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Amoebic dysentry

Amoebic dysentry
Amoebic dysentry

Amoebic dysentry

AMOEBIC DYSENTRY= PATHOGENESIS-     1- it results 4m infection of large intestine by Entamoeba histolytica.  2-caused by ingestion of tetra-nucleated cysts.  3-after ingestion cysts undergo further nuclear division n eight trophozoites r released in terminal ileum. Later they carried to large intestine n produse 'flask shaped' amoebic ulcerations. 4-Incubation period 2-6 wks.     CLINICAL FEATURES= 1-

Atherosclerosis

Atherosclerosis
Atherosclerosis

Atherosclerosis

Defn
a progresiv inflmatory disorder of arterial wall i.e charctrised by focal lipid-rich deposits of atheroma dat remain clinicaly silent until they becom large enough 2 impair arterial perfusion / until ulceration / disruption of lesion results in thrombotic oclusion / embolisation of afectd vessel.


Risk factors

i)major constitutionl risk factors
-age mostly byond 4th d
-sex more in men
-genetic factors
-familial & racial factrs

ii)major acquird risk factrs
-hyperlipidaemia
-HTN
-smoking
-DM

iii)minor risk factrs
-obesity
-exognous harmons lik oral contraceptivs
-endogenous estrogen defi
-physicl inactivity
-stresful lif style
-environmental influencs
-heavy alcohol


pathophysiology


i)early atherosclerosis
fatty streaks @ alterd arterial shear stress -> abnormal endothlial function -> dvlpmnt of inflmn -> inflmatry cels mainly monocyts binds 2 receptors of endothelial cels -> migrate into intima -> take up oxidizd LDL 4m plasma -> lipid laden foam cels or macrophages -> extracelular lipid pool in intima -> foam cels die -> releas of contents -> cytokines, grwth factrs releasd -> smooth muscle cels migration into intima & change 4m contractile 2 a repair phenotype in atempt 2 stabiliz atherosclrotic lesion -> formn of atherosclerotic plaque

ii)Advancd athrsclros
-in establishd atherosclerotic plaque macrophages mediate inflmn & smooth muscl cels promot repair
-if inflmn predominates plaque becmes active/unstabl & may b complicted by ulceration & superaded thrombosis
-cytokines by activtd macrophges & may caus intiml smoth muscl cels ovrlying plaque 2 becom senescent
-thining of fibrous cap
-any breach in intgrity of plaque wil expose contents 2 circulatry bld
-platlet agregation & thrombosis dat extnds in2 athromtous plaque & arterial lumen


Clinicl efects

dpends on siz, typ of artries
1)slow luminl narowing causing ischaemia & atrophy
2)suden luminl oclusn causing infarction necr
3)propagation of plaque by formn of thrombi, emboli
4)formn of aneurysml dilatation & eventual ruptur


#Primary prevention
2 complementary strategies

1)Population strategy
-risk factors in whole population thru diet & lifstyle
-advice on smoking / avg cholestrol / exercise / diet / obesity

2)Targeted strategy
-treat high risk
-consider absolut risk of atheromatous cvs diseas
-antihypertensivs, lipid lowring therapy
-apropriate Rx

#Secondry prevention

in whom evidnc of atheromtous vascular diseas e.g periphral vasc diseas / MI offered a variety of Rx
-energetic corection of risk factors lik smoking, HTN, hypercholstrolmia 

AMPUTATION

AMPUTATION
AMPUTATION

AMPUTATION  

Amputation is a procedure where a part of the limb is removed through one or more bones.
   Amputations of lower limb are performed more commonly than that of upper limb.
 
     *INDICATIONS
1. injury is commonest cause of amputation in developing countries. Common cause in adults (25- 30 yrs)
2. Peripheral vascular diseases including DM - common in elderly (50- 75 yrs)
3. Infections eg. Gas gangrene
4. Tumours
5. Nerve injuries
6. Congenital anomalies
     * TYPES
     A) Guillotine or open amputation
   skin is not closed over wound as wound is not healthy
    Operation done after some period to construct stump:-
  1. Secondary closure
  2. Plastic repair
  3. Revision of stump
  4. Re-amputation

       B) Closed amputation
   Skin is closed primarily
   Surgical Principles:-
   1. Torniquet - except in ischaemic limb.
   2. Ex-sanguination - limb is squeezed with Esmarch bandage before torniquet application.
    Contraindicated in malignancy & infection
   3. Level of amputation :-
 decided on the basis of
    - Disease :- disease for which amputation is indicated. Be conservative with dry gangrene & trauma, but liberal with acute life-threatening infection & malignancy
     - Anatomy :- joint must be saved    
      - Suitability for proper functionig :- sometimes length is compromised for efficient functionig.
    4) Skin flaps :- skin over stump should be mobile & normally sensitive.
     5) Muscles :- muscles are cut distal to level of bone with
   - Myoplasty :- opposite group of muscles sutured together
   - Myodesis :- muscles sutured to end of stump
     6) Nerves :- are gently pulled distally into wound & divided with a sharp knife. Large nerves like sciatic nerve contain large vessel & should be ligated before dividing
      7) Major blood vessel should be isolated & doubly ligated using non-absorbable sutures. Torniquet should be before closure
      8) bone level is decided. Sharp edges of cut bone should be made smooth.
      9) Drain :- corrugated rubber drain is used for 48-72 hours.
     10) After Rx
        - Dressing :- two types of dressings are used 1) Soft
                          2) Rigid
     soft dressing is advantageous for wound healing  & early prosthetic fitting
         - Positing & elevation of stump to prevent contracture & promote healing.
          - Exercises :- for maintaining range of motion of proximal joint
           - Wrapping the stump with crepe-bandage helps in healing, shrinkage & maturation
           - Prmsthetic fitting & gait-training started after 3 months
       *COMPLICATIONS
    1. Haematoma :- due to
- inadequate haemostasis
- loosening of ligature
- inadequate drainage
- it results in delayed wound healing & infection
- Rx aspiration  &  a pressure bandage        
   2. Infection :-
- due to PVD, DM or haematoma
- Rx wth AMA
   3. Skin flap necrosis :-
- indicates insufficient blood
circulation
- avoided by taking care at time of designing
   4. Deformities of joints :-
- improper positionig of amputation stump leads to contracture
- Rx passive stretching exercises
    5. Neuroma
- always forms at the end of but nerve
- adhesion to scar makes it painful
- prevented by dividing the nerves sharply at proximal level & allowing it to retract proximally
- Rx excision at more proximal level
   6. Phantom sensation :-
- sensation of amputed limb being  still present
- most prominent immediately after amputation gradually diminish with time
     
   
             

Aphakia

Aphakia
Aphakia

APHAKIA

Aphakia literally means absence of crystalline lens from the eye. However,from the optical point of view,it may considered a condition in which  lens is absent from pupillary area. Aphakia produces high degree of hypermetropia.

CAUSES
1. Congenital absence of lens.
2. Surgical aphakia occuring after removal of lens is commonest presentation.
3. Aphakia due to absorption of lens matter is noticed rarely after trauma in children.
4. Traumatic extrusion of lens from eye.
5. Posterior dislocation of lens in vitreous causes optical aphakia.

OPTICS of APHAKIC EYE
1. Eye becomes highly hypermetropic.
2. Total power of eye is reduced to about +44D from +60D.
3. Anterior focal point  becomes 23.2 mm in front of cornea.
4. Posterior focal point is about 31 mm behind the cornea.
5. There occurs total loss of accomodation.

CLINICAL FEATURES
Symptoms
1. Defective vision. Main symptom in aphakia is marked defective vision for both far and near due to high hypermetropia and absence of accommodation.
2. Erythropsia and cyanopsia. Seeing red and blue images. This occurs due to excessive entry of ultraviolet and infrared rays in absence of crystalline lens.

Signs
1. Limbal scar may be seen in surgical aphakia.
2. Anterior chamber is deeper than normal.
3. Iridodonesis. Tremulousness of iris can be demonstrated.
4. Pupil is jet black in colour.
5. Purkinje's image test shows only two images.
6. Fundoscopy examination shows hypermetropic small disc.
7. Retinoscopy reveals high hypermetropia.

Treatment
Modalities for correcting aphakia include..
1. Spectacles prescription has been the most commonly employed method of correcting aphakia.
Advantages- it is cheap,easy and safe method.
Disadvantage- 1. Image is magnified by 30 percent, so not useful in unilateral aphakia.
2. Problem of spherical and chromatic aberrations of thick lenses.
3. Field of vision is limited
4. Prismatic effect of thick glasses
5. Roving ring scotoma
6. Cosmetic blemish.

2. Contact lenses.
Advantages-
1. Less magnification of image.
2. Elimination of aberrations and prismatic effect of thick glasses.
3. Wider and better field of vision.
4. Cosmetically more acceptable.
5. Better suited for uniocular aphakia
Disadvantages
1. More cost
2. Cumbersome to wear.
3. Corneal complications.

3. Intraocular lens implantation. It is commonest modality being employed.

4. Refractive corneal surgery.
1. Keratophakia.
2. Epikeratophakia
3. Hyperopic lasik.

Assisted breech

Assisted breech
Assisted breech

Assisted breech

ASSISTED Breech delivery :carried by skilled obs  principles :never to rush never pull from bellow  keep fetus with back anterior
STEPS pt is brought to table when anterior buttock and fetal anus r visible  she is placed lithotomy  position or tilted  Antiseptic cleaning  pudendal block is done episiotomy done in all case Patient is encouraged to bear down for easy descent  No touch of fetus policy is used until buttocks delivered with legs flexed
Soon after trunk upto umbilicus born following done  extend leg Pull cord down and nobilised to one side Rotate trunk to bring it anterior BABY is wraped with towel
delivery of arms :should not be extension of arms Arms are delivered one after other only when one axilla is visible by hooking down elbow
HEAD DELIVERY crucial stage  various methods BURNS MARSHALL METHOD  FORCEP delivery method
process baby allowed to hang by  own weight  Supra pubic pressure by hand in downward backward direction  when neck is visible baby is grasped traction is done
Resuscitation of baby 

Asthama

Asthama
Asthama

Asthama

DEF#
chronic imflamatory disease of airway charcterised by an increased responsiveness of tracheobronchial tree to variety
of stimuli.
         Manifest as paroxysm of dyspnoea,cough,wheezing as result of musclespasm,mucosal oedema,&bronchial secreations.
CLASSIFICATION#
1.Erly onset asthama(atopic,allergic,extrinsic)
2.Late onset asthama(non-atopic,intrinsic,idiosyncratic)
ETIOPATHOGENESIS#
2major factors.
1.Bröchial hyperresponsiveness
2.Inflamatory reaction in bronchial wall
3.Roll of allergans
PATHOGENESIS_
cell                 triggers
[                       [
Mediators___>bronchial
[             hyperresponse
]                      |
Inflamation         |
       |               |
       |_Symptoms__|            
CELLS INVOLVED inreleas mediator
¤Mast cells¤macrophages
¤eosinophil¤lymphocytes
MEDIATORS
¤histamine¤prostaglandins(d2,f2,E2)¤thrombaxane¤PAF¤bradykinin
¤leucotrienes(B4,C4,D4,E4)¤subP
¤adenosine¤oxygen radicals
TRIGGERS
¤exercise¤hyperventilation
.¤cold air¤dust & fumes
¤respiratory viral infection
¤emotional stress¤tobaco smoke
¤aspirin,beta blockers
CLINICAL FEATURES
discussed under 3 headings
1.EPISODIC ASTHAMA
¤occurs in episodes with asymptomatic period between
¤spontaneos in onset triggered
by allergans,exerecise,viral infe
2.SEVERE ACUTE ASTHAMA
also called
status asthamaticus
symptoms persist instid of initial
Rx¤severe dyspnoea,unproductiv
cough
¤Signs-sweating,central cyanosis
tachycardia,pulsus paradoxus
3.CRONIC ASTHAMA
chronic cough with mucoid sputum,¤episodes of cough&wheeze during night
PHYSICAL SIGN IN CHEST
seen onely during attack
1.Tachycardia use of accesory
muscles of respiration
2.Percussion,Hyper-resonant
3.Breath sonds-vesicular
4.Rhonchi&wheeze
5.Silent chest airflow insufficient
to produce rhonchi
INVESTIGATIONs
1.Chest radiography
in attck lungs r hyperinflated
complications like pigeon chest,
lobar/segmental collapse may occur
2.Pulmonary function tests
forced expiratory volume in 1min
[FEV1] vital capacity[VC],peak
expiratory flo rate[PEF]
3.Arterial Blood Gas analysis
it shows hypoxia&hypocarbia
4.Skin hypersensitivity test for
allergans & there avoidance
5.Blood& sputum for eosinophilia
#MANAGEMENT#
3 broad headings
A].Avoidance of allergans
B] .Desensitisation imunotherpy
C].Drugs therapy

A].Avoidance of allergans
it is possible when there is single allergan
.B].Desensitisation
repeated S.C inj of extract of
allergans
.C].Drugs
seven catagories of drugs r use
1}.BETA-ADRENERGIC AGONISTS
b1=heart b2=bronchial smoothmu
¤adrenaline_dose0.3-0.5ml of1:1000 sol route-sc ripeated at
interval of 20minutes
¤salbutamol
dose2-4mg tds oraly/2puff 100ug
¤salmeterol
2puffs of25 ug each2/3timeday
¤formeterol
2puffs of6 ug each1/3times day
2}.METHYL XANTHINES
¤theophylline
dose:100-200mg tds 300mg bds
or450-600mg od
¤aminophylline
dose:loading 5mg/kg slowly ouer
20minute.Maitenance:0.5mg/kg/hr
3}CORTICOSTEROIDS
¤hydrocortisone
dose loading-4mg/kg iv followed
by2-3mg 6 hourly
¤prednisolone
40-60mg oraly single mornig dose
¤beclomethasone (200ug) budesonide(200ug),
4}CHROMONES
¤nedocromil sodium
route-inhalation 4mg2/4time
5}.ANTICHOLINERGICS
¤ipratropium bromide
2puffs of20ug each time 4/day
6}LEUKOTRIENE INHIBITORS
¤zafirlukast 20mg 4times a day
¤montelukast10mg once day 

Anc antenatal care

Anc antenatal care
Anc antenatal care


Anc antenatal care

Systematic supervision (examination and care ) of a women during pregnacy is called antenatal care
anc comprie of

careful history taking and examination (general and obstretical)
advice given to pregnant women

procedure at first visit

Anxiety disorder And Its Types

Anxiety
Anxiety

Anxiety

Anxiety disorder : classification 1anxiety state 2 phobic @ anxiety -panic disorder generalised anxiety post traumatic stress disorder @phobic-agoraphobia social phobia simple phobia 1 panic disorder- recurrent attack of severe anxiety r sudden and unpredictable physical attack prominent such as palpitation chest pain sweating chill nausea fear of dying numbness and feeling of detachment last for 1o 15 min 2 generalised anxiety disorder st have persistent excessive unrealistic worry with other feature such as impaired concentration autonomic arousal restlessness and insomnia 3phobic persistent recurring irrational severe anxiety of sp object activities or situation with secondary avoidance behaviour of phobic stimulus  @treatment 1use of selective serotonin reuptake inhibitor 2selective serotonin nor epinephrine reuptake inhibitor eg venlafaxine 3anxiolytic agent benzodiazepine 4 cognative behaviour therapy          

ASOM

ASOM
ASOM

ASOM

Acute suppurative otitis media is a common infection affecting d mucosa of d middle ear cleft and may cause severe pain.

AETIOLOGY:
1) Age: occurs in all ages, common in children
2) sex: affects both equally
3) geograpical distribution: all over d world



Asherman syndrome

Asherman syndrome
Asherman syndrome

Asherman syndrome

A codition in wich amenorrhoea n infertility follow a major haemorrhage in pregnacy.

AETIOLOGY
-It may result from overvigourous curettage of the uterus in an attempt to control the bleeding this remove the lining
- the wall adherent n the cavity is oblitertated to greater or lesrer degree. -50'/.  of such pt. R subsequently infertile n of those who become pregnant only minority achieve an uncoplicted delivery.
-It may be occur after hystroscopic resction of the septum.
-In the tb of genital tract the caseating material collects in the uterine cavity to forn apyometra these adhesion within uterin cavity lead to formation of synechiae n to asherman syndrom when pt complent of amenorrhoea.
-after vaccume evacuation.

PATHOLOGY
-in this disease uterin cavity is shrivelled n obliterated by adhasion.

TREATMENT
uSe IUCD.

Arthroscopy

Arthroscopy
Arthroscopy

Arthroscopy

Defn
A techniqu of surgry on joints in whch tip of a thin(4mm diamtr) telescop called arthroscope is intrducd in2 a joint & inside of joint examind.Dis is called diagnostic arthroscopy.

Once diagno is made, necesary corectn can b done der & den by introducing microinstrmnts thru



Arf

Arf
Arf

 Arf

It is a life threatning condition with abrupt impairment of renal function resulting in retension of nitrogenous wastes.Oliguria n anuria is prominant feature. Etiology-pre renal-acute gastroenteritis,haemorrhage, shock,chf. Intrinsic-acute tubular necrosis, gn,hus,renal vein thrombosis. Post renal-calculus,post urethral valve. Pathophysiology-gfr n rbf r markedly decreased.Intravascular

Aquired aplastic anaemia

Aquired aplastic anaemia
Aquired aplastic anaemia

Aquired aplastic anaemia

Causes-drugs like chloramphenicol,oxyphenbutazone,sulfonamides,cimetidine,phenytoin,carbamazepine.Exposure to ionising radiatn..,.Infections -parvovirus,hepatitis b,c,d,EB virus...Chemicals lik DDT,benzene,aromatic hydrocarbons..Metals like-gold,arsenic,lead..CLINICAL features-progressive anaemia,assc

Aplastic anaemia

Aplastic anaemia
Aplastic anaemia

Aplastic anaemia:

     Results from colonyforming progeniters of mature granulocytes, megakaryocytes, erythroid cells and true stem cells.
     Haemopoetic failure is mediated by activated cytotoxic T cells in bood and marrow by producing gamma interferon and tumour necrosis factor.
     Differenciation of haemopoetic cells is regulated by humoral factors. Disturbances in these pathways lead to aplasia in

Aphasia

Aphasia
Aphasia

Aphasia

APHASIA= 1=SENSORY APHASIA- a) it is a disorder of language wid enability to encode or decode d signals used in d language.  b) sensory aphasia denotes dysfunction in afferent area, i.e. failure to comprehend verbal written messages.  c) lesions hn dominent post. perisylvian areas r responsible.  d) signs- poor comprehension of spoken speech n inability to read through person is able to hear n

Aortic stenosis

Aortic stenosis
Aortic stenosis


AORTIC STENOSIS


-The site of obstruction may be at the level of valve, above the level (supravalvar) or below valve (subvulvar)
 1 ) At the level of valve the stenosis either results frm an unicuspid or bicuspid aortic valve.
 2) Supravulvar due to stenosis in root of arota above the aortic valve .
 3) Subvalvar :- may be


Aortic regurgitation

Aortic regurgitation
Aortic regurgitation


Aortic Regurgitation

Aortic valve involv in RHD results in AR

**Hemodynamics:-
-Backward leak 4m aorta into left ventricle during diastole. -Dis increases volume of blood reaching d left ventricle. Left ventricle increases in size 2 accomodate d extra volume. -So dat forward flow impaired.
-Peripheral pulse pressure is wide becoz of increased systolic &

Antinuclear antibodies

Antinuclear antibodies
Antinuclear antibodies

Antinuclear antibodies

1. These are antibodies that bind to various nuclear antigens.they are generally detected using indirect immunofluorescence. Most laboratories employ a HEp-2 cell line.
2. Higher titres of ANA  are more likely to be true -positive than low titres.
3. ANA is  positive in several conditions. In SLE and drug -

Angina pectoris

Angina pectoris
Angina pectoris


Angina pectoris

*it is a clinical syndrome of discomfort due to transient myocardial ischaemia
*transient ischaemia is due to
1) obstruction of coronary flow by atheroma
2) coronary arterial spasm
3) risk factors -exercise, hypertension, AS, AR, hyperthyroidism
Clinical features
1- retrostermal pain which is squeezing crushing in character. It

Aneurysm

Aneurysm
Aneurysm


Aneurysm

DEF
.
Its a localired or diffuse dilatation of an artery.

TYPES.

1. True: It contains all 3 layers of artery wall.
2. False: it has a pinke layer of fibrous tissue as the wall of the sac and does not contain the three layers of the artery wall as the

Anorexia nervosa

Anorexia nervosa
Anorexia nervosa

Anorexia nervosa

There is marked weight loss arising from food avoidance. often c- purging bingeing . exce
exercise or the use of diuretcs&
laxatives.
Patient Still feel overweight
false beliefs r delusional
Anxiety n depression.
Downy hairs.
ETIOLGY
unknown but probably
enviorn n genetisc factors
social pressure on women.

Anaemia in pregnancy

Anaemia in pregnancy
Anaemia in pregnancy


Anaemia in pregnancy

Classification of anamia:
1) physiological anaemia of prg.
2) pathological
 A) iron deficiency anaemia
     iron, folic acid, vit B 12 and protein def
 B) haemorrhagic anaemia
        a) acute - following bleedin in early months
        b) chronic - hookworm infestation and

Analgesic nephoropathy

Analgesic nephoropathy
Analgesic nephoropathy

Analgesic Nephoropathy

 Heavy use of amalgesic mixture of phenacetin in combination with aspirin acetaaminophen
Morphology
 papillary necrosis
 tubulo interstetial infalmation
damage to vascular supply of inner medulla lead to local intersti inflam reaction
 
c/f          
proteinuria
hematuria
pyuria
renal coli
nephrocalcinosis

invest

urine -proteinuria
     hematuria
     pyuria

IPV
 ring sign

CT
 gasRland paTERN

TREATMENT
discourage use of this combinatio n phenactin              

Astigmatism

Astigmatism
Astigmatism

Astigmatism

Astigmatism is type of refractive eror in which refraction varies in diffrent media.
Types-regular and irregular.
Regular=refractiue power changes uniformly frm one meridian to another.
ETIOLOGY-1.Corneal astigmatism is d result of abnormalities of curvature of cornea.Most comon.
2.Lenticular astigmatism-a)curvatural due to abnormalities of curvature of lens.
b)positional due to tilting of lens as in subluxation..
c)index astigmatisms may ocur rarely.
Types of regular astigmatism-1.With rule astigmatism=when 2 principal meridia r placd at right angles to one another but vertical meredian is more curvd than horizontal.Corection requires cocave cylindes at 180 +-20 degree or convex cylindrical at 90+-20
2.Against rule astigmatism refers to condition in which horizontal meridian is more curvd than vertical.Correction requires convey cylindrical lens at 180+-20degree.
3.Oblique astigmatism-in which two principal media s nt horizontal and vertical thougi these are at right angle to 1 another.Corection requires cylindrical lens at 30 in both eyes.Or comlimentary cylindrical in 30 in 1 eye and 150 in other eye.
4.Bioblique astigmatism-two principal media r nt at right angle to each other..
Refractive type of regular astigmatism-1.Simple when rays r focussd in one meridian and either in front or behind. Simle myopic or simple hypermetropic respectively.
2.Compound-in which rays of light in both the meridia r focusd either in front or behind.
3.Mixed astigmatism in which light rays in 1 meridian r focusd in front and in other meridian behind the retina.Thus 1 meridian eye is myopic and another hypermetropic.
Symptoms-1.Defective vision 2.Blurin of objects .3.Object may b proportionaly elongated4.Asthenopic symptoms.
Signs-1.Difrent power in 2 media.
2.Oval or tilted disc
3.Head tilt-may develop torticolis to have good vision.
4.Half closure of eyelid.
INVESTIGATIONS-
1.Retinoscopy reveal difrent power in 2 difrent axis
2.Keratometry
3.Astigmatic fan test and jackson cross cylinder test.
TREATMENT-1.Optical treatment of regular astigmatism comprises following
a)spectacle with ful corection of cylindrical power and corect axis.
b)contact lenses-rigid contact lenses may corect upto 2-3 of regular astigmatism
2.Surgical correction of astigmatism is quite efective.
IRREGULAR ASTIGMATISM-
Characterisd by an irregular change of refractive power in diffrent media.
Etiological types-
1.Curvatural irregular astigmatis m found in patient of extensive corneal scar.
2.Index irregular astigmatirm due to variable refractive index in difrent parts in lens.
Symptoms-1.Defective vision
2.Distortion of objects
3.Polyopia
Investigations-1.Placido disc test reveals distorted circles.
2.Photokeratoscopy and computerisd corneal topography reveal irregular corneal curvature.
TREATMENT-1.Optical treatment consists of contact lens which replaces anterior surface of cornea.
2.Phototherapeutic keratectomy may b helpful.
3.Surgical treatment indicated in extensive corneal scarring and consists of penetrating keratoplasty.

Atrial fibrillation

Atrial fibrillation
Atrial fibrillation


Atrial Fibrillation

Definition:
 This is an arrhythmia where atria are disorganised and multiple atrial foci fire impulses at a rate of 350-600 per minute. There is no atrial contraction but only fibrillation. The ventricles respond at irregular intervals, usually at a rate of 100-140/min.
 It can be paroxysmal or persistent.

Aetiology:
1. Rheumatic heart disease.
2. Ischaemic heart disease.

Atrial flutter




Atrial flutter
Atrial flutter

Atrial flutter

Def....atrial flutter is characterised by a regular rapid atrial rate of 250-350/min.where ventricles respond to every second,third or fourth heart beat (2:1,3:1 atrioventricular block).

Causes
-Organic heart disease (ischaemic,rheumatic,congenital).
-pericarditis
-acute respiratory failure
-1st week following open heart

Atrial septal defect


Atrial septal defect
Atrial septal defect

Atrial septal defect

Asd is an abnormal communication between two atria .  Congenital heart disease wth lt to rt shunt
  *TYPES
1. Ostium secondum type - located at fossa ovalis.Ten times more common
2. Ostium primum type - inf. to fossa ovalis
   *HEMODYNAMICS
-There is leak of oxygenated blood from lt to rt atrium
- pressure diff. betwn 2 atria is small hence shunt is silent on auscultation
-rt. atrium enlarges in size to accomodate extra volume of blood from left atrium
-large volume of blood passes through normal sized tricuspid valve resulting in delayed diastolic murmur audible at lower lt. sternal border.
-pulm. ejection murmur. Pulmn. valve closes late resulting in delayed P2 .Second sound is widely split & fixed P2 is also accentuated
-cardiac apex formed by rt. ventricle

AV block and Its Functionality


AV block and Its Functionality
AV block and Its Functionality
fIRRT DEGREE BLOCK

AV block and Its Functionality

fIRRT DEGREE BLOCK
A>asso wth electrolyte disturbance,use of digitalis,B blocker,ca chanel blocker,acute MI B>asymptomatic C>in ECG,P-R interval is prolong to >than 0.20 sec.All P wave r conducted n QRS is normal D>Rx-correction of eletrolytes imbalance n removal of offending agent
SECOND DEGRRE BLOCK
A>subdivided into mobitz type 1 n 2

ATROPHIC RHINITIS

ATROPHIC RHINITIS

ATROPHIC RHINITIS And Its Effect
ATROPHIC RHINITIS

It an chronic inflammation of nose characterised by atrophy of nasal mucosa and turbinate bone.
The nasal cavities are roomy and full of foul smelling crusts. Atrophic rhinitis is of two type primary and secondary.

ATIOLOGY
A PRIMARY
1 AGE bet the age 15-40 start at puberty
2 SEX common in female
3 common in tropical counties like india
4 heredity may be responsibe.
5 HORMONAL
6 NUTRITION  poorly nourished person.
7 VIT A DEFICIENCY
8 AUTONOMIC IMBALANCE may be the cause of the disease.

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