This document discusses pulmonary embolism (PE), including its definition, epidemiology, pathophysiology, risk factors, diagnosis, and treatment. PE refers to obstruction of the pulmonary artery or its branches by material originating elsewhere in the body. It affects around 5 million people annually worldwide and can be life-threatening. Diagnosis involves evaluating risk factors, symptoms, imaging tests like CT scans, and blood tests like D-dimer. Timely diagnosis and treatment are important to prevent right heart failure or death from PE.
whom that have sx of swelling leg, painful when walking and raise up leg, redness of leg skin, have history of accident or long journey u are suspected had deep vein thrombosis.
It is estimated that 20% of American women and 7% of American men suffer from venous disease. Venous disease results in symptoms such as aching, fatigue, swelling, and pain in the legs which can interfere with daily living.Cosmetic issues may affect quality of life.
At least 20% of patients with venous disease will develop leg ulcers. This presentation outlines the normal anatomy and physiology of venous drainage of the extremities as well as the common venous disorders such as varicose veins and deep vein thrombosis.
whom that have sx of swelling leg, painful when walking and raise up leg, redness of leg skin, have history of accident or long journey u are suspected had deep vein thrombosis.
It is estimated that 20% of American women and 7% of American men suffer from venous disease. Venous disease results in symptoms such as aching, fatigue, swelling, and pain in the legs which can interfere with daily living.Cosmetic issues may affect quality of life.
At least 20% of patients with venous disease will develop leg ulcers. This presentation outlines the normal anatomy and physiology of venous drainage of the extremities as well as the common venous disorders such as varicose veins and deep vein thrombosis.
Pulmonary embolism (PE) occurs when a blood clot gets lodged in an artery in the lung, blocking blood flow to part of the lung. Blood clots most often start in the legs and travel up through the right side of the heart and into the lungs.
Pulmonary embolism (PE) occurs when a blood clot gets lodged in an artery in the lung, blocking blood flow to part of the lung. Blood clots most often start in the legs and travel up through the right side of the heart and into the lungs.
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Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
3. PE refers to obstruction of the pulmonary artery
or one of its branches by material (eg, thrombus,
tumor, air, or fat ) that originated elsewhere in
the body
DEFINITIONS
5. PE
Epidemiology
Five million cases of venous thrombosis each year
10% of these will have a PE
10% will die
Correct diagnosis is made in only 10-30% of cases
Up to 60% of autopsies will show some evidence of past
PE
6. PE
Epidemiology
90-95% of pulmonary emboli originate in the deep
venous system of the lower extremities
Other rare locations include
Uterine and prostatic veins
Upper extremities
Renal veins
Right side of the heart
7. Risk Factors
CHF
Malignancy
Obesity
Estrogen/OCP
Pregnancy (esp post
partum)
Lower ext injury
Coagulopathy
Venous Stasis
Prior DVT
Age > 70
Prolonged Bed Rest
Surgery requiring > 30
minutes general
anesthesia
Orthopedic Surgery
8. Virchow’s Triad
Rudolf Virchow postulated more than a century ago
that a triad of factors predisposed to venous
thrombosis
Local trauma to the vessel wall
Hypercoagulability
Stasis of blood flow
It is now felt that pts who suffer a PE have an
underlying predisposition that remains silent until a
acquired stressor occurs
10. Vessel Wall Injury
Acute or chronic injury to vessel endothelium.
Leads to activation of platelets and clotting cascade.
Promotes thrombus formation.
15. Alternations in Coagulation
Increase in procoagulant factors.
By trauma to vascular wall or extravascular tissues.
Releases tissue thromboplastin and phospholipid.
Leads to formation of prothrombin activator.
Prothrombin Thrombin
16. Alterations in Coagulation
Decrease in anticoagulant factors.
Thrombomodulin
Antithrombin III
Heparin
Alpha2-Marcoglobulin
Plasmin
Leads to hypercoagulable state by formation of
thrombin.
17. Thrombosis Formation
Platelet nidus at site of injury.
Growth by aggregation of platelets and fibrin.
Activation of clotting cascade.
Larger growth to a red fibrin thrombus.
Thrombus fractures and embolizes to other areas of
the body.
18. Predisposing Factors or Diseases for
Development of PTE
Hypercoagulable state
Nephrotic syndrome
Immobilization
Amyloidosis
Early DIC
Hyperadrenocorticism
Capillary fragility
Activation of clotting cascade.
19. Predisposing Factors or Diseases for
Development of PTE
Hypercoagulable state
Capillary fragility
Diabetes Mellitus
Immune–mediated hemolyitc anemia
Sepsis
Hyperadrenocorticism
Activation of clotting cascade.
20. Factor V Leiden mutation
Protein C deficiency
Protein S deficiency
Antithrombin deficiency
Prothrombin gene mutation A20210
Anticardiolipin antibodies
Lupus anticoagulant
Hyperhomocystinemia
21. Predisposing Factors or Diseases for
Development of PTE
Hypercoagulable state
Capillary fragility
Activation of clotting cascade.
Sepsis
Pneumonia/pyothorax
Heartworm disease
Surgery
Bacterial endocarditis
Neoplasia
22. Factor V Leiden
Most frequent inherited predisposition to
hypercoagulability
Resistance to activated Protein C
Single point mutation (Factor V Leiden)
Single nucleotide substitution of glutamine for arginine
Frequency is about 3% in healthy American male .
23. PE
When venous emboli become dislodged from their site
of origin, they embolize to the pulmonary arterial
circulation or, paradoxically to the arterial circulation
through a patent foramen ovale
About 50% of pts with pelvic or proximal leg deep
venous thrombosis have PE
Isolated calf or upper extremity venous thrombosis pose
a lower risk for PE
29. Intrapulmonary Shunts
Blood that has not been to areas of ventilated lung and
enters systemic circulation without gas exchange
taking place.
Poorly oxygenated blood enters the arterial system
lowering the PaO2.
Not responsive to oxygen therapy.
30. Ventilation/Perfusion Inequality
V/Q inequality occurs when distribution of blood is
altered to the alveoli.
O2 increase in the alveoli and CO2 decreases.
31. Hemodynamic Changes
Increase in pulmonary vascular resistance.
Increased afterload to the right heart.
Can lead to circulatory collapse and shock.
32. Right Ventricular Dysfunction
Progressive right heart failure is the usual immediate
cause of death from PE
As pulmonary vascular resistance increases, right
ventricular wall tension rises and perpetuates further
right ventricle dilation and dysfunction
Interventricular septum bulges into and compresses
the normal left ventricle
33. Clinical Syndromes
Pts with massive PE present with systemic arterial
hypotension and evidence of peripheral thrombosis
Pts with moderate PE will have right ventricular
hypokinesis on echocardiogram but normal systemic
arterial pressure
Pts with small to moderate PE have both normal right
heart function and normal systemic arterial pressure
34. Well’s Criteria
Clinical Signs and Symptoms of DVT?
(Calf tenderness, swelling >3cm, errythema, pitting
edema affected leg only)
+3
PE Is #1 Diagnosis, or Equally Likely +3
Heart Rate > 100 +1.5
Immobilization at least 3 days, or Surgery in the
Previous 4 weeks
+1.5
Previous, objectively diagnosed PE or DVT? +1.5
Hemoptysis +1
Malignancy w/ Rx within 6 mo, or palliative? +1
>6: High Risk
2 to 6: Moderate Risk
2 or less: Low
Adapted with permission from Wells PS, Anderson DR, Rodger M, Ginsberg JS, Kearon C, Gent M, et al. Derivation of a simple
clinical model to categorize patients probability of pulmonary embolism: increasing the models utility with the SimpliRED d-dimer.
Thromb Haemost 2000;83:416-20.
35. Diagnosis
H&P
Always ask about prior DVT, or PE
Family History of thromboembolism
Dyspnea is the most frequent symptom of PE
Tachypnea is the most frequent physical finding
Dyspnea, syncope, hypotension, or cyanosis suggest a
massive PE
Pleuritic CP, cough, or hemoptysis
36. Signs of P.E.
Tachypnea
Rales
Tachycardia
Hypoxia
S4
Accentuated pulmonic component of S2
Fever: T <102 F
37. Signs in Massive P.E.
“Massive PE”: hemodynamic instability with SBP <90
or a drop in baseline SBP by >/=40mmHg for more
then 30 min
Signs as before PLUS:
Acute right heart failure
Elevated J.V.P.
Right-sided S3
Parasternal lift
38. P.E. & Leg Symptoms
Most patients with P.E. do not have leg symptoms at
time of diagnosis
Patients with leg symptoms may have asymptomatic
P.E.
39. Differential Diagnosis
USA, MI
Pneumonia
CHF
Asthma
Costochondritis, Rib Fx,
Pneumothorax
PE can coexist with other illnesses!!
41. Diagnosis
Serum Studies
D-dimer
Elevated in more than 90% of pts with PE
Reflects breakdown of plasmin and endogenous thrombolysis
Not specific: Can also be elevated in MI, sepsis, or almost any
systemic illness
Negative predictive value
ABG-contrary to classic teaching, arterial blood gases
lack diagnostic utility for PE
42. Diagnosis
CXR
Usually reveals a non specific abnormality. 14% normal
Classic abnormalities include:
Westermark’s Sign - focal oligemia
Hampton’s Hump - wedge shaped density
Enlarged Right Descending Pulmonary Artery (Palla’s sign)
43. Chest X-ray Eponyms of PE
Westermark's sign
A dilation of the pulmonary vessels proximal to the
embolism along with collapse of distal vessels,
sometimes with a sharp cutoff.
Hampton’s Hump
A triangular or rounded pleural-based infiltrate with the
apex toward the hilum, usually located adjacent to the
hilum.
43
49. How About This???
Westermark's Sign: an abrupt tapering of a vessel caused by
pulmonary thromboembolic obstruction.
This CXR shows enlargement of the left hilum accompanied by left
lung hyperlucency, indicating oligemia (Westermark's sign).
52. Lab Findings in P.E.
(ABG)
ABG:
Hypoxemia
Hypocapnia (low CO2)
Respiratory Alkalosis
Massive PE: hypercapnia, mix resp and metabolic
acidosis (inc lactic acid)
Patients with RA pulse ox readings <95% are at
increased risk of in-hospital complications, resp failure,
cardiogenic shock, death
53. Lab Findings in P.E. (BNP)
BNP (beta natruretic peptide)
Insensitive test
Patient’s with PE have higher levels than pts without,
but not ALL patients with PE have high BNP
Good prognostic value measure: if BNP >90
associated with adverse clinical outcomes (death, CPR,
mechanical vent, pressure support, thrombolysis,
embolectomy)
54. Lab Findings in P.E. (Troponin)
Troponin
High in 30-50% of pts with mod to large PE
Prognostic value if combined pro-NT BNP
Trop I >0.07 + NT-proBNP >600 = high 40 day mortality
55. Lab Findings in P.E.
(D-dimer)
D-dimer:
Degredation product of fibrin
>500 is abnormal
Sensitivity: High, 95% of PE pts will be positive
Specificity: Low
Negative Predictive Value: Excellent
56. Lab Findings in P.E. (cont’d)
EKG
2 Most Common finding on EKG:
Nonspecific ST-segment and T-wave changes
Sinus Tachycardia
Historical abnormality suggestive of PE
S1Q3T3
Right ventricular strain
New incomplete RBBB
60. Venous Ultrasonography
Relies on loss of vein compressibility as the primary
criterion
About 1/3 of pts will have no imaging evidence of
DVT
Clot may have already embolized
Clot present in the pelvic veins (U/S usually inadequate)
Workup for PE should continue even if dopplers (-)
in a pt in which you have a high clinical suspicion
61. V/Q Scan Historically, the principal imaging test for the
diagnosis of PE
A perfusion defect indicates absent or decreased
blood flow
Ventilation scan obtained with radiolabeled gases
A high probability scan is defined as two or more
segmental perfusion defects in presence of nl
ventilation scan
62. V/Q Scan
Useful if the results are normal or near normal, or if
there is a high probability for PE
As many as 40% of pts with high clinical suspicion for
PE and low probability scans have a PE on angiogram
64. Pulmonary Angiogram
Most specific test available for diagnosis of PE
Can detect emboli as small as 1-2 mm
Most useful when the clinical likelihood of PE differs
substantially from the lung scan result or when the
lung scan is intermediate probability
67. Echocardiogram
Useful for rapid triage of pts
Assess right and left ventricular function
Diagnostic of PE if hemodynamics by echo are consitent
with clinical
68. Spiral CT Scan
Identifies proximal PE (which are the ones usually
hemodynamically important)
Not as accurate with peripheral PE
73. SPIRAL CT SCAN
Criteria for PE extension:
obstruction index according to the scoring system
of Qanadli
∑ (n · d)
n = number of segmental
branches
d = obstruction degree
(1 if partial 2 if complete)
74. 2-slice CT
1992
2 x 2.7 mm
25 sec
4-slice CT
1998
4 x 1 mm
25 sec
64-slice
2004
64 x 0.625 mm
4 sec
16-slice CT
2002
16 x 0.75 mm
10 sec
PE at MDCT
77. Clinical probability assessment
Low or intermediate High (≈ 30%)
Diagnosis of PE in stable patients
D-dimer
Normal Elevated
PE excluded (≈30%)
Multi-detector CT
Positive for PE No PE
Treat
78. Echocardiography
RVD present No RVD
Diagnosis of PE in un-stable patients
Treat & stabilize
Multidetector CT
Search for alternative
diagnosis
79. Treatment
Begin treatment with either unfractionated
heparin or LMWH, then switch to warfarin
(Prevents additional thrombus formation and permits endogenous
fibrinolytic mechanisms to lyse clot that has already been formed,
Does NOT directly dissolve thrombus that already exists)
Warfarin for atleast 3 months, INR 2-3
80. Treatment
Pain Relief
Supplemental Oxygen
Dobutamine for pts with right heart failure and
cardiogenic shock
Volume loading is not advised because increased right
ventricular dilation can lead to further reductions in
left ventricular outflow
81. Anticoagulation
Start during resuscitation phase itself
If suspicion high, start emperic anticoagulation
Evaluate patient for absolute contraindication
(i.e.: active bleeding)
82. Anticoagulation (cont’d)
HEPARIN:
Lovenox: if hemodynamically stable, no renal function
1mg/kg BID OR 1.5mg/kg QDay
Heparin gtt: if hypotension, renal failure
80units/kg bolus then 18units/kg infusion
Goal PTT1.5 to 2.5 times the upper limit of normal
COUMADIN:
Start once acute anticoagulation achieved
Start with 5mg PO qday OR 10mg PO q day
If start with 10mg then achieve therapeutic INR 1.4 days sooner
Complications and morbidity no different in 5mg or 10mg start
Goal INR 2 to 3
83.
84.
85. Duration of Anticoagulation for DVT or
PE*
Event Duration Strength of
Recommendation
First Time event of
Reversible cause
(surgery/trauma)
At least 3 mos A
First episode of
idiopathic VTE
At least 6 mos A
Recurrent idiopathic
VTE or continuing risk
factor (e.g.,
thrombophilia, cancer)
At least 12 mos B
Symptomatic isolated
calf-vein thrombosis
6 to 12 weeks A
*From American College of Chest Physicians
86. Thrombolysis
Considered once P.E. diagnosed
If chosen, hold anticoagulation during
thrombolysis infusion, then resumed
Associated with higher incidence of major
hemorrhage
Indications: persistent hypotension, severe
hypoxemia, large perfusion defecs, right
ventricular dysfunction, free floating right
ventricular thrombus, paten foramen ovale
Activase or streptokinase
87. IVC Filter
Indication:
Absolute contraindication to anticoagulation (i.e.
active bleeding)
Recurrent PE during adequate anticoagulation
Complication of anticoagulation (severe bleeding)
Also:
Pts with poor cardiopulmonary reserve
Recurrent P.E. will be fatal
Patient’s who have had embolectomy
Prophylaxis against P.E. in select patients
(malignancy)
88. Embolectomy
Surgical or catheter
Indication:
Those who present severe enough to warrant
thrombolysis
In those where thrombolysis is contraindicated or fails
89. Recommendations Heparin therapy should be continued for at least five
days.
Oral anticoagulation should be overlapped with
heparin therapy for four to five days.
Heparin and warfarin therapy can be initiated
simultaneously, with heparin therapy discontinued
on day five or six if the INR has been therapeutic for
two consecutive days.
Longer periods of initial heparin therapy may be
considered in the case of massive pulmonary
embolism or iliofemoral thrombosis.
90. Recommendations
Therapy of acute deep vein thrombosis or
pulmonary embolism should be initiated with IV
heparin …
91. Recommendations Heparin therapy should be continued for at least five
days.
Oral anticoagulation should be overlapped with
heparin therapy for four to five days.
Heparin and warfarin therapy can be initiated
simultaneously, with heparin therapy discontinued
on day five or six if the INR has been therapeutic for
two consecutive days.
Longer periods of initial heparin therapy may be
considered in the case of massive pulmonary
embolism or iliofemoral thrombosis.
92. Recommendations
LMW heparin may be used in place of
unfractionated heparin.
Dosing requirements are individualized for each
product.
93. Recommendations
Duration of therapy
First thromboembolic event in the context of a
reversible risk factor
-- treated for three to six months
Idiopathic first thromboembolic event
-- AT LEAST full six months of treatment
-- further therapy at discretion of clinician
Recurrent venous thrombosis or a continuing risk
factor -- treated indefinitely.
94. Recommendations IVC filter placement is recommended when
-- anticoagulation is contraindicated
-- recurrent thromboembolism despite adequate
anticoagulation
-- chronic recurrent embolism with pulmonary
hypertension
-- high-risk of recurrent embolization
-- conjunction with the performance of pulmonary
embolectomy or endarterectomy
95. Treatment
IVC filter With filter 5% risk of
recurrent pulmonary
embolus, especially after 6
mos.
complication of leg swelling
can occur.
anticoagulation is continued
if possible.
96. Conclusion
PE is often a misdiagnosed clinical disorder.
Rapid identification and appropriate treatment may
often prevent unnecessary morbidity and mortality.