referred to as
    the reticular endothelial system Stages are
  • Continued recruitment of monocytes from
    circulation, via chemotaxis
  • Local Proliferation of Macrophages
  • Immobilization of Macrophages

109
Reticulo Endothelial System
  • Primary (or "central") lymphoid organs - the
    sites where the cells of the RES are produced.
    The cells of the RES are produced in the bone
    marrow.
  • The thymus is also included as it is the required
    site for T cell maturation.
  • Secondary (or "peripheral") lymphoid organs - the
    sites where the cells of the RES function.
  • MALT is further divided into the GALT
    (gut-associated lymphoid tissue) and the BALT
    (bronchus-associated lymphoid tissue).
  • The Kupffer cells of the liver act as part of
    this system but are not organized into a tissue
    rather, they are dispersed throughout the liver
    sinusoids

110
RES
111
(No Transcript)
112
Macrophages
  • These cells are part of the innate
    response. Unlike T and B cells, they do not
    contain any specific receptors. Macrophages
    continuously phagocytose self-proteins and cells
    in their vicinity, during normal tissue repair
    and aging (e.g. old red blood cells). All of
    these proteins are degraded and presented on
    MHC-II. These self-proteins however, do not
    activate T cells, because in the absence of
    infection, macrophages express low levels of
    MHC-II, and almost no co-stimulator (B7).
    Further, T cells with high affinity receptor for
    self-peptides have been deleted during T cell
    development in the thymus. In the case
    of infection, however, macrophages posses certain
    types of receptors that recognize differential
    carbohydrate patterns on foreign cells. They also
    have receptors for specific bacterial products
    such as lipopolysaccharide (LPS) (endotoxin).
    When these molecules bind their bacterial
    ligands, they stimulate the macrophages to up
    regulate MHC-II and B7, providing these cells
    with strong antigen presentation properties. They
    also start to secrete Cytokines   that aid in
    their functions. (note IL-1, 6, 8, 12 and
    TNF-a). It is at this point that antigen
    presentation by MHC II will activate Th cells.

113
(No Transcript)
114
Products released by
Macrophages
  • Enzymes
  • Elastase
  • Collagenases
  • Plasma Proteases
  • Complement
  • Coagulaton factors
  • Reactive oxygen species
  • Eicosenoids
  • Cytokines (IL-1, TNF, IL-8)
  • Growth factors
  • Nitric oxide

115
Connective Tissue Repair
  • FIBROSIS HAS (4) COMPONENTS TO THE PROCESS
  • FORMATION OF NEW BLOOD VESSELS
  • (ANGIOGENESIS)
  • MIGRATION AND PROLIFERATION OF FIBROBLASTS
  • DEPOSITION OF EXTRACELLUALR MATRIX
  • MATURATION AND REMODELING OF TISSUE

116
Granulomatous Inflammation
  • Bacterial
  • Tuberculosis
  • Leprosy
  • Syphilis
  • Cat Scratch Fever
  • Parasitic
  • Schistosomiasis
  • Fungal
  • Crypyococcus
  • Coccidioidis
  • Inorganic Metals
  • Unknown

117
Lymphatic Inflammation
  • Lymphatics are very delicate channels that are
    often very difficult to visualize because they
    readily collapse.
  • Lymphadenititis may be caused by a bacteremia of
    ,the vascular system that prevents drainage that
    way.
  • The constellation of nodal involvement is usually
    termed reactive or inflammatory because of the
    loose pattern of the infective process.

118
Serous Inflammation
  • Serous inflammation is marked by an outpouring of
    thin non proteinacious fluid.
  • The fluid is a cause of effusions amd skin
    blistering that may be a result of various
    sources to include (viral, osmotic, and other
    non-bacterial sources)

119
Fibrinous Inflammation
  • With more severe injuries, resulting is greater
    vascular permeability, larger molecules including
    fibrin pass the vascular barrier.
  • Histologically, fibrin appears as an eosinopholic
    meshwork of threads.
  • Conversion of this fibrinous exudate leads to
    scar tissue organization, and sometimes a
    thickening of the tissue itself.

120
Purulent Inflammation
  • This type of inflammation is what can cause
    abscesses, pus, or exudate consisting mainly of
    neutrophils and necrotic cells.
  • There is usually a necrotic foci of
    staphylococcus or other pyogenic bacteria.

121
Ulcers
  • An ulcer is a local defect, or excavation of the
    surface of an organ that is produced by continual
    (shedding) sloughing or inflammatory necrotic
    tissue.
  • It is common to the GI tract, and during the
    acute phase there is intense polymophonuclear
    infiltration and vascular dilation.
  • Chronically fibroblastic proliferation continues

122
Systemic effects of
Inflammation
  • Release in interleukins, prostaglandins, after an
    initial leukocytosis can cause serum proteins,
    including amyloid, complement and coagulation
    factors to invade surrounding tissue.
  • Certain infection increase the risk of such an
    inflammatory state, creating a tissue
    eosinophilia that may briefly impede tissue
    repair until treated.

123
(No Transcript)
124
(No Transcript)
125
Wound Healing
  • Within 24 hours, neutrophil appear at margin of
    insult. The cut edges thicken as a result of
    mitotic activity of basal cells
  • By day 3, granulation tissue continues to invade
    the area
  • By day 5, the area in granulated and
    neo-vascularization begins to develop
  • During the second week there is an accumulation
    of collagen, accompanied by a regression of
    vascular channels.
  • Hypoxia lead to pain, and prostaglandin release
  • By the end of the 1st month, inflammatory tissue
    has ceased and tensile strength element begin to
    develop.

126
Wound Healing
127
(No Transcript)
128
(No Transcript)
129
FEVER
130
Infectious Disease
131
General Principles
  • Improved living conditions, help in decreasing
    infection in developed countries, yet in
    undeveloped or developing countries, unsanitary
    living condition (sewage/ water) and malnutrition
    leave the massive burden of infectious disease 10
    million people each year.
  • Most of these are children that die from
    complicated respiratory and diarrheal infections
    caused by viruses and bacteria

132
Kochs Postulate
  • 1 The microganism is regularily found in the
    lesion
  • The organism can be isolated as single colonies
    on a solid medium
  • Inoculation of the culture organism can cause a
    lesion in experimental animals
  • The organism can be recovered from experimental
    animals

133
Categories of Infection Agents
  • Viruses
  • Bacteriophages, plasmids
  • Bacteria
  • Chlamydia, Rickettsia
  • Fungi
  • Protozoa
  • Helminths
  • Ectoparacytes

134
Respiratory Viruses
  • Adenovirus
  • Echovirus
  • Cocksackie virus
  • Coronavirus
  • Inluenza A, B
  • Parainfluenza Type 1-4
  • RSV

135
Digestive Viruses
  • Mumps
  • Rotavirus
  • Norwalk
  • Hepatitis A
  • Hepatitis B
  • Hepatitis C
  • Hepatitis D
  • Hepatitis E

136
Systemic and Skin Viruses
  • Measles
  • Rubella
  • Parvavirus
  • Vacinnia
  • Varicella-zoster
  • HSV I
  • HSV II

137
Systemic and Blood Viruses
  • Cytomegalovirus (CMV)
  • Epstein-barr virus (Mono)
  • HTLV I virus
  • HTLV II virus
  • HIV I II virus

138
Arbor and Hemmorrhagic Viruses
  • Denguevirus 1-4
  • Yellow fver
  • Colorado Tick
  • Regional Hemmorhagic (Hanta, Marburg, Ebola )

139
Warty Growth Virus
  • Papillomavirus (HPV)
  • Molluscum Virus

140
CNS Viruses
  • Polivirus
  • Rhabdovirus
  • JC virus
  • Arboviral encphalitis virus

141
Bacteria
142
Pyogenic Cocci Bacteria
  • Staphylococcus aurues
  • Streptococcus pyogenes
  • Streptococcus Pneumoniae
  • Neisseria Menegitidis
  • Neisseria Gonorrhoeae

143
Common Gram Negative Infections
  • Escherichia Coli
  • Klebsiella Pneumonae
  • Enterobacter Aerogenes
  • Proteus spp.
  • Pseudomonas sp.
  • Legionella spp.

144
Rare Gram Negative
Infections
  • Calymmatatobacterium donavons
  • Heamophilis ducreyi
  • Klebseilla rhinoschleromatis
  • Bartonella bacilliforms

145
Contagious Childhood Bacteria
  • Hemophilus influenze
  • Hemophilus pertusis
  • Cornyobacterium diptheria

146
Enteropathic Infections
  • Enterpathogenic E-coli
  • Shigella Sp
  • Vibrio cholera
  • Campylobacter jejuni
  • Yersinia enterocolitica
  • Salmonella spp (1000 strains)

147
(No Transcript)
148
K, H, O Antigens
149
Mycobacterium Tuberculosis
  • Tuberculosis (TB) survives in the United States
    and has been infecting people for more than 3,000
    years.  It is truly a global menace with
    remarkable staying power.  TB remains one of the
    worlds leading killers, responsible for nearly 2
    million deaths every year.  Today, this bacterium
    infects some one-third of all human beings
    worldwide.  It was estimated that in 2005 alone,
    9 million people will be diagnosed with the
    infection and more than 2 million will die. 
    During this same year, about 40 million, most
    unknowingly, will quietly become infected. 
    Mycobacterium tuberculosis, which is the name of
    the bacterium that causes most cases of
    tuberculosis, often times will lie latent
    (dormant), awaiting a future time and place to
    awaken.  This disease is capable of lingering
    undetected in the body for years in its latent
    form, with potentially devastating consequences
    if it becomes active

150
(No Transcript)
151
Vibrio Chorela
  • Annually 5-7 million cases, 100,000 deaths
    worldwide. Cholera gravis, the most severe form
    of the disease, has a 10 death rate.
  • Cholera is actually hard to catch. Normal levels
    of stomach acidity make it necessary to ingest
    great volumes of the pathogen--enough to make the
    water cloudy. Water filtration and waste
    treatment are an important part of controlling
    the spread of cholera.

152
Malaria
  • Humans infected with malaria parasites can
    develop a wide range of symptoms. These vary from
    asymptomatic infections (no apparent illness), to
    the classic symptoms of malaria (fever, chills,
    sweating, headaches, muscle pains), to severe
    complications (cerebral malaria, anemia, kidney
    failure) that can result in death. The severity
    of the symptoms depends on several factors, such
    as the species (type) of infecting parasite and
    the human's acquired immunity and genetic
    background.

153
Malaria Transmission
  • Malaria is transmitted among humans by female
    mosquitoes of the genus Anopheles. Female
    mosquitoes take blood meals to carry out egg
    production, and such blood meals are the link
    between the human and the mosquito hosts in the
    parasite life cycle. Of the approximately 430
    known species of Anopheles, only 30-50 transmit
    malaria in nature. The successful development of
    the malaria parasite in the mosquito (from the
    "gametocyte" stage to the "sporozoite" stage)
    depends on several factors. The most important is
    ambient temperature and humidity (higher
    temperatures accelerate the parasite growth in
    the mosquito) and whether the Anopheles survives
    long enough to allow the parasite to complete its
    cycle in the mosquito host ("sporogonic" or
    "extrinsic" cycle, duration 10 to 18 days).
    Differently from the human host, the mosquito
    host does not suffer noticeably from the presence
    of the parasites.

154
Zoonotic Bacteria Infections
  • Bacillus Anthracis
  • Listeria monocytogenes
  • Yersinia pestis
  • Franciella tuleremia
  • Brucella sp
  • Lerptospira sp (many groups)
  • Borrelia burgodorferi

155
Various Adhesin Factors
156
Helminths
  • Refer to Helminths chapter it is very inclusive
    as to life cycles and treatment of Helminths

157
Ectoparasites
  • Ectoparasites are arthropods (lice, ticks,
    bedbugs, fleas) that attach and can burrow into
    skin.
  • An example of this is
  • LYME Disease (Borrellia Borgedorferi, which is
    transmitted by ticks) it causes an erthymatous
    plaque skin lesion

158
Fungi
  • Pathogenic fungi is describes inclusively in the
    Mycology section of IMECs Series

159
Chlamydia
  • Is a common sexually transmitted disease (STD)
    caused by the bacterium, Chlamydia trachomatis,
    which can damage a woman's reproductive organs.
    Even though symptoms of chlamydia are usually
    mild or absent, serious complications that cause
    irreversible damage, including infertility, can
    occur "silently" before a woman ever recognizes a
    problem. Chlamydia also can cause discharge from
    the penis of an infected man.

160
Trichomoniasis
  • Trichomoniasis is caused by the single-celled
    protozoan parasite, Trichomonas vaginalis. The
    vagina is the most common site of infection in
    women, and the urethra (urine canal) is the most
    common site of infection in men. The parasite is
    sexually transmitted through penis-to-vagina
    intercourse or vulva-to-vulva (the genital area
    outside the vagina) contact with an infected
    partner. Women can acquire the disease from
    infected men or women, but men usually contract
    it only from infected women.
  • Trichomoniasis is the most common curable STD in
    young, sexually active women. An estimated 7.4
    million new cases occur each year in women and
    men.

161
Legionaires Disease
  • Legionnaires disease (LEE-juh-nares) is caused
    by a type of bacteria called Legionella. The
    bacteria got its name in 1976, when many people
    who went to a Philadelphia convention of the
    American Legion suffered from an outbreak of this
    disease, a type of pneumonia (lung infection).
    Although this type of bacteria was around
    before1976, more illness from Legionnaires
    disease is being detected now. This is because we
    are now looking for this disease whenever a
    patient has pneumonia
  • PONTIAC FEVER !!!

162
Environmental Disease
163
Factors
  • Air pollution
  • Cigarette smoking
  • Ultra-violet light
  • Chemical Injury
  • Drugs injury
  • Physical injuries
  • Nutritional disease

164
Air Pollution
  • Daily we inhale and exhale 10-20 thousand liters
    of air, that has a myriad of pollutants from
    bacteria, gases, fibers, particles .
  • Some pollutants are restricted to specific
    industries and are carefully monitored in the US,
    and in general creat less of a health problem.

165
Environmental Considerations
  • All disease are not purely genetic in nature,
    many are aquired through environmental exposure.
    Consideration are almost limitless, but they can
    divided into
  • The magnitude of the environmental problem
  • The adverse affects associated
  • Injuries induced by exposure
  • Overall health consequences of nutritional
    adjustments needed

166
Air Pollutants
  1. Tobacco Smoke
  2. Wood coal Stoves
  3. Gas Ranges ( NO, CO2, NO2 )
  4. Dust Mites
  5. Formaldehyde
  6. Radon
  7. Solvents Cleaning
  8. Pesticides and herbicides
  9. ASBESTOS

167
Lung Diseases
  • Acute/Chronic inflammation
  • Emphysema
  • Asthma
  • Hypersensitivity pneumonitis
  • Pneumococcal Infections
  • Neoplasma

168
Ultra-violet light
  • Increased ultra-violet exposure may have serious
    threats with increasing global warming and
    depletion of the ozone.
  • The direct injury can lead to basal cell
    carcinoma and melanoma.
  • Not to mention that the depletion of
    phytoplankton can cause a disruption in the CO2
    and changes in the food change.

169
Chemical Injury
  • All chemicals are capable of injury.
  • In the United States , OSHA is supposed to
    regulate all of these.
  • Yet recently, a dramatic industrial exposure in
    (BHOPAL, India) in 2000 released gaseous cyanide.
  • It must be expected that at any time similar
    incidences could happen again.
  • LEAD, SILICON, MERCURY

170
Drug Injuries
  • Blood dyscrasias
  • Agranulocytosis, aplastic anemia, hemolytic
    anemia
  • Cutaneous
  • Uticaria
  • Cardiac
  • Arrhythmia
  • Renal
  • Glomerulonephritis
  • Hepatic
  • Fatty Changes
  • Pulmonary
  • Systemic
  • CNS

171
Common Drug Injuries
  • Tricyclic antidepressants
  • Dopamine, serotonin terminals
  • Acetominophen
  • Toxic metabolite binds to gluthathione
  • Aspirin
  • Respiratory depression, gastritis
  • Oral Contraceptives
  • Endometrial defects, cardio, venous thrombus
  • Osteoporosis
  • Halothane
  • Hepatic necrosis, hypersensitivity reaction
  • Ethanol
  • To many to list

172
(No Transcript)
173
Major Environmental Carcinogens
  • Arsenic ----- Skin, Lung, liver CA
  • Asbestos ---Bronchogenic CA
  • Benzene----mylogenous leukemia
  • Beta-naphylamine ---- bladder
  • Cadmium---- Prostate
  • Nickel---- Stomach Carcinoma
  • Vinyl Chloride-----angio-sarcoma

174
Major Environmental Toxins
  • Mercury---Neuronal changes
  • Cyanidecytochome oxidase inhibitor
  • Mushrooms blocks RNA polymerase
  • Insectides Neuronal changes
  • MethanolForladehyde and formic acid

175
Physical Injuries
  • Abrasions
  • Lacerations
  • Incisions
  • Contusions
  • Gunshot wounds
  • Burns
  • Electrical Injuries
  • Radiological Injuries

176
Nutritional Disorders
  • Protein/Calorie- under-nutrition
  • Fat Soluble Vitamin Deficiency
  • Water Soluble Vitamin Deficiency

177
Protein/Calorie Under-nutrition
  • Decreased Intake
  • Poor Teeth
  • Dysphagia
  • Anorexia
  • Systemic disease
  • Mal-absorption
  • Biliary/Pancreatic Diseases
  • Enteric and Vit B12 Malabsorption
  • Increase Requirements
  • Trauma
  • Burns
  • Excessive protein loss

178
Protein/Calorie Under-nutrition
  • Kwashiorkor is characterized by apathy,
    peripheral edema, sub Q fat, moon face, enlarged
    fatty liver and low serum albumin
  • Marismus is muscle wasting , no edema or hepatic
    enlargement

179
Kwashiorkor
180
Fat Soluble Vitamin Deficiency
  • Vitamin A------ Night Blindness
  • Vitamin D------ Rickets, Osteomalacia
  • Vitamin E------ Spinocerebellar effects
  • Vitamin K------ Bleeding diathesis

181
Severe Vitamin A defect
182
Water Soluble Vitamin
Deficiency
  • Vitamin B1 (Thiamine)---Beriberi
  • Vitamin B2 (Riboflavin)---Stomatitis
  • Niacin--- Pellegra (demtentia, dermatitis,
    diarrhea)
  • Vitamin B6 --- (Peripheral neuropathy)
  • Vitamin B12---Megaloblatsic/perniscious anemia
  • Vitamin C--Scurvy
  • Folate----Megaloblastic anemia

183
Obesity
  • Few problems in America have been talked about
    more, yet one quarter of americans are
    overweight, and 1/8th would be considered obese
  • Body Mass Index ( BMI ) in whatever form must be
    evaluated to patients morphology
  • Obesity in itself can be due to eating habit, as
    well as lower metabolic rates
  • Consequences include Heart Disease, Hypertension,
    Diabetes Mellitus, and other coronary artery
    insults

184
Diet and Systemic Disorder
  • There is significant studies that show variable
    ratios of HDL, LDL, and VLDL effect coronary
    heart disease
  • Hypertension although not entirely clear is
    related to sodium channels, and sodium
    restriction would be the first line of therapy

185
Diet and Cancer
  • There is great concern that aromatic compound can
    effect cancer
  • Cyclymates, and saccharin although now regulated
    enhance cancinogenic influences
  • High fat diet and less bulk grains attribute to
    colon cancer
  • Anti-oxidants, such as Vitamins A, E, C, are
    essential as free radical scavengers

186
Vascular Disease
187
Arteries Veins
  • Arteries and veins have been distinctively
    structures.
  • Artery walls are generally thicker than venous
    counterparts.
  • Vein have an overall larger diameter, a larger
    lumen and a more narrow wall.

188
(No Transcript)
189
(No Transcript)
190
Arterial and Venous Lumen
  • Under normal situations the Intima layer of
    arteries is less exaggerated than veins
  • Whereas under most situations in elastic arteries
    the Media layer is much more prominent than
    corresponding veins
  • Arterioles, the smallest branches of the
    arteries, is normally responsible for blood
    pressure regulation

191
Intima Cells
192
Endothelial Cell Activation
193
Endothelial Cell Adhesion
194
Endothelial Cell Properties
  • Maintenance of permeability barrier
  • Extra cellular Matrix (collagen, procollagen)
  • Elaboration of anticoagulant /anti-thrombotic
    molecules
  • Prostacyclin
  • Plasminogen Activator
  • Heparin like molecules
  • Elaboration of pro-thrombotic molecules
  • Von Willebrand factors (Factor VIIIa)
  • Tissue Factor
  • Plasminogen Activator Inhibitors

195
Endothelial Cell Properties
  • Modulation of Blood Blow Factors
  • Vasoconstrictors ACE, endothelin
  • Vasodilators NO/EDRF, prostacyclin
  • Regulation of Inflammation Factors
  • IL-1, IL-6, IL-8
  • Adhesion Molecules
  • Histocompatibility Antigens
  • Regulation of Cell Growth
  • Growth Stimulators PDGF, CSF, FGF
  • Growth Inhibitors Heperin, TGF-B
  • Oxidation of LDL

196
LDL Oxidative Stress
197
(No Transcript)
198
(No Transcript)
199
Endothelial Dysfunction
  • In all realization, the term endothelial
    dysfunction refers to potentially reversible
    changes in the state of the endothelial cell that
    occurs in response to environmental stimuli

200
Intimal Thickening
  • Healing and damage of blood vessels comprise SMC
    proliferation in the migration from the media to
    the intima, and subsequent multiplication and
    modification of intimal cells.
  • An extensive or chronic injury induces a very
    complex and repair sequence. Which include
    proliferation activities of promoters and
    inhibitors.

201
Intimal Thickening
202
Atherosclerosis
203
Atherosclerosis
204
Major Rick Factors
  • Diet Hyperlipidemia
  • Hypertension
  • Cigarette Smoking
  • Diabetes

205
Minor Risk Factors
  • Obesity
  • Activity level
  • Male gender
  • Age
  • Family history
  • Stress (Type A)

206
(No Transcript)
207
Inflammatory Vasculitis
208
Inflammatory Vasculitis
  • Large Vessel
  • Giant Cell (Temporal) Arteritis
  • Takayasus Arteritis
  • Medium Size Vessel
  • Polyarteritis Nordosa
  • Kawasaki Disease
  • Small Vessel Vasculitis
  • Wegeners Granulomatous
  • Churg-Strauss Syndrome
  • Henloch-Schonlein Purpura

209
Giant Cell (Temporal) Arteritis
  • Giant cell arteritis (GCA) is an inflammation of
    the lining of your arteries
  • Although giant cell arteritis can affect the
    arteries in your neck, upper body and arms, it
    occurs most often in the arteries in your head,
    especially those in your temples. For this
    reason, giant cell arteritis is sometimes called
    temporal arteritis or cranial arteritis.
  • Giant cell arteritis frequently causes headaches,
    jaw pain, and blurred or double vision, but the
    most serious potential complications are
    blindness and, less often, stroke. These problems
    can occur when swelling in your arteries impairs
    blood flow to your eyes or brain.

210
Takayasus Arteritis
  • TA often affects young Oriental women, but it can
    affect children, women and men of all ages and
    ethnic backgrounds. At diagnosis, TA patients are
    often between 15-35 years old.
  • Every year in the United States, two to three new
    cases of TA per million Americans are diagnosed

211
Polyarteritis Nordosa
  • Polyarteritis nodosa (PAN) is a rare autoimmune
    disease characterized by spontaneous inflammation
    of the arteries (arteritis) of the body. Because
    medium sized arteries are involved, the disease
    can affect any organ of the body. The most common
    areas of involvement include the muscles, joints,
    intestines, nerves, kidneys, and skin
  • Within several weeks of onset the patient
    condition may lead to paralysis and death. At
    autopsy, nodular swellings is found along the
    course of muscular arteries.

212
Kawasaki Disease
  • About 80 percent of the people with Kawasaki
    disease are under age five. Children over age
    eight are rarely affected. The disease occurs
    more often among boys (over 60 percent) and among
    those of Asian ancestry
  • The coronary arteries are most often affected.
    Part of a coronary wall can be weakened and
    balloon (bulge out) in an aneurysm. A blood clot
    can form in this weakened area and block the
    artery, sometimes leading to a heart attack. The
    aneurysm can also burst, but this rarely happens.

213
Wegeners Granulomatous
  • Because Wegeners so often involves the upper
    respiratory tract (sinuses, nose, ears, and
    trachea windpipe) and because biopsy of these
    tissues is a relatively noninvasive procedure,
    these sites are frequently biopsied in patients
    suspected of Wegeners
  • Since 1982, when ANCAs (antineutrophil
    cytoplasmic antibodies) were first described, the
    role of these antibodies in the diagnosis of
    Wegeners has grown. ANCA testing, which involves
    the performance of a simple blood test, has
    achieved wide availability during the 1990s

214
Churg-Strauss Syndrome
  • Churg Strauss syndrome is a type of vasculitis
    (blood vessel inflammation) that occurs
    throughout the body.
  • Asthma
  • High numbers of eosinophils, a type of white
    blood cell, in the blood
  • Pain, numbness, or tingling in the arms and legs
    (called mononeuropathy)
  • Lung abnormalities
  • Sinus problems such as abnormal growths (polyps)
  • A tissue sample showing a blood vessel with
    eosinophils around it
  • A person with Churg Strauss syndrome may have
    some or all of these symptoms

215
Henloch-Schonlein Purpura
  • Henoch-Schonlein purpura (HSP or anaphylactoid
    purpura) is a form of blood vessel inflammation
    or vasculitis. There are many different
    conditions that feature vasculitis. Each of the
    forms of vasculitis tends to involve certain
    characteristic blood vessels. HSP affects the
    small arterial vessels called capillaries in the
    skin and frequently the kidneys
  • HSP occurs most often in the spring and
    frequently follows an infection of the throat or
    breathing passages. HSP seems to represent an
    unusual reaction of the body's immune system that
    is in response to this infection (either bacteria
    or virus). Aside from infection, drugs can also
    trigger the condition

216
Buergers Disease
  • Buerger's disease (also known as thromboangiitis
    obliterans) is a rare disease characterized by a
    combination of acute inflammation and thrombosis
    (clotting) of the arteries and veins in the hands
    and feet. The obstruction of blood vessels in the
    hands and feet reduces the availability of blood
    to the tissues, causes pain and eventually
    damages or destroys the tissue. It often leads
    skin ulcerations and gangrene of fingers and
    toes. Rarely, in advanced stages of the disease,
    it may affect vessels in other parts of the body

217
INFECTIOUS ARTERITIS
218
Raynauds Syndrome
  • Raynaud's phenomenon (RAY-noz), in medicine, is a
    vasospastic disorder causing discoloration of the
    fingers, toes, and occasionally other
    extremities. The cause of the phenomenon is
    unknown, but emotional stress and cold are
    classically triggers, and the discoloration
    follows a characteristic pattern in time white,
    blue and red. It comprises both Raynaud's disease
    (primary Raynaud's), where the phenomenon is
    idiopathic, and Raynaud's syndrome (secondary
    Raynaud's), where it is secondary to something
    else.

219
KIDNEY DISEASES
220
Kidney
  • Each human adult kidney weighs about 150 gm. As
    the ureter enters the kidney at the hilus, it
    dilates into a funnel shaped pelvis, from derive
    2-3 major calyces, and then about 12 minor
    calyces
  • The kidney is richly supplied with a blood flow
    that branch as follows
  • Interlobar, Arcuate, Interlobar
  • The glomerulus which is in the cortex and
    surrounding tubules are the function branch,
    which exist in the renal medulla

221
(No Transcript)
222
Renal Glomerulus
223
(No Transcript)
224
The Glomerular Basement Membrane
  • The (GBM), is a this electron dense central
    layer, called the lamina densa
  • It is made up of a collagen rich, polyanionic
    proteoglycan ( mainly Heperan Sulfate)
    fibronectin, and severel other glycoprotiens
  • The visceral epithelim is made up of podocytes
    (or Foot Processes)

225
Basement Membrane
226
Tubules
  • The structure of the renal tubules varies
    considerably at different levels of the nephron.
  • The proximal tubule is particularily vulnerable
    to ischemic disease.
  • The juxta cell snuggle closely to the glomerulus
    ad sense changes in Renin, therefore very very
    important cell in the regulation of fluid volume
  • In the distal tubule the cells are more crowded
    so less ionic transfer occurred
  • The Loop of Henle is a diuretic area of the
    tubules

227
Pathology of Renal DX
  • Renal disease is responsible for a great deal of
    morbidity, in the USA about 35,000 deaths are
    related directly to this.
  • Twenty percent of women contract UTI is their
    lifetime
  • The glomerular diseases are most often
    immunologically mediated, whereas tubular disease
    and interstitial disease are more often caused by
    toxic or infectious diseases.

228
Diagnosis of Renal Disease
  • Although is standard practice renal failure is
    simple evaluated by output, BUN, and Creatinine.
  • Whereas in Renal Disease the widespread use of
    biopsy has changes our concepts dramitically,
    especially with Glomerulonephritis Test inclde
  • Periodic Acid-Schiff stain (PAS)
  • Basement membrane and mesangial matrix
  • Silver Impregnation
  • Tubular basement membranes
  • Immunoflourescence
  • Electron Microscopy when available

229
Clinical Manifestations
  • Acute Nephritic Syndrome
  • Nephrotic Syndrome
  • Hematuria
  • Acute renal failure
  • Chronic Renal Failure
  • Nephrolithiasis

230
Acute Nephritic Syndrome
  • Acute nephritic syndrome most often results from
    infection by streptococcus, a type of bacteria.
    Acute nephritic syndrome after a streptococcal
    infection (post-streptococcal glomerulonephritis)
    typically develops following a throat or skin
    infection in children between the ages of 2 and
    14. Infections by other types of bacteria, such
    as staphylococcus and pneumococcus, viral
    infections such as chickenpox, and parasitic
    infections such as malaria can also result in
    acute nephritic syndrome. Membranoproliferative
    glomerulonephritis, IgA nephropathy,
    Henoch-Schönlein purpura, systemic lupus
    erythematosus, mixed cryoglobulinemia,
    Goodpasture's syndrome, and Wegener's
    granulomatosis are all noninfectious causes of
    acute nephritic syndrome.

231
Nephrotic Syndrome
  • Nephrotic syndrome is a condition marked by very
    high levels of protein in the urine
    (proteinuria) low levels of protein in the
    blood swelling, especially around the eyes,
    feet, and hands and high cholesterol. Nephrotic
    syndrome results from damage to the kidneys'
    glomeruli (the singular form is glomerulus).
    Glomeruli are tiny blood vessels that filter
    waste and excess water from the blood and send
    them to the bladder as urine
  • Nephrotic syndrome may go away once the
    underlying cause, if known, has been treated. In
    children, 80 percent of cases of nephrotic
    syndrome are caused by minimal change disease,
    which can be successfully treated with
    prednisone.

232
Hematuria
  • Hematuria is the presence of red blood cells
    (RBCs) in the urine. In microscopic hematuria,
    the urine appears normal to the naked eye, but
    examination under a microscope shows a high
    number of RBCs. Gross hematuria can be seen with
    the naked eyethe urine is red or the color of
    cola.
  • Several conditions can cause hematuria, most of
    them not serious. For example, exercise may cause
    hematuria that goes away in 24 hours. Many people
    have hematuria without any other related
    problems. Often no specific cause can be found.
    But because hematuria may be the result of a
    tumor or other serious problem, a doctor should
    be consulted.
  • To find the cause of hematuria, or to rule out
    certain causes a series of tests including
    urinalysis, blood tests, intravenous pyelogram,
    and cystoscopic examination

233
Acute renal failure
  • Acute (sudden) kidney failure is the sudden loss
    of the ability of the kidneys to remove waste and
    concentrate urine without losing electrolytes
  • There are many possible causes of kidney damage.
    They include
  • Decreased blood flow, which may occur with
    extremely low blood pressure caused by trauma,
    surgery, serious illnesses, septic shock,
    hemorrhage, burns, or dehydration
  • Acute tubular necrosis (ATN)
  • Urinary tract obstruction (obstructive uropathy)
  • Autoimmune kidney disease such as interstitial
    nephritis or acute nephritic syndrome
  • Disorders that cause clotting within the thin
    blood vessels of the kidney
  • Idiopathic thrombocytopenic thrombotic purpura
    (ITTP)
  • Transfusion reaction
  • Malignant hypertension
  • Scleroderma,
  • Hemolytic-uremic syndrome

234
Chronic Rena
About PowerShow.com