Madelung deformity is an abnormality of the palmar ulnar part of the distal radial physis in which progressive ulnar and volar tilt develops at the distal radial articular surface, with dorsal subluxation of the distal ulna.
Avascular necrosis (AVN) or Aseptic Necrosis of the hip is caused by a disruption to the hip’s blood supply which results in the deterioration and often collapse of the ball of the thigh bone (femoral head). Early identification and treatment of the condition increases the likelihood that a patient’s hip will recover. Surgery may be required in severe cases to repair or revascularize (restore circulation) the hip or to replace the hip in neglected/end stage cases.
http://www.davidsfeldmanmd.com/specialties/avascular-necrosis-hip
hip osteoarthritis is most disabling condition and surgery is a consequence of the same. but if this condition can assess on time so it can be manageable with conservative treatment and decrease the prevalence of AVN. further life of an individual become better.
Hi ! Med Students . In this slide, you will learn a summary definition of elbow dislocation and subluxation their causes, symptoms and treatments. I hope this will help to make your notes. Good luck with your studies.
My seminar presentation slides. Please correct me if I've did something wrong in it. You can also leave any message thru my email, nurhanisahzainoren@gmail.com
Madelung deformity is an abnormality of the palmar ulnar part of the distal radial physis in which progressive ulnar and volar tilt develops at the distal radial articular surface, with dorsal subluxation of the distal ulna.
Avascular necrosis (AVN) or Aseptic Necrosis of the hip is caused by a disruption to the hip’s blood supply which results in the deterioration and often collapse of the ball of the thigh bone (femoral head). Early identification and treatment of the condition increases the likelihood that a patient’s hip will recover. Surgery may be required in severe cases to repair or revascularize (restore circulation) the hip or to replace the hip in neglected/end stage cases.
http://www.davidsfeldmanmd.com/specialties/avascular-necrosis-hip
hip osteoarthritis is most disabling condition and surgery is a consequence of the same. but if this condition can assess on time so it can be manageable with conservative treatment and decrease the prevalence of AVN. further life of an individual become better.
Hi ! Med Students . In this slide, you will learn a summary definition of elbow dislocation and subluxation their causes, symptoms and treatments. I hope this will help to make your notes. Good luck with your studies.
My seminar presentation slides. Please correct me if I've did something wrong in it. You can also leave any message thru my email, nurhanisahzainoren@gmail.com
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
Follow us on: Pinterest
Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
2. CLASSIFICATION
1)Immediate: (Occur atthetimeofinjury)
Systemic:
Local :
Hypovolaemic shock
Injury to major vessels, peripheral nerves, muscles and
tendons,, joints and viscera.
2)Early:
Systemic:
(occur on initial few days (1-2
days) after injury)
Hypovolaemic shock
ARDS and Fat embolism
syndrome.
DVT and pulmonary embolism
Crush syndrome
Aseptic traumatic fever
Septicaemia ( in open fractures)
Local: infection
Compartment syndrome
3. 3) Late : (Occur long time after injury)(1-2 weeks)
Delayed union
non union
Malunion
cross union
Others :
Avascular necrosis
Shortening
joint stiffness
Reflex sympathetic dystrophy (sudeck dystrophy)
myositis ossificans
Osteomyelitis
osteoarthritis
. Ischemic contrature
4. Sourceofhaemorrhage:
HYPOVOLEMIC SHOCK
a) External: In compound fractures, c or s injury to
major vessel
b) Internal: In blunt injury abdomen,&chest and
pelvic fractures etc.
Blood loss :
• Femoral shaft fractures range 1000 – 1500 ml.
• Pelvic fractures range 1500– 2000 ml.
• Tibial shaft fractures range 500 – 1500 ml.
6. Clinical features :
•Hypotension, Tachycardia
•Oliguria, Clouded sensorium
•Cool, clammy, moist skin.
•Increased respiratory rate, Low volume rapid / thready pulse.
•Sweating, Sunken eyeballs, Tongue – pale and dry
•Patient gradually becomes drowsy, BP falls and renal output
decreases ; patient may become unconscious and die.
7. management
Starts even before the cause is established
• Two large bore iv cannulas put
• Infuse 2000 ml of crystalloids (ringer lactate) followed by
colloid (haemaccel) and blood if needed
• Venous cut down & central line if peripheral
vasoconstriction is present
• Localise the site of bleed- if in body cavities, perform
chest aspiration or diagnostic peritoneal lavage.
Sometimes a simple x ray is enough.
• Chest bleeding----chest tube
• Abdominal bleeding---- laparotomy
• Blood loss from # ---- immobilisation
• Pelvis stabilisation c external fixator
• Advanced---- emergency angiography & embolisation of
vessel
9. c/f of ischemic limb
Pain palor
Paraesthesia pulseless
Paralysis
Diagnosis
Clinical
Doppler study
Angiogram (ischemia)
Consequences
No effect ( good collateral circulation)
Exercise ischemia
Ischaemic contracture
gangrene
10.
11. Injury to nerves
How damaged?
# fragments
Entrapment btw # fragment during reduction
Entrapment in callus /fibrous tissue
Sharp object direct injury
Consequences:
Neuropraxia ( compression) --- physiological disruption of
conduction. local myelin damage with nerve still intact
Axonotmesis (crush) --- discontinuity of axons
Neurotmesis – complete rupture of nerve
12. c/f:
neuropraxia: numbness & tingling sensation (
dermatomes)
axonotmesis: dec sensation & motor weakness
neurotmesis: complete loss of sensation & no power
13. Dx: clinical
Electromyography ( EMG)
nerve conduction study
MRI
Rx: neuropraxia : splint & vit B1/B6/B12
axonotmesis: exploration
end to end anast
nerve grafting
physiotherapy
14. ARDS (Acute Respiratory Distress Syndrome)
Respiratory distress following a trauma
release of Inflammatory cells and proteinaceous fluid
that accumulate in the alveolar spaces
Disruption of microvasculature of pulm system
decrease in diffusing capacity and hypoxemia.
Onset- 24 hours after injury
16. Fat embolism syndrome
One of the most serious comp
Seen in fracture of long bone ( # shaft femur)
Pathogenesis ( 2 theories)
# bone
Hormonal changes thrombosis
FAT
Lipase
FREE FATTY ACID plt & firbin agg
Release into circulation vasculitis
Attack wall of vessels
17. 2)Disrupted bone marrow /adipose tissue
fat globules forced into torn venules
lung capillaries
18. c/f
made clinically ( 24 to 72 hrs)
Pulm: tachypnoea
spo2 < 50%
resp distress
Cerebral: drowsy
restlessness
disoriented
coma
Others: petechial rash
conjunctival petechia
retinopathy
tachycardia
22. DEEP VEIN THRMBOSIS AND
PULMONARY EMBOLISM
Is common in lower limb injuries, pelvic fractures and
spinal injury.
Commonly occurs in leg veins (calf)/ but may also
involve thigh.
Pulmonary embolism is a complication of DVT where
clot is detached from its site of formation and passes
via I.V.C. and right heart to pulmonary arteries
which may lead to collapse and sudden death.
25. c/f ( DVT)
oedema
Erythema
dilated veins of the leg
Dull aching or nagging pain in calf muscles.
Superficial blebs in the skin, skin red and warm.
Low grade fever with increased pulse rate is characteristic.
Patient complains of swelling, difficulty in standing, walking and cramps
in the leg.
26. Diagnosis
Dvt:
Homans test : Forcible dorsiflexion at foot ----- calf or
popliteal region pain.
Constrast venography
Doppler ultrasound
D-dimers
Pulmonary embolism
D-dimer
Blood gas- resp alkalosis
Ecg- S1Q3T3
CXray
CT pulm angiography (gold standard test)
V/Q Scan
27. treatment
DVT
Prophylaxis
1)Active/ passive calf pump and toe
movement
2)Elevation
3)Deep breathing exercise
4)Elastic TED stockings
5)Early internal fixation to provide
early mobility.
Management
1)Bed rest
2)Elevation
3)Inj LMWH
4)Warfarin
5)Venous bypass
6)IVC filters
PE
Management
1)Pulm support
2)Anticoagulant
OR thrombolysis
3)Surgical embolectomy
4)IVC filter
29. c/f ( ARF) appear within 2 -3 days
1)Oliguria
2)Hyperkalemia & m/b acidosis
3)Dec urine output
4) Restlessness
5) Delirium
Treatment
Prophylaxis
Application of tourniquet and gradual release to slowly
allow the myoglobin to reach the kidneys
Management
rx as acute renal failure – aggressive fluid resuscitation
maintenance of electrolyte
imbalance
30. • What is Compartment syndrome?
An elevation of the interstitial pressure in a closed
osteofascial compartment that results in
microvascular compromise.
Compartment syndrome
31. • Compartments are groups of
muscles surrounded by
inelastic fascia.
• Increased pressure within a
muscle compartment causes
decreased blood supply to
affected muscles.
• Any swelling of muscles leaves
no room for expansion and
blood supply is progressively
shut off.
• If affected muscles are
deprived of blood supply for
> 6 hours, nerve and muscle
tissue can be permanently
damaged.
32. etiology
1) Decrease compartment size
-Tight dressings/closure of fascial defect
-External pressures : casts, splints ,lying on limb for long
period,
2)Increase compartment contents
Hemorrhage -- vascular injury, coagulopathy
Muscle edema -- severe exercise , crush injury
Burn -- increase capillary permeability
33. Pathophysiology
This vicious cycle continues
until total vascularity of mm
& nerves within compartment
is compromised
Leading to mm necrosis & nerve
damage
Necrotic mm undergo healing
with fibrosis
contactures
34. Clinical Presentation:
• Swelling/ Tightness of compartment
• pain out of proportion
• decrease power in mm within affected comp
• Pallor/Cyanosis
• Hyperesthesia/Paresthesia
• Paralysis : full recovery is rare
35. diagnosis
1) Stretch test ( earliest sign)
Pain on passive stretching of mmm
Ex: passive extension of fingers --- pain flexor comp of
forearm
2) Measure pressure in each compartment
>40mm h2o
36.
37. treatment
Limb elevation & active movement as prevention
Remove any bandage /slab /cast then readjust
Early surgical decompression within 6hrs
Like fasciotomy & fibulectomy(middle 3rd of fibula is
excised to decompress all comp of legs)
38. Delayed & non union
Delayed union : When a fracture takes more than the
usual time to unite
Non union : When the process of healing stops before
completion. To diagnose non union the fracture has
to be minimum 6 months old & progressive
evaluation of xray done.
39.
40. TYPES
1. Atrophic: no or minimal callus formation
2. Hypertrophic: callus is present but it does not
bridge the fracture site.
COMMON SITES
Neck of femur
Scaphoid
Lower third of tibia
Lower third of ulna
Lateral condyle of humerus
41. C/F
Persistent Pain
Increase deformity @ fracture site ( non union)
Abnormal mobility(non union)
Refracture
Radiological findings
Delayed union: inadequate callus, visible fracture
line
Non union: ends are rounded, smooth sclerotic.
Medullary cavity may be obliterated. visible fracture
line.
42.
43. treatment
1)Asymptomatic – no Rx ( scaphoid)
2)ORIF & bone grafting
3)Excision & replacement by prothesis ( THR)
4) ILIZAROV’s mtd:
44. MALUNION
MALUNION : When a fracture does not unite in
proper position
Causes:
1.Improper reduction
2.Unchecked muscle pull ( # clavicle)
3.Excessive comminution ( colle’s #)
Common sites: supracondylar # of humerus
colle’s #
olecranon #
# both forearm bone
45. C/F
Deformity
Shortening of limb
Limitation of movements
Treatment
1.osteoclasis:
2.Redoing the fracture surgically: most common. ORIF
is generally done along with bone grafting.
3.Corrective osteotomy:
4.Excision of protruding bone.
46. Cross union : 2 bones unites with each other
common in # forearm
47. shortening
Common comp of malunion, crushing, growth defect
Treatment:
<2cm : not noticeable
shoe raise
>2cm : elderly: shoe raise
young: limb length equalisation procedure
48. Avascular necrosis
# blood supply to a part of bone
necrosis of that part
Common sites:
Site
-head of the femur
-Proximal pole of scaphoid
-Body of talus
Cause
-fracture neck of femur
-post disclocation of hip
-# thru waist of scaphoid
- # thru neck of talus
49.
50. c/f
1)Early stage – asymptomatic
2)Later stage – 2* osteoarthristis
Painful limitation of joint movement
Stiffness
Diagnosis:
Suspected in # where it is known to occur because pain and
stiffness appear late
51. Xray changes
1)Sclerosis of necrotic area; with revascularisation, new bone is
deposited around dead bone resulting in increase bone density
2)Subchondral cysts
3) deformity of bone because of collapse of necrotic bone
4)Osteoarthritis: dec joint space, osteophytes
52.
53. treatment
Prevented by early, energetic reduction
Rx:
1)Delay weight bearing for revascularisation
2)Revascularisation procedure by vascularised bone
graft
3)Excision of avascular segment not hampering
functions
4)Excision & prosthesis
5)Total joint rep or arthrodesis
55. Causes
1)Severe injury to a joint when capsule & periosteum
stripped from bone by violent disp of the fragments
2)Common in children: periosteum is loosely attached to
bone
3)Common arnd elbow jt
4)Massage foll trauma aggr myositis
Consequences / clinical features
1)Stiffness of jt
2)Restriction of jt
3)Complete loss of mvnt
56. Xray:
Active myositis: fluffy margins of bone mass
Mature myositis : trabeculated with well defined margins
Rx
Active: early ; rest, NSAIDS, physiotherapy
late: physiotherapy & french osteotomy
57. Sudeck’s dystrophy
Is a group of disorder where there is dysfunction in
the normal “ injury and repair process” leading to an
exaggerated response to anoxious stimulus.
Trauma is relatively minor and hence symptoms and
signs are out of proportion to the trauma
c/f
Pain
Hyperaesthesia
Tenderness
Swelling
Skin: red shiny warm ( early stage)
Late: prog atrophy of skin mm & nails
Joint deformities & stiffness