This document discusses various types and causes of glaucoma, including:
- Angle closure glaucoma which can be pre-trabecular, trabecular, or post-trabecular
- Neovascular glaucoma which involves the growth of new blood vessels in the angle
- Pigmentary and pseudoexfoliation glaucoma caused by pigment dispersion and buildup
- Lens-induced glaucoma from phacolytic mechanisms, particles, or phacoanaphylaxis
- Glaucoma caused by trauma, hemorrhage, tumors, corticosteroids, and after cataract surgery
Treatment options vary depending on the type and stage of glaucoma but
Ischemic condition affecting the eye.
The ischemia can occur secondary to systemically problem [or] particulary the eye.
Many retinal vascular disorders {like CRAO,CRVO,Diabetic retinopathy,Hypertensive Retinopathy} shows ischemic signs.
Ischemic condition affecting the eye.
The ischemia can occur secondary to systemically problem [or] particulary the eye.
Many retinal vascular disorders {like CRAO,CRVO,Diabetic retinopathy,Hypertensive Retinopathy} shows ischemic signs.
Heard of people being unable to see other people's faces if not fr failure of recognition of people's faces (prosapagnosia)...then they need to get their retina in particular macula checked! And a bunch of other macular disorders are enlisted nd elaborated in the presentation
Retinal Arterial Obstructions is a common eye disease that causes loss of vision due to the blockage of the blood flow, runs into the retina which is to be found in the back of your eye.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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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7. Stages of neovascular glaucoma.
(A)Pre-glaucoma stage with new vessels appearing at pupillary margin
and in angle.
(B) Open-angle glaucoma stage with new vessels spreading and
fibrovascular tissue covering angle.
(C) Heavy neovascularization and extensive peripheral anterior
synechiae.
(D) Regression stage with angle sealed and vessels less visible.
8.
9. Treatment options of neovascular glaucoma
• Atropine and steroids to decrease inflammation
• Beta-bockers
•intravitreal VEGF inhibitor injection
Panretinal photocoagulation
- in early cases
Artificial filtering devices
- in very advanced cases
Cyclodestructive procedures
- to relieve pain
Retrobulbar alcohol
injection to relieve pain
Topical
10.
11. (A)Membrane forms in one area of angle.
(B) Additional areas of angle are involved, and contraction of
membrane displaces pupil.
13. Pigmentary glaucoma
B/L condition due to pigment dispersion in AC
Risk factors is young adolescent male, whites, high
myopic, AD located at 7q35-36
Pathogenesis is rubbing of pig. Epi. Of iris against
zonules -> liberation of pig -> deposited in angle by
convection current in aq.
Signs are:- cornea – krukenberg’s spindle
AC – deep, homogeneous fine hyperpig.
over post. Trabeculum
Iris – radial, spoke like, mid peripheral
transillumination defect, concave iris
Lens – Scheie’s line/Zentmayer’s ring
Zonules - pigmentation
16. Exfoliation glaucoma
TM clogging up by PXF material &/or pig. From iris
Risk factors are –fem, in Scandinavia, mutation in
LOXL1 gene at 15q22 locus
Patho ---grey-white fibrillary extracellular material
composed of protein core surrounded by GAGs
produced by abnormal BM of ageing epi. Cells of
TM, equatorial lens capsule & CB.
Signs –cornea -> dandruff like deposi, in endo.
AC -> Sampolesi’s line
iris -> absence of pupi. Ruff, moth-eaten
trans illumination defect
lens -> cataract, exfo. Deposi. As central
disk with peri. Band & a clear zone in
middle
17. Pseudoexfoliation glaucoma
Pseudoexfoliative material Iris sphincter atrophy Gonioscopy
Central disc with
peripheral band
Trabecular hyperpigmentation
- may extend anteriorly
(Sampaolesi line)
On retroillumination
19. Lens induced glaucoma
1) PHACOLYTIC:-
. Due to protein leakage from mat./hypermat. cat
. mechanism is –a) high molecular wt. soluble
protein directly block
b)macrophages engulf the
proteins & block
. c/f – seen in elderly with h/o poor vision for mons
- acute onset of uniocular pain, redness & watering
- grossly decres. Vision & raised IOP
- signs of uveitis
-hypermat/ morgagnian cat
- AC shows heavy flare a/w hyper refringent crystals which are
ca++ oxalate / cholesterol crystals
. t/t – medical (hyperosmotic, CA inhi.,topical b-blockers & steroids
- surg ( ECCE with PCIOL)
21. Calcium oxalate crystal in the lens of a
patient with glaucoma associated with
hypermature cataract. (Hematoxylin and
eosin stain.)
Phacolytic glaucoma with bloated
macrophages and lens material
obstructing the trabecular
meshwork.
22. Contd…
2) LENS PARTICLE:-
. k/a phacotoxic uveitis
. Mechanism is – due to trauma/ surg.retained lens material
disruption of lens capsule
lens material liberation raised IOP
inflammatory response
raised IOP
. c/f – features of uveitis, rai IOP, chunky white particles in AC,
hypopyon
. Diag. by paracentesis
. t/t – medical as phacolytic
- surg. ( removal of lens material)
23. Contd…
3)PHACOANAPHYLAXIS :-
. occur when patients become sensitized to their own lens
protein k/a endophthalmitis anaphylactica
. typically develops after penetrating trauma or
extracapsular cataract extraction
. granulomatous inflammation of the lens with
polymorphonuclear leukocytes, lymphocytes, epithelioid
cells, and giantcells.
. t/t is surg. Removal of residual lens material
24. Glaucoma after trauma
1) CHEMICAL :-
. Alkali>acid
. caused by scleral shrinkage and release of active
substances, including prostaglandins
. IOP measured more accurately with the
pneumatic or MacKay-Marg tonometers
.managed by – medical ( topical and systemic
medications)
2) ELECTRIC :-
. pressure rise to venous dilation, contraction of
the extraocular muscles, and pigment dispersion
. No therapy due to transient rise of IOP
25. Contd…
3) RADIATION :-
. Mechanism are neovascularization/ ghost-cell
glaucoma associated with radiation retinopathy and
vitreous hemorrhage.
4) PENETRATING :-
. Due to retained organic material / FB / severe
inflammation / TM damage
5) CONTUSION :-
. can cause hyphema, iridocyclitis, iris sphincter tears,
iridodialysis, cyclodialysis, lens subluxation, retinal
tear or dialysis, retinal detachment, vitreous
hemorrhage, choroidal rupture, and glaucoma.
27. Glaucoma a/w intraocular
haemorrhage
1) GHOST CELL:-
.mecha. - retinal disease/ trauma/surgery /snake poisoning
vitreous haem.
degenerated RBC’s travel thr. Disruped ant
hyaloid face
obstructs TM
. Diag. by paracentesis & cyto. Exam. which shows HEINZ bodies
i.e. RBCs in the vitreous degenerate to tan-colored spheres
(ghost cells), which appear empty except for clumps of
denatured hemoglobin
. t/t is AC wash / pars plana vitrectomy to remove remaining ghost
cells
28. Contd…
2) HEMOLYTIC :-
. Due to macrophages laden with pigments, RBC’s &
debris
3) HEMOSIDEROSIS :-
. Due to iron liberted from Hb causing siderosis of
TM
4) HYPHEMA :-
. Due to blood & blood products
. Total hyphema changing color from red to black
(black-ball or eightball hyphema)
. t/t – topical anti glaucoma
- surgical removal of hyphema
29. Glaucoma a/w uveitis
. Mechanism are-
(1) increased viscosity of aqueous humor;
(2) obstruction of the trabecular meshwork by
inflammatory cells and debris
(3) swelling and dysfunction of the trabecular
meshwork;
(4) liberation of active substances such as
prostaglandins;
(5)scarring of the outflow channels;
(6) development of a cuticular endothelial membrane
over the angle;
(7) neovascularization;
(8) elevation of episcleral venous pressure;
30. Contd…
Causes are:-
1) FUCH’S HETEROCHROMIC
IRIDOCYCLITIS
. Mild form of anterior uveitis associated with
cataract and glaucoma.
.c/f – mild uveitis, fine filaments on the
endothelium between the keratic precipitates, a
patchy loss of the iris pigment epithelium,
hypochromia, grey-white nodules on the anterior
iris, a few opacities in the anterior vitreous, and
chorioretinal scars
. Gonioscopy reveals fine vessels that bridge the
angle
31. Contd…
2) GLAUCOMATOCYCLITIC CRISIS:-
. k/a POSNER – SCHLOSSMAN SYNDROME
. young to middle-aged adults and consists of
recurrent episodes of mild anterior uveitis and
marked elevations of IOP
. mild ciliary flush, a dilated or sluggishly reactive
pupil, corneal epithelial edema, IOP in the range
of 40–60 mmHg, decreased outflow facility, open
angles, faint flare, and 1–20 fine
keratic precipitates
32. Contd…
3) JRA:-
. most common in young girls with iridocyclitis and
monoarticular or pauciarticular involvement
. Due to inflammation of the trabecular meshwork
4) HERPES :-
. Due to trabeculitis , inflamm. Of TM
. Commonly in disciform & necrotising sromal type
5) SYPHILIS:-
. Due to acute interstitial keratitis
33. Contd…
6) SARCOIDOSIS:-
. swelling and dysfunction of the trabecular meshwork,
obstruction of the trabecular meshwork by inflammatory
cells and debris
7) PRECIPITATES IN THE TM
Diag. by lab. & imaging technique
t/t- medical ( topical, sys. & periocular steroids, cycloplegics,
NSAIDS, immunomodulators, anti glaucoma)
- surg (ALT, filtering procedure, tube shunts, cycloablative,
Nd:YAG laser cyclophotocoag.)
34. Glaucoma a/w intraocular
tumors
Mechanisms are:-
(1) direct extension of the tumor into the trabecular
meshwork
(2) seeding of tumor cells into the outflow channels
(3) pigment dispersion
(4) inflammation
(5) Hemorrhage,inducing hemolytic glaucoma, and
suprachoroidal hemorrhage
(6) neovascularization of the angle
(7) obstruction of the trabecular meshwork by
macrophages containing melanin released by a
necrotic tumor (melanomalytic glaucoma)
37. Corticosteroid glaucoma
Seen in steroid responders who use topical, creams, oientment
on eyelids, systemic, periocular, inhaled steroids
Steroid responders are those who showed rai. IOP to topical
steroids in 4-6 wks as compared to general population
3 groups- low (manifest with no change in IOP)
intermediate ( mod. Elevation of IOP to 22-30)
high ( marked rise to >30)
Patho.:- stabilize lysosomal memb. Prevents polymerization of
GAG GAG accumulation in TM
t/t :- dicontinuation of drug
- anti glaucoma medication
- trabeculectomy / seton implantation in uncontrolled
38. Glaucoma after cataract surgery Mechanism are:-
1. Inflammation with the release of active
substances, including prostaglandins and the
formation of secondary aqueous humor.
2. A watertight wound closure with multiple fine
sutures limiting the ‘safety valve’ leak of aqueous
humor.
3. Deformation of the limbal area, reducing
trabecular outflow.
4. Obstruction of the trabecular meshwork by
pigment, blood,lens particles, inflammatory cells,
and viscoelastic substances.
39. Contd…A. Early onset (within first postoperative week)
1. Pre-existing chronic open-angle glaucoma
2. alpha- Chymotrypsin-induced glaucoma
3. Hyphema/debris
4. Viscoelastic material
5. Idiopathic pressure elevation
B. Intermediate onset (after first postoperative week)
1. Pre-existing chronic open-angle glaucoma
2. Vitreous in the anterior chamber
3. Hyphema
4. Inflammation
5. Lens particle glaucoma
6. Corticosteroid-induced glaucoma
7. Ghost-cell glaucoma
C. Late onset (more than 2 months postoperatively)
1. Pre-existing chronic open-angle glaucoma
2. Ghost-cell glaucoma
3. Neodymium:yttrium-aluminum-garnet (Nd:YAG) laser capsulotomy
4. Vitreous in the anterior chamber
5. Late-occurring hemorrhage
6. Chronic inflammation
40. 1.alpha-Chymotrypsin
Glaucoma
used widely to facilitate intracapsular cataract
extraction.
mechanism for alpha-chymotrypsin glaucoma
is that zonular fragments obstruct the outflow
channels
t/t by using a lesser concentration of the drug (1:10 000
instead of 1:5000) in a lower volume(0.25–0.5 ml
instead of 2 ml)
anterior chamber should be irrigated before lens
extraction to remove zonular fragments
41. Scanning electron micrograph of the zonular fragments
obstructing the trabecular meshwork after alpha-
chymotrypsin administration
42. 2. Glaucoma From Viscoelastic
Substances
Sodium hyaluronate blocks TM
tiny ruby-like globs of hemorrhage on the iris surface
or suspended in the anterior chamber
43. 3. Glaucoma with Pigment
Dispersion from Intraocular
Lenses
Mechanism:-
Decentered, tilted, excessively mobile, too small, or
reversed in position
excess friction between the optic or haptic and the iris
pigment epithelium
Pigment particles block TM
c/f :- geographical loss of iris pigment
44. 4. Uveitis-Glaucoma-Hyphema
Syndrome
Seen in iris supported ACIOL / PCIOL
c/f:- rai.IOP, iridocyclitis & recurrent hyphema for wks
to mons after surg.
Due to excessive chafing of the iris by the
pseudophakics because the lenses are too mobile
45. 5.Glaucoma After nD: yag Laser
Posterior Capsulotomy
occurs within 2–4 hours of the laser treatment and
then abates spontaneously over the next 24 hours
usually associated with particulate debris clogging the
trabecular meshwork
Pretreatment with apraclonidine 1% 1 hour prior to
surgery and one drop 1 hour after surgery has been
shown to decrease the number and severity of
postoperative pressure spikes
46. 6. Glaucoma from Vitreous in
the Anterior Chamber
Common in aphakic eyes
after a spontaneous rupture of the hyaloid face or after
an extensive posterior vitreous detachment.
47. Retinal detachment and glaucoma
Due to vitreous loss
Schwartz Syndrome- RD + Rai. IOP + decrea.
Outflow + open angles + cells & flare in AC
Mechanism:- a)angle recession,inflammation,
pigment granules released by the retinal pigment
epithelium, and glycosaminoglycans synthesized by
the photoreceptors blocks TM
- b) photoreceptor outer segments migrate through
the retinal hole and obstruct the trabecular meshwork
48. Glaucoma after vitrectomy
Pre-existing glaucoma
Angle recession
Ghost cell
Primary open-angle glaucoma
Pigmentary glaucoma
Associated with intraocular hemorrhage
Hyphema
Ghost cell
Hemolytic
Hemosiderosis
Related to lens material
Phacolytic
Lens particle
Phacoanaphylactic
Neovascular
Inflammatory
Corticosteroid induced
Intraocular gas or liquid
Air
Viscoelastic substances
Perfluorocarbons
Silicone
49. Post- trabecular causes
TM is normal but aq. Flow is impaired due to elevated
episcleral venous pressure
For every 1mm rise in EVP-> 0-8 mm rise in IOP
Causes are :-
I. Obstruction of venous drainage
A. Episcleral-1. Chemical burns 2. Radiation
B. Orbital -1. Retrobulbar tumors 2. Thyroid eye disease
3. Pseudotumor 4. Phlebitis
C. Cavernous sinus thrombosis
D. Jugular vein obstruction
E. Superior vena cava obstruction
F. Pulmonary venous obstruction
II. Arteriovenous fistulas
A. Orbital
B. Intracranial-1. Carotid-cavernous fistula 2. Dural fistula
3. Venous varix 4. Sturge-Weber syndrome
III. Idiopathic
50. Superior Vena Cava
Obstructions
Mainly due to tumors, aortic aneurysms,
mediastinal masses, hilar adenopathy, and
intrathoracic goiter
produces edema and cyanosis of the face and
neck (pumpkinhead appearance) as well as
dilated vessels in the head, neck, chest, and upper
extremities
ocular findings include exophthalmos,
papilledema, and prominent blood vessels in the
conjunctiva, episclera, and retina
IOP is elevated mainly in supine position
51. Arteriovenous Fistulas
Carotid-cavernous fistulas-
- It provide a free communication between the
internal carotid artery and the surrounding
cavernous sinus in high blood flow and high
mean pressure in the shunt
- reversal of blood flow in the vessels leads to
congestion of the orbital veins and soft tissues
- c/f--- pulsating exophthalmos, chemosis, lid edema,
vascular engorgement, and restriction of ocular
motility