The potential risk factors for POVL that are listed are:
- Obesity
- Long Prone Cases
- Anemia
- Pressure on the globe
- Hypotension
- Glaucoma
Cataracts is not a risk factor for POVL.
Enumerates the effect of different anesthetic agents on the CNS and compares their relative efficacy and safety in providing good outcome in neuroanesthesia
Enumerates the effect of different anesthetic agents on the CNS and compares their relative efficacy and safety in providing good outcome in neuroanesthesia
One of the hardest specialties is neuro anesthesia. When I initially started, I were so dumb founded. The things in brain did not only change, they become instantly harder. The drugs which were supposed to work now did not because the brain had developed edema or there was no blood supply. I worked real hard on this presentation. Took help from the textbooks and my teachers and has helped me. I hope you will found it somewhat helpful. Some of the answers are beyond the scope of this presentation due to the diversity of the field.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
7. Blood Flow to the Spinal Cord
Anterior Spinal Artery (1)
Anterior 2/3 of spinal cord
Posterior Spinal Arteries (2)
posterior 1/3 of spinal cord
These 3 arteries depend on a network of
collateral vessels to provide adequate blood
supply to the spinal cord.
8. Artery of Adamkiewicz
arteria radicularis magna
Largest most consistent
radicular artery
Located in the
thoracolumbar region
(T5-L3)
Supplies blood to the ASA
(anterior 2/3 of cord)
Responsible for most of
the spinal cord blood flow
beneath its point of entry
If obstructed Anterior
Artery Syndrome
9. Spinal Cord Blood Flow
Autoregulation determines the amount of blood
flow to the sp cd.
Limits: 50-150 mmHg. Outside these limits
pressure dependant.
Spinal cord blood flow increases when CO2
levels are high and decreases when CO2 levels
are low. (similar to cerebral blood flow)
Injury to the spinal cord alters both
autoregulation and CO2 responsiveness.
11. Spinal Cord Injury
Trauma Partial or Complete transection of the cord
Transections above C 3-5 = Diaphragmatic innervention
(ventilator required for survival)
Transections above T 1 = Quadraplegia
Transections above L4 = Paraplegia
Most Common C 5-7 & T 12 - L 1
(least protected / most mobile)
12. Acute Spinal Cord Injury
Spinal shock may begin within an hour after injury and
last from several minutes to several months, after which
reflex activity gradually returns:
Flacid paralysis
Complete loss of reflex and sensory activity below level
of lesion.
Loss of vasomotor tone, CV instability, Hypotension,
Bradycardia, Venous pooling.
Paralytic ileus with distension
Hypothermia
13. Scoliosis
Lateral curvature of the
spine, usually accompanied
by rotation.
Cobb angle is a method
used to measure the
curvature.
The greater the angle, the
greater the progression and
severity of complications.
14.
15. Causes of Scoliosis
Neuromuscular Scoliosis - the result of muscle
imbalance and lack of trunk control. (i.e. cerebral
palsy, muscular dystrophy, or leg length
discrepancy)
Congenital Scoliosis - the result of asymmetry of
the vertebrae secondary to congenital anomalies.
(i.e. hemivertebrae, failure of segmentation)
Idiopathic Scoliosis - no definite etiology.
Diagnosis of exclusion. Most common type
accounting for 80-85% of cases
16. Effects of scoliosis
Increased curvature =
narrowing of thoracic
cage, which leads to
abnormal CV and Pulm
function.
Increased curvature causes
increased co-morbidities
Restrictive lung
disease, dyspnea on
exertion, pulmonary
hypertension, cor pulmonale
and alveolar hypoventilation.
18. PROGRESSION OF RESPIRATORY DISEASE WITH
INCREASING DEGREE OF SCOLIOSIS
< 10 normal
> 25 increased PA pressures
> 40 surgery considered
> 65 restrictive lung disease
> 100 exertional dyspnoea
> 120 alveolar hypoventilation
19. NEUROMUSCULAR SCOLIOSIS – severe respiratory
dysfunction
weak resp muscles
ineffective cough, unable to clear secretions
incoordinate swallowing, impaired airway
defences
impaired central resp drive
exaggerated resp depressant effect of drugs
immobile, retain secretions
recurrent chest infections
23. Spinal Cord Injury & Succinylcholine
Succinylcholine- Induced Hyperkalemia.
Safe to administer Succs within first 48 hours after
spinal cord injury.
Avoid Succs in all spinal cord injuries after 48 hours
24. Epidural Steroid Injections
Methylprednisone 80 mg (smaller amounts
in diabetics who may be at increased risk for
formation of epidural abscess) is injected into
epidural space close to the nerve root.
The addition of 3-4 mL of local anesthetic
(lidocaine) to the injected solution produces
analgesia, confirming proper drug placement
26. Epidural Steroid Injection (cont.)
Few pts get relief from repeated injections if first one
was unsuccessful.
Relief can last from weeks to months - injections are
repeated every 3-4 months.
Little risk of serious complications ; Aseptic
meningitis and bacterial meningitis
Adrenal Suppression may occur but recovers in 1-3
months.
27. High Dose Steroid Therapy
(methylprednisone)
Acute Spinal Cord Injury
Severe spine disease undergoing major spinal surgery.
Recommendation = bolus dose of 30 mg/kg over 15
minutes, then 5.4 mg/kg/hr for 23 hrs, within 8 hours of
injury.
If therapy is started 8 hours after injury, the duration of
the methylprednisone therapy should be continued for
48 hours
Pitfalls = Immunosuppression,wound infections & GI
bleeds.
28. Tricyclic Antidepressants
• Useful for chronic pain, producing analgesic
effect via inhibition of reuptake of serotonin and
norepinephrine.
• Other benefits include: normalization of sleep
patterns, reduction in anxiety and depression.
29. Anticonvulsants
May have some efficacy in treatment of
chronic pain syndromes
Chronic anticonvulsants lead to an
increased resistance to non-depolarizing
neuromuscular relaxants
31. Management of Spinal Cord Injuries
Immediate management is critical.
Improper handling can cause further
damage and loss of functioning
Always assume there is a spinal cord
injury until it is ruled out
Immobilize
Prevent flexion, rotation or extension of
neck
Avoid twisting patient
32. Management cont’d
• Management is aimed at preventing
further injury and observing for
progression of neuro deficits
• Consists of emergency treatment
following an A-B-C-D-E sequence.
33. Airway Management
First priority.
Open airway with jaw-thrust maneuver.
Use bag-valve-mask device initially, if
necessary intubate.
High conc. of 02 will prevent bradycardia or
asystole for patients exhibiting signs of
neurogenic shock.
34. Breathing
Lesions above C5 level will cause partial to
complete diaphragmatic paralysis (diaphragm is
innervated at C3-5 levels).
Lesions at C5 and below will allow full
diaphragmatic movement, but intercostal muscles
(innervated at T1) and abdominal muscles
(innervated at T12) are affected.
35. Circulation
Cardiac output is affected by external or
internal hemorrhage and neurogenic
shock.
IV fluids
Blood transfusion
Vasopressors
37. Anesthesia Implications for
Acute Spinal Cord Transection
In-line stabilization of neck. Consider fiberoptic
intubation, especially if cervical spine injury is suspected.
Prepare for CV instability, position changes, mild blood
loss, ..
Guard against hypothermia.
Succinylcholine may be administered within the first 24
hrs of acute injury
Blood flow (maintain perfusion pressure, normal CO2)
SSEP, MEP, wake up test
38. Anesthesia Implications for
Chronic Spinal Cord Transection
Monitor for autonomic hyperreflexia. Have
rapid-acting vasodilators available.
Bradycardia / absence of compensatory
tachycardia (cardioaccelerators T1-4).
Use nondepolarizing muscle relaxants only.
Guard against hypothermia.
Position carefully (osteoporosis).
39. Autonomic Hyperreflexia
Sympathetic system reflex
response below the level of a
spinal cord transection.
At T5 or above.
After the resolution of
spinal shock.
Triggers : stimulation below
the level of injury.
44. Preoperative preparation
Clear chest infection .
Wake up test explaining.
Posibility of post operative mechanical
ventilation
Premedication: atropine?
Heavy sedation should be avoided in severe
scoliosis.?
45. Anesthetic Problems associated with
Scoliosis Surgery
Problems related to the patient:
Respiratory , cardiovascular
neuromuscular abnormalities or
syndromes.
46. Problems related to the surgery
Prone position
Blood loss and third space loss: solution?
Lengthy operation
Preservation and monitoring of spinal
cord function.
Heat loss.??
Postoperative visual loss.
47. Monitoring
Routine monitors:
oximeter, ECG, capnography, esophageal
stethoscope and core body temp
Arterial catheter to monitor beat to beat
changes.
CVP
Urinary catheter
Blood loss and replacement are
monitored.
Patient’s position
48. Induction of anesthesia
Two large IV lines
Suxamethonium. is avoided in paralyzed
patients or neuromuscular etiology.
Intermediate non depolarizing ms. relaxent
like Atracurium or Rcuronium is used for
intubation and maintenance of relaxation.
50. Prone position
Maintain alignment of head / neck, support
head in neutral position w/ pillow or head
holding device.
Avoid hyperextension of arms by tucking them
against the body or extending them <90
degrees alongside the head on armboards
Compression stockings to avoid the pooling of
blood.
Frequently examine
eyes, ears, chin, nose, shoulders, breasts, and
genitalia for areas of pressure.
51. Spinal Cord Protection
Methylprednisolone
Reestablish normotension, normooxia and normocarbia to avoid
secondary insult.
Instruct surgeon to decrease traction on spinal cord.
Monitoring of the spinal cord: wake up test, SSEP and MEPs
52. Post Op Visual Loss -POVL
Unkown Cause, may Risk Factors:
hypoperfusion +edema Hypotension
+stretching of the optic Anemia
nerve. Glaucoma
Long prone cases Preventative measures:
Keep IV fluid to reasonable
Large amounts of IV level
fluid. HCT > 27
MAP >70 mmHg
Avoid pressure on globe
53. SPINAL CORD MONITORING
The Wake Up Test:
2 assisstants
Monitors motor function, simple to
perform
Problems -
extubation/lines/hardware, air
embolism, awareness, false neg.
Containdications – paresis, uncoop.
Modified for use in small children
(withdrawal to tetanic stimulus)
55. MOTOR EVOKED POTENTIALS
MEP is basically an EMG potential
recorded over muscles in the hand or foot
in response to depolarization of the
motor cortex using transcranial stimulus.
MEP profoundly affected by anesthetic
agents, recordable only during TIVA
MEP cannot be recorded in the presence
of complete neuromuscular blockade.
56. Extubation of the patient
Extubation may be performed immediately
Extubation in the ICU
57. Indications for postoperative mechanical ventilation:
VC was < 30% of predicted.
Severe gas exchange abnormality (↑PaCO2).
Duchenne muscular dystrophy.
Severe CP.
Patient with congenital heart.
Severe face edema.
PaO2 on mask ↓70 mmHg
Respiratory rate > 35 breath /min.
59. Case Study
29 ys male pt. 110 kg. 9 days s/p MVA
SCI. hx = asthma, donated one kidney.
Planned surgery is a C1-3 Cervical
fusion. dx: occipitoatlantal instability?
61. Question
All of the following are potential risk factors for
POVL except for 2 of the following.
• A. Obesity
• B. Long Prone Cases
• C. Anemia
• D. Pressure on the globe
• E. Hypotension
• F. Glaucoma
• G. Cataracts
62. Question
• Paraplegia is the result of which of the following
injuries?
• A. Occlusion of the artery of adamkiewicz
• B. Spinal cord transection at C7
• C. Spinal cord transection at L2
• D. A & C are both correct
• E. All of the above are correct