This is a presentation on the topic of hemodynamic disorders, thromboembolic diseases and shock, prepared by Dr Ashish Jawarkar, he is MD in pathology and a teacher at Parul institute of Medical sciences and research Vadodara.
Dear all, Pathologybasics is out with a new series of power point presentations on general Pathology.. Following is link presentation on seventh and the most difficult to understand chapter of robbins.. chapter 7,neoplasia. Any suggestions/feedback/constructive criticism are welcome on facebook.com/pathologybasics or pathologybasics@gmail.com
This is a presentation on the topic of Inflammation and repair, prepared by Dr Ashish Jawarkar, he is MD in pathology and a teacher at Parul institute of Medical sciences and research Vadodara.
Dear all, Pathologybasics is out with a new series of power point presentations on general Pathology.. Following is link presentation on seventh and the most difficult to understand chapter of robbins.. chapter 7,neoplasia. Any suggestions/feedback/constructive criticism are welcome on facebook.com/pathologybasics or pathologybasics@gmail.com
This is a presentation on the topic of Inflammation and repair, prepared by Dr Ashish Jawarkar, he is MD in pathology and a teacher at Parul institute of Medical sciences and research Vadodara.
Cellular adaptations, injury and death.. Lecture 1Ashish Jawarkar
This is a series of lectures on general pathology useful for undergraduate and postgraduate pathology students. The ppts here have are enriched with explanatory pictures as well as useful video links.. hope you find them useful
This is a powerpoint presentation on the Topic of Diseases of the immune system, part 1 - Chapter 6, based on Robbin's textbook of pathology. Prepared by Dr. Ashish Jawarkar, who is Assistant professor at Parul institute of medical sciences and research, Vadodara. Please subscribe to our youtube channel https://www.youtube.com/channel/UCwjkzK-YnJ-ra4HMOqq3Fkw . Our facebook page: facebook.com/pathologybasics. Instagram handle @pathologybasics
Disorders that perturb cardiovascular, renal, or hepatic function are often marked by the accumulation of fluid in tissues (edema) or body cavities (effusions).
Cellular adaptations, injury and death.. Lecture 1Ashish Jawarkar
This is a series of lectures on general pathology useful for undergraduate and postgraduate pathology students. The ppts here have are enriched with explanatory pictures as well as useful video links.. hope you find them useful
This is a powerpoint presentation on the Topic of Diseases of the immune system, part 1 - Chapter 6, based on Robbin's textbook of pathology. Prepared by Dr. Ashish Jawarkar, who is Assistant professor at Parul institute of medical sciences and research, Vadodara. Please subscribe to our youtube channel https://www.youtube.com/channel/UCwjkzK-YnJ-ra4HMOqq3Fkw . Our facebook page: facebook.com/pathologybasics. Instagram handle @pathologybasics
Disorders that perturb cardiovascular, renal, or hepatic function are often marked by the accumulation of fluid in tissues (edema) or body cavities (effusions).
Slide Note: Edema Congestion
Title: Edema Congestion: Understanding the Mechanisms and Clinical Implications
Introduction:
Edema congestion is a pathological condition characterized by the abnormal accumulation of fluid within tissues or body cavities, leading to swelling and impaired tissue function. It is a complex physiological process that can arise due to various underlying factors and may manifest in different regions of the body. Understanding the mechanisms and clinical implications of edema congestion is crucial for healthcare professionals to effectively diagnose, manage, and treat patients presenting with this condition.
I. Mechanisms of Edema Congestion:
A. Increased Capillary Hydrostatic Pressure:
- Elevated pressure within the capillaries due to factors such as venous obstruction, heart failure, or localized inflammation.
- Higher hydrostatic forces cause an excessive filtration of fluid from the capillaries into the interstitial spaces, contributing to tissue swelling.
B. Decreased Plasma Oncotic Pressure:
- Reduction in plasma protein levels, particularly albumin, results in decreased oncotic pressure.
- Lower oncotic pressure leads to reduced fluid reabsorption from the interstitial spaces back into the capillaries, exacerbating fluid accumulation.
C. Lymphatic Obstruction or Insufficiency:
- Impaired lymphatic drainage due to lymphatic vessel obstruction, surgical intervention, or congenital malformations.
- Inadequate lymphatic clearance results in the retention of interstitial fluid, leading to edema.
D. Sodium and Water Retention:
- Dysregulation of sodium and water balance in conditions like kidney dysfunction, cirrhosis, or hormonal imbalances.
- Sodium retention leads to increased osmotic pressure, causing water to accumulate in the interstitial spaces.
II. Clinical Implications:
A. Peripheral Edema:
- Swelling predominantly in the extremities, commonly observed in conditions such as heart failure, deep vein thrombosis, or venous insufficiency.
- Patients may experience discomfort, reduced mobility, and skin changes due to chronic edema.
B. Pulmonary Edema:
- Accumulation of fluid in the lungs, often resulting from heart failure, acute respiratory distress syndrome (ARDS), or pneumonia.
- Respiratory compromise, cough, and shortness of breath are common symptoms requiring urgent medical intervention.
C. Cerebral Edema:
- Swelling within the brain due to trauma, stroke, or tumors.
- Potentially life-threatening, as it can lead to increased intracranial pressure, neurological deficits, and herniation.
D. Ascites:
- Edema within the peritoneal cavity, commonly associated with liver cirrhosis, malignancies, or congestive heart failure.
- Abdominal distension, discomfort, and respiratory compromise are typical manifestations.
III. Diagnostic Approach:
A. Clinical Examination:
- Careful assessment of the patient's medical history, physical symptoms, and risk factors.
This is a powerpoint presentation on the Topic of Male and female genital tract, based on Robbin's textbook of pathology. Prepared by Dr. Ashish Jawarkar, who is Assistant professor at Parul institute of medical sciences and research, Vadodara. Please subscribe to our youtube channel https://www.youtube.com/channel/UCwjkzK-YnJ-ra4HMOqq3Fkw . Our facebook page: facebook.com/pathologybasics
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This is a presentation covering all techniques in histopathology. Comprehensive coverage of all related aspects.. Useful for postgraduate Pathology students and practitioners.
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Dear all, Pathologybasics is out with a new series of power point presentations on General Pathology.. Following is link presentation on amyloidosis covered in chapter 6 of Robbins. Remaining topics will be uploaded as a separate presentation soon.
Dear all, Pathologybasics is out with a new series of power point presentations on Systemic Pathology.. Following is link presentation on 12th chapter of robbins - the heart.This presentation includes valvular heart diseases, endocarditis, cardiomyopathies, pericardial diseases and tumors of the heart. Remaining topics will be uploaded as a separate presentation soon.
This is a series of notes on clinical pathology, useful for postgraduate students and practising pathologists. It covers all internal and external quality control techniques. The topics are presented point wise for easy reproduction.
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Medical Technology Tackles New Health Care Demand - Research Report - March 2...pchutichetpong
M Capital Group (“MCG”) predicts that with, against, despite, and even without the global pandemic, the medical technology (MedTech) industry shows signs of continuous healthy growth, driven by smaller, faster, and cheaper devices, growing demand for home-based applications, technological innovation, strategic acquisitions, investments, and SPAC listings. MCG predicts that this should reflects itself in annual growth of over 6%, well beyond 2028.
According to Chris Mouchabhani, Managing Partner at M Capital Group, “Despite all economic scenarios that one may consider, beyond overall economic shocks, medical technology should remain one of the most promising and robust sectors over the short to medium term and well beyond 2028.”
There is a movement towards home-based care for the elderly, next generation scanning and MRI devices, wearable technology, artificial intelligence incorporation, and online connectivity. Experts also see a focus on predictive, preventive, personalized, participatory, and precision medicine, with rising levels of integration of home care and technological innovation.
The average cost of treatment has been rising across the board, creating additional financial burdens to governments, healthcare providers and insurance companies. According to MCG, cost-per-inpatient-stay in the United States alone rose on average annually by over 13% between 2014 to 2021, leading MedTech to focus research efforts on optimized medical equipment at lower price points, whilst emphasizing portability and ease of use. Namely, 46% of the 1,008 medical technology companies in the 2021 MedTech Innovator (“MTI”) database are focusing on prevention, wellness, detection, or diagnosis, signaling a clear push for preventive care to also tackle costs.
In addition, there has also been a lasting impact on consumer and medical demand for home care, supported by the pandemic. Lockdowns, closure of care facilities, and healthcare systems subjected to capacity pressure, accelerated demand away from traditional inpatient care. Now, outpatient care solutions are driving industry production, with nearly 70% of recent diagnostics start-up companies producing products in areas such as ambulatory clinics, at-home care, and self-administered diagnostics.
The Importance of Community Nursing Care.pdfAD Healthcare
NDIS and Community 24/7 Nursing Care is a specific type of support that may be provided under the NDIS for individuals with complex medical needs who require ongoing nursing care in a community setting, such as their home or a supported accommodation facility.
R3 Stem Cells and Kidney Repair A New Horizon in Nephrology.pptxR3 Stem Cell
R3 Stem Cells and Kidney Repair: A New Horizon in Nephrology" explores groundbreaking advancements in the use of R3 stem cells for kidney disease treatment. This insightful piece delves into the potential of these cells to regenerate damaged kidney tissue, offering new hope for patients and reshaping the future of nephrology.
Defecation
Normal defecation begins with movement in the left colon, moving stool toward the anus. When stool reaches the rectum, the distention causes relaxation of the internal sphincter and an awareness of the need to defecate. At the time of defecation, the external sphincter relaxes, and abdominal muscles contract, increasing intrarectal pressure and forcing the stool out
The Valsalva maneuver exerts pressure to expel faeces through a voluntary contraction of the abdominal muscles while maintaining forced expiration against a closed airway. Patients with cardiovascular disease, glaucoma, increased intracranial pressure, or a new surgical wound are at greater risk for cardiac dysrhythmias and elevated blood pressure with the Valsalva maneuver and need to avoid straining to pass the stool.
Normal defecation is painless, resulting in passage of soft, formed stool
CONSTIPATION
Constipation is a symptom, not a disease. Improper diet, reduced fluid intake, lack of exercise, and certain medications can cause constipation. For example, patients receiving opiates for pain after surgery often require a stool softener or laxative to prevent constipation. The signs of constipation include infrequent bowel movements (less than every 3 days), difficulty passing stools, excessive straining, inability to defecate at will, and hard feaces
IMPACTION
Fecal impaction results from unrelieved constipation. It is a collection of hardened feces wedged in the rectum that a person cannot expel. In cases of severe impaction the mass extends up into the sigmoid colon.
DIARRHEA
Diarrhea is an increase in the number of stools and the passage of liquid, unformed feces. It is associated with disorders affecting digestion, absorption, and secretion in the GI tract. Intestinal contents pass through the small and large intestine too quickly to allow for the usual absorption of fluid and nutrients. Irritation within the colon results in increased mucus secretion. As a result, feces become watery, and the patient is unable to control the urge to defecate. Normally an anal bag is safe and effective in long-term treatment of patients with fecal incontinence at home, in hospice, or in the hospital. Fecal incontinence is expensive and a potentially dangerous condition in terms of contamination and risk of skin ulceration
HEMORRHOIDS
Hemorrhoids are dilated, engorged veins in the lining of the rectum. They are either external or internal.
FLATULENCE
As gas accumulates in the lumen of the intestines, the bowel wall stretches and distends (flatulence). It is a common cause of abdominal fullness, pain, and cramping. Normally intestinal gas escapes through the mouth (belching) or the anus (passing of flatus)
FECAL INCONTINENCE
Fecal incontinence is the inability to control passage of feces and gas from the anus. Incontinence harms a patient’s body image
PREPARATION AND GIVING OF LAXATIVESACCORDING TO POTTER AND PERRY,
An enema is the instillation of a solution into the rectum and sig
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As we watch Dr. Greene's continued efforts and research in Arizona, it's clear that stem cell therapy holds a promising key to unlocking new doors in the treatment of kidney disease. With each study and trial, we step closer to a world where kidney disease is no longer a life sentence but a treatable condition, thanks to pioneers like Dr. David Greene.
Empowering ACOs: Leveraging Quality Management Tools for MIPS and BeyondHealth Catalyst
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In this session, we will explore how a robust quality management solution can empower your organization to meet regulatory requirements and improve processes for MIPS reporting and internal quality programs. Learn how our MeasureAble application enables compliance and fosters continuous improvement.
Antibiotic Stewardship by Anushri Srivastava.pptxAnushriSrivastav
Stewardship is the act of taking good care of something.
Antimicrobial stewardship is a coordinated program that promotes the appropriate use of antimicrobials (including antibiotics), improves patient outcomes, reduces microbial resistance, and decreases the spread of infections caused by multidrug-resistant organisms.
WHO launched the Global Antimicrobial Resistance and Use Surveillance System (GLASS) in 2015 to fill knowledge gaps and inform strategies at all levels.
ACCORDING TO apic.org,
Antimicrobial stewardship is a coordinated program that promotes the appropriate use of antimicrobials (including antibiotics), improves patient outcomes, reduces microbial resistance, and decreases the spread of infections caused by multidrug-resistant organisms.
ACCORDING TO pewtrusts.org,
Antibiotic stewardship refers to efforts in doctors’ offices, hospitals, long term care facilities, and other health care settings to ensure that antibiotics are used only when necessary and appropriate
According to WHO,
Antimicrobial stewardship is a systematic approach to educate and support health care professionals to follow evidence-based guidelines for prescribing and administering antimicrobials
In 1996, John McGowan and Dale Gerding first applied the term antimicrobial stewardship, where they suggested a causal association between antimicrobial agent use and resistance. They also focused on the urgency of large-scale controlled trials of antimicrobial-use regulation employing sophisticated epidemiologic methods, molecular typing, and precise resistance mechanism analysis.
Antimicrobial Stewardship(AMS) refers to the optimal selection, dosing, and duration of antimicrobial treatment resulting in the best clinical outcome with minimal side effects to the patients and minimal impact on subsequent resistance.
According to the 2019 report, in the US, more than 2.8 million antibiotic-resistant infections occur each year, and more than 35000 people die. In addition to this, it also mentioned that 223,900 cases of Clostridoides difficile occurred in 2017, of which 12800 people died. The report did not include viruses or parasites
VISION
Being proactive
Supporting optimal animal and human health
Exploring ways to reduce overall use of antimicrobials
Using the drugs that prevent and treat disease by killing microscopic organisms in a responsible way
GOAL
to prevent the generation and spread of antimicrobial resistance (AMR). Doing so will preserve the effectiveness of these drugs in animals and humans for years to come.
being to preserve human and animal health and the effectiveness of antimicrobial medications.
to implement a multidisciplinary approach in assembling a stewardship team to include an infectious disease physician, a clinical pharmacist with infectious diseases training, infection preventionist, and a close collaboration with the staff in the clinical microbiology laboratory
to prevent antimicrobial overuse, misuse and abuse.
to minimize the developme
2. Overview
• Distribution of body water
• Edema and effusions
• Hyperaemia and congestion
• Haemostasis, haemorrhagic
disorders, thrombosis, DIC
• Embolism
• Infarction
• Shock
10. MECHANISMS OF EDEMA AND EFFUSION
• Increased hydrostatic pressure
– Increases in hydrostatic pressure are mainly caused by disorders that impair
venous return.
• If the impairment is localized (e.g., a deep venous thrombosis [DVT] in a lower
extremity), then the resulting edema is confined to the affected part.
• Conditions leading to systemic increases in venous pressure (e.g., congestive heart
failure) are associated with more widespread edema
• Reduced plasma colloid oncotic pressure
– Under normal circumstances albumin accounts for almost half of the total
plasma protein; conditions leading to inadequate synthesis or increased loss
of albumin from the circulation are common causes of reduced plasma
oncotic pressure
• Reduced albumin synthesis occurs mainly in severe liver diseases (e.g., end-stage
cirrhosis) and protein malnutrition
• An important cause of albumin loss is the nephrotic syndrome
13. Types –
Inflammatory
(Exudate)
& Non
inflammatory
(Transudate)
• These protein-rich exudates accumulate due to
increases in vascular permeability caused by
inflammatory mediators.
• Usually, inflammation-associated edema is
localized to one or a few tissues, but in systemic
inflammatory states, such as sepsis, that produce
widespread endothelial injury and dysfunction,
generalized edema may appear
Inflammation-related edema
• protein-poor fluids called transudates
• are common in many diseases, including heart
failure, liver failure, renal disease, and severe
nutritional disorders
Noninflammatory edema and effusions
17. Clinical
features
Subcutaneous edema –
is important primarily because it signals potential underlying
cardiac or renal disease
Pulmonary edema –
fluid collects in the alveolar septa around capillaries and impede
oxygen diffusion, but edema fluid in the alveolar spaces also
creates a favourable environment for bacterial infection
Pulmonary effusions
often accompany edema in the lungs
Peritoneal effusions (ascites)
resulting most commonly from portal hypertension are prone to
seeding by bacteria, leading to serious and sometimes fatal
infections
19. Morphology
• Gross
1. EDEMA
• Subcutaneous edema - can be diffuse or more
conspicuous in regions with high hydrostatic pressures.
• Dependent edema - Its distribution is often
influenced by gravity (e.g., it appears in the legs
when standing and the sacrum when recumbent)
• Pitting edema - Finger pressure over markedly
oedematous subcutaneous tissue displaces the
interstitial fluid and leaves a depression
20. Morphology
• Edema resulting from renal dysfunction
• periorbital edema - often appears initially
in parts of the body containing loose
connective tissue, such as the eyelids
• Pulmonary edema
• the lungs are often two to three times their
normal weight, and sectioning yields frothy,
blood-tinged fluid—a mixture of air, edema,
and extravasated red cells
• Brain edema
• Narrowed sulci and distended gyri, which
are compressed by the unyielding skull
21. Morphology
2. Effusions
• Transudative effusions are typically protein poor,
translucent and straw coloured
• Chylous effusion -peritoneal effusions caused by
lymphatic blockage which may be milky due to
the presence of lipids absorbed from the gut
• Exudative effusions - are protein-rich and often
cloudy due to the presence of white cells.
25. Hyperaemia
• An active process
• Arteriolar dilation leads to increased blood
flow
• E.g. at sites of inflammation or in skeletal
muscle during exercise
• Affected tissues turn red (erythema) because
of increased delivery of oxygenated blood.
27. Congestion
• Passive process
• Resulting from reduced outflow of blood
from a tissue
• It can be systemic, as in cardiac failure, or
localized, as in isolated venous obstruction
• Congested tissues take on a dusky reddish-
blue color (cyanosis) due to red cell stasis
and the presence of deoxygenated
haemoglobin
28. Pulmonary
congestion
• Acute pulmonary congestion exhibits
engorged alveolar capillaries, alveolar septal
edema, and focal intra-alveolar
haemorrhage. In
• Chronic pulmonary congestion - the septa
are thickened and fibrotic, and the alveoli
often contain numerous hemosiderin-laden
macrophages called heart failure cells
29. Venous congestion-
LIVER
• Acute hepatic congestion –
• the central vein and sinusoids are distended
• centrilobular hepatocytes may undergo
ischemic necrosis while the periportal
hepatocytes—better oxygenated because of
proximity to hepatic arterioles—may only
develop fatty change.
• Chronic passive hepatic congestion –
• the centrilobular regions are grossly red-
brown and slightly depressed (because of cell
death) and are accentuated against the
surrounding zones of uncongested tan liver
(nutmeg liver)
• Microscopically, there is centrilobular
haemorrhage, hemosiderin-laden
macrophages, and variable degrees of
hepatocyte dropout and necrosis
33. Definition
Haemostasis is a precisely orchestrated process
that occurs at the site of vascular injury
That culminates in the formation of a blood clot
Involving platelets, clotting factors, and
endothelium
Which serves to prevent or limit the extent of
bleeding
35. Events
1. Arterial
Vasoconstriction
• Occurs immediately,
markedly reduces blood
flow to the injured area
• Mediated by reflex
neurogenic mechanisms
• Augmented by the local
secretion of factors such
as endothelin
36. Events
2. Primary Haemostasis –
formation of platelet
plug (adherence,
activation,
aggregation)
• Disruption of the
endothelium exposes
subendothelial von
Willebrand factor (vWF) and
collagen, which promote
platelet adherence and
activation
• Activation of platelets results
release of secretory granules
• Within minutes the secreted
products recruit additional
platelets, which undergo
aggregation to form a
primary haemostatic plug
37. Events
3. Secondary
Haemostasis –
deposition of fibrin
• Tissue factor is exposed at the
site of injury
• Tissue factor binds and activates
factor VII, setting in motion a
cascade of reactions that
culminates in thrombin
generation
• Thrombin cleaves circulating
fibrinogen into insoluble fibrin,
creating a fibrin meshwork
• This sequence, referred to as
secondary haemostasis,
consolidates the initial platelet
plug
38. Events
4. Clot stabilization and
resorption
• Polymerized fibrin and
platelet aggregates
undergo contraction to
form a solid permanent
plug that prevents further
haemorrhage
• At this stage,
counterregulatory
mechanisms (e.g., tissue
plasminogen activator, t-
PA) are set into motion that
limit clotting to the site of
injury and eventually lead
to clot resorption and
tissue repair.
40. Role of -
Platelets
• Platelets main role is in primary haemostasis
• Their function depends on several glycoprotein
receptors, a contractile cytoskeleton, and two
types of cytoplasmic granules.
1. α-Granules
1. have the adhesion molecule P-selectin on
their membranes
2. contain proteins involved in coagulation, such
as fibrinogen, coagulation factor V, and vWF
3. protein factors that may be involved in
wound healing, such as fibronectin, platelet
factor 4 (a heparin-binding chemokine),
platelet-derived growth factor (PDGF), and
transforming growth factor-β.
2. Dense (or δ) granules
1. contain adenosine diphosphate (ADP) and
adenosine triphosphate, ionized calcium,
serotonin, and epinephrine.
42. Role of – Clotting cascade
• The coagulation cascade is series of amplifying enzymatic reactions
that leads to the deposition of an insoluble fibrin clot
43. Role of –
Coagulation
cascade
PT and aPTT
• PT (Prothrombin time) and aPTT (Activated partial
thromboplastin time) assays are of great utility in
evaluating coagulation factor function in patients
• PT
• Tissue factor, phospholipids, and calcium are added to
plasma and the time for a fibrin clot to form is
recorded
• Assesses the function of the proteins in the extrinsic
pathway (factors VII, X, V, II, and fibrinogen)
• aPTT
• In this assay, clotting of plasma is initiated by addition
of negative charged particles (e.g., ground glass) that
activate factor XII (Hageman factor) together with
phospholipids and calcium, and the time to fibrin clot
formation is recorded.
• Screens the function of the proteins in the intrinsic
pathway (factors XII, XI, IX, VIII, X, V, II, and fibrinogen)
45. Role of – Coagulation cascade
Limiting coagulation and fibrinolysis
• Once initiated, coagulation must be restricted to
the site of vascular injury to prevent deleterious
consequences
• Limiting factors
1. Dilution; blood flowing past the site of
injury washes out activated coagulation
factors, which are rapidly removed by the
liver.
2. Negatively charged phospholipids which
are mainly provided by platelets that have
been activated are required for
coagulation, are in short supply
3. fibrinolytic cascade that limits the size of
the clot and contributes to its later
dissolution
46. Role of – Coagulation cascade
Fibrinolytic system
• Fibrinolysis is largely accomplished
through the enzymatic activity of
plasmin which breaks down fibrin
• Plasmin is generated by enzymatic
catabolism of precursor
plasminogen, by t-PA (tissue
plasminogen activator)
• This characteristic makes t-PA a
useful therapeutic agent
• Once activated, plasmin is in turn
tightly controlled by
counterregulatory factors such as α2-
plasmin inhibitor
• An elevated level of breakdown
products of fibrinogen (often called
fibrin split products), most notably
fibrin-derived D-dimers, are a useful
clinical markers of several thrombotic
states
47. Role of Endothelium
• The balance between the anticoagulant
and procoagulant activities of
endothelium often determines whether
clot formation, propagation, or
dissolution occurs
• if injured or exposed to proinflammatory
factors, endothelial cells lose many of
their antithrombotic properties
• Antithrombotic factors include –
• Platelet inhibition
• Anticoagulant effects
• Fibrinolysis effects
50. Defects in primary haemostasis
(platelets defects and von Willebrand disease)
• Present with small bleeds in skin or
mucosal membranes
• These bleeds typically take the form
of
• petechiae, minute 1- to 2-mm
haemorrhages or
• purpura, which are slightly larger (≥3
mm)
52. Defects in secondary hemostasis
(coagulation factor defects)
• Present with bleeds into soft tissues (e.g.,
muscle) or joints (hemarthrosis) following
minor trauma
• Particularly characteristic of haemophilia
54. Defects involving small vessels
• Present with “palpable purpura” and
ecchymoses
• Ecchymoses (sometimes simply called bruises)
are hemorrhages of 1 to 2 cm in size
• Characteristic of systemic disorders that disrupt
small blood vessels (e.g., vasculitis) or that lead
to blood vessel fragility (e.g., amyloidosis,
scurvy)
59. 2. Alterations
in normal
blood flow
• Normal blood flow is laminar
• Stasis and turbulence therefore
• Promote endothelial activation
• Disrupt laminar flow and bring
platelets into contact with the
endothelium
• Prevent washout and dilution of
activated clotting factors by fresh
flowing blood
61. Heparin induced
thrombocytopenia
Syndrome (HIT)
• HIT occurs following the administration of
unfractionated heparin, which may induce the
appearance of antibodies against heparin and
platelets
• Binding of these antibodies to platelets results
in their activation, aggregation, and
consumption (hence the thrombocytopenia)
• This effect on platelets and endothelial damage
induced by antibody binding combine to
produce a prothrombotic state, even in the face
of heparin administration
• Low-molecular-weight heparin preparations
induce HIT less frequently
62. Anti
phospholipid
antibody
syndrome
• Most important pathologic effects of antibodies are
mediated through binding of to epitopes on protein
antigens that are somehow induced or “unveiled” by
phospholipids
• In APLA, suspected antibody targets include β2-
glycoprotein I, a plasma protein that associates with the
surfaces of endothelial cells
• In vivo, it is suspected that these antibodies induce a
hypercoagulable state through uncertain mechanisms.
• This syndrome (previously called the lupus anticoagulant
syndrome) has protean clinical manifestations, including
• recurrent thromboses,
• repeated miscarriages,
• cardiac valve vegetations, and
• thrombocytopenia.
• The antibodies also frequently give a false-positive
serologic test for syphilis because the antigen in the
standard assay is embedded in cardiolipin.
65. Morphology
of thrombus
• Arterial or cardiac thrombi
• usually begin at sites of turbulence or
endothelial injury, whereas
• Venous thrombi
• characteristically occur at sites of
stasis.
66. Morphology of thrombus
Arterial thrombi Venous thrombi
Begin at the site of turbulence Occurs at site of stasis
Grow retrograde (towards heart) Extend in direction of blood flow (towards
heart)
Arterial thrombi are occlusive Venous thrombi are also occlusive
consist of a friable meshwork of platelets, fibrin,
red cells, and degenerating
Leukocytes, superimposed on a ruptured
atherosclerotic plaque
tend to contain more enmeshed red cells (and
relatively few platelets) and are therefore
known as red, or stasis,
thrombi.
Most common sites in decreasing order of
frequency are the coronary, cerebral, and
femoral arteries
veins of the lower extremities are most
commonly involved (90% of cases); however,
upper extremities, periprostatic plexus, or the
ovarian and periuterine veins
67.
68. Morphology
of thrombus
• Antemortem thrombi
• Have grossly and microscopically apparent
laminations called lines of Zahn, which are
pale platelet and fibrin deposits alternating
with darker red cell–rich layers
• focally attached to the underlying vascular
surface
• Postmortem thrombi
• gelatinous and have a dark red dependent
portion where red cells have settled by
gravity and a yellow “chicken fat” upper
portion,
• usually not attached to the underlying
vessel wall.
69. Morphology of thrombus
Mural thrombi
• Occurring in heart chambers or in the
aortic lumen
• Due to
• Abnormal myocardial contraction
(arrhythmias, dilated cardiomyopathy, or
myocardial infarction)
• Endomyocardial injury (myocarditis or
catheter trauma)
• Ulcerated atherosclerotic plaque and
aneurysmal dilation
76. Arterial and
cardiac
thrombi
Arterial thrombi
• The chief clinical problem is more related
to occlusion of a critical vessel (e.g., a
coronary or cerebral artery)
• They can also embolize and cause
downstream infarctions
Venous thrombi
• Venous thrombi can cause painful
congestion and edema distal to an
obstruction
• mainly of concern due to their tendency
to embolize to the lungs
78. Disseminated intravascular
coagulation (DIC)
• Disorders ranging from obstetric complications to advanced
malignancy to sepsis can cause DIC
• DIC leads to widespread formation of thrombi in the
microcirculation.
• These microvascular thrombi can cause diffuse circulatory
insufficiency and organ dysfunction, particularly of the brain,
lungs, heart, and kidneys.
• To complicate matters, thrombosis “uses up” platelets and
coagulation factors (hence the synonym consumptive
coagulopathy) and often activates fibrinolytic mechanisms.
• Thus, symptoms initially related to thrombosis can evolve into a
bleeding catastrophe, such as haemorrhagic stroke or
hypovolemic shock.
82. Embolism
• Detached intravascular solid, liquid, or gaseous mass
• That is carried by the blood from its point of origin to a
distant site
• Where it often causes tissue dysfunction or infarction
84. Pulmonary embolism
• Pulmonary emboli originate from deep venous
thromboses
• Are carried through progressively larger veins and the
right side of the heart before slamming into the
pulmonary arterial vasculature.
• Depending on the size of the embolus, it can occlude
• Main pulmonary artery,
• Straddle the pulmonary artery bifurcation (saddle embolus),
• Pass out into the smaller, branching arteries
• Most pulmonary emboli (60% to 80%) are clinically
silent
• Sudden death, right heart failure (cor pulmonale), or
cardiovascular collapse occurs when emboli obstruct
60% or more of the pulmonary circulation
85. Systemic thromboembolism
• Most systemic emboli (80%) arise from intracardiac mural thrombi
• Arterial emboli can travel to a wide variety of sites; the point of arrest
depends on the source and the relative amount of blood flow that
downstream tissues receive
• Most come to rest in the lower extremities (75%) or the brain (10%)
86. Fat and marrow embolism
• After fractures of long bones /soft tissue trauma/burns
• Microscopic fat globules can be found in the pulmonary
vasculature
• Most cases are asymptomatic
• Fat embolism syndrome is the term applied when it is
symptomatic
• It is characterized by pulmonary insufficiency, neurologic symptoms, anemia
(rbc in fat emboli), and thrombocytopenia (platelets in fat emboli), and is fatal
in about 5% to 15% of cases.
87. Air embolism
• Air can be inadvertently introduced in circulation
• during obstetric or laparoscopic procedures
• consequence of chest wall injury
• Gas bubbles within the circulation can coalesce to form
frothy masses that obstruct vascular flow and cause distal
ischemic injury
• A larger volume of air, generally more than 100 cc, is
necessary to produce a clinical effect
89. Amniotic fluid embolism
• Ominous complication of labour and the immediate
postpartum period.
• The underlying cause is the infusion of amniotic fluid or
fetal tissue into the maternal circulation via a tear in the
placental membranes or rupture of uterine veins
92. Infarction
• An area of ischemic necrosis caused by
occlusion of either the arterial supply or the
venous drainage
• Examples
• Myocardial infarction following
atherosclerosis of coronary arteries
• Cerebral infarction (stroke) following DVT
• Pulmonary infarction following DVT
• Bowel following DVT
• Ischemic necrosis of the extremities
(gangrene) in diabetics
94. Causes
• Arterial
• Thrombosis or embolism
• Atherosclerosis
• Local vasospasm like Raynaud’s phenomenon
• Haemorrhage into an atheromatous plaque
• Extrinsic vessel compression (e.g., by tumour)
• Torsion of a vessel (e.g., in testicular torsion or bowel volvulus)
• Traumatic vascular rupture
• Vascular compromise by edema (e.g., anterior compartment
syndrome)
• Entrapment in a hernia sac
• Venous
• Although venous thrombosis can cause infarction, the more common
outcome is just congestion
• Infarcts caused by venous thrombosis are more likely in organs with a
single efferent vein (e.g., testis and ovary).
96. Types
Red infarcts White infarcts
Seen in tissues with
(1) with venous occlusions(e.g.,
testicular torsion),
(2) in loose, spongy tissues (e.g.,
lung) where blood can collect in
the infarcted zone,
(3) in tissues with dual circulations
(e.g., lung and small intestine)
that allow blood to flow from an
unobstructed parallel supply into
a necrotic zone,
(4) in tissues previously congested by
sluggish venous outflow
(5) when flow is re-established to a
site of previous arterial occlusion
and necrosis (e.g., following
angioplasty of an arterial
obstruction)
occur with arterial occlusions in solid
organs with end-arterial circulation
(e.g., heart, spleen, and kidney), and
where tissue density limits the
seepage of
blood from adjoining capillary beds
into the necrotic area.
98. Morphology
• Gross
• Wedge-shaped
• with the
occluded vessel
at the apex and
the periphery of
the organ
forming the base
• When the base is a
serosal surface
there may be an
overlying fibrinous
exudate.
99. Morphology
• Microscopy
• Ischemic coagulative
necrosis
• Acute inflammation is
present along the margins of
infarcts
• Most infarcts are ultimately
replaced by scar
101. Factors influencing infarct development
Anatomy of the vascular supply
• The availability of an alternative blood supply
• Lungs and liver have a blood supply that protects against infarction.
• In contrast, renal and splenic circulations are end-arterial, and vascular obstruction generally causes tissue death.
Rate of occlusion
• Slowly developing occlusions are less likely to cause infarction, because they provide time for development of collateral
pathways
Tissue vulnerability to hypoxia
• Neurons undergo irreversible damage when deprived of their blood supply for only 3 to 4 minutes.
• Myocardial cells die after 20 to 30 minutes of ischemia
• In contrast, fibroblasts within myocardium remain viable even after many hours of ischemia
Hypoxemia
• Understandably, abnormally low blood O2 content (regardless of cause) increases both the likelihood and extent of
infarction
104. Shock
• Shock is a state in which diminished
cardiac output or reduced effective
circulating blood volume impairs
tissue perfusion and leads to cellular
hypoxia
106. • Neurogenic shock - in the setting of an anaesthetic accident or a spinal cord injury
• Anaphylactic shock - IgE–mediated hypersensitivity reaction
• In both of these forms of shock, acute vasodilation leads to hypotension and tissue
hypoperfusion.
Shock - Types
108. Pathogenesis (septic shock)
• With a mortality rate exceeding 20%, septic shock ranks first among the
causes of death in intensive care units
• Its incidence is rising, ironically due to
• improvements in life support for critically ill patients
• growing ranks of immunocompromised hosts (due to chemotherapy,
immunosuppression, advanced age or HIV infection)
• the increasing prevalence of multidrug resistant organisms in the hospital
setting
• Septic shock is most frequently triggered by gram-positive bacterial infections,
followed by gram-negative bacteria and fungi
111. Stages of shock
1. An initial non-progressive phase during
which reflex compensatory
mechanisms are activated and
perfusion of vital organs is maintained
2. A progressive stage characterized by
tissue hypoperfusion and onset of
worsening circulatory and metabolic
imbalances, including lactic acidosis
3. An irreversible stage that sets in after
the body has incurred cellular and
tissue injury so severe that even if the
hemodynamic defects are corrected,
survival is not possible
112. Morphology
• The cellular and tissue changes induced by shock are essentially those of hypoxic
injury
• Adrenal gland - cortical cell lipid depletion
• Kidneys - acute tubular necrosis
• Lungs - diffuse alveolar damage
• Brain, heart, lungs, kidney, adrenal glands, and gastrointestinal tract - Fibrin-
rich microthrombi, particularly in the– due to disseminated intravascular
coagulation
• Petechial haemorrhages on serosal surface and the skin – due to consumption
of platelets and coagulation factors
114. Clinical features
• Patient presents with hypotension; a
weak, rapid pulse; tachypnoea; and
cool, clammy, cyanotic skin
• Rapidly, however, shock begets
cardiac, cerebral, and pulmonary
dysfunction, and eventually
electrolyte disturbances and
metabolic acidosis