Sure Shahbaz Khan Sir

Acute congestive glaucoma

Acute congestive glaucoma

An attack of acute primary angle closure glaucoma occurs due to a sudden total angle closure leading to severe rise in IOP.

Clinical features
Symptoms
- pain: sudden önset of very severe pain
- nausea, vomiting and prostrations



- redness, photophobia and lacrimation with progresv impairment of vision
- past history: previous attcks of same

Signs
- lids may b oedematous
- conjunctiva is chemosed and cyanosed
- cornea bcomes insensitive and oedmatous.
- angle of anterior chamber closd
- iris may b discoloured
- pupil is semidilated, verticly oval, fixed.
- IOP is raised.
- optic disc oedematous and hypermic

Management
A. Medical therapy
1. Systemic hyperosmotic agent intravemous mannitol
2. Acetozolamide 500mg i.v. Inj followd by 250 mg tab thrice a day
3. Analgesics and antiemetics
4. Pilocarpine eyedrops
5. Beta blocker eyedrops like 0.5 timolol maleate
6. Corticosteroid eyedrops like dexamethasone and betamethasone

B. Surgical therapy
1. Peripheral iridotomy- it is indicated when the peripheral ant synechiae are formed in less than 50% of ant chamber and as prophylaxis in other eye.

2. Filtration surgery- when IOP is not controlled wid the best medical therapy folwnp an attack of angle closure glaucoma and also when peripheral ant synechiae is formed inp more than 50% of angle of ant. Chamber.

3. Clear lens extractn by phacoemulsifictn with intraocular lens implantation

C. Prophylaxis treatment in normal fellow eye
 Prophylactic laser iridotomy or surgical peripheral iridectomy should be performed on the fellow asymptomatic eye.. 

Acute dacrocystitis

ACUTE DACRYOCYSTITIS...

 It is an acute suppurative inflammation of lacrimal sac , characterised by presence of painful swelling in the region of sac..
ETIOLOGY,
1. As an acute exacerbation of chronic dacryocystitis..
2. As an acute peridacryocystitis due to direct involvement from the neighbouring infected structures ..



Causative organisms are streptococus haemolyticus,pnemococus, staphylococus...

CLINICAL PICTURE:
it is divided into 3 stages
1. Stage of cellulitis... It is characterised by a painful swelling in the region of lacrimal sac epiphora , fever , malaise.. Swelling is red hot firm and tender. If treated resolution occurs at this stage..
2. Stage of lacrimal abscess: continued inflammation causes occlusion of the canaliculi due to oedema.. The sac is filled with pus  distends and its anterior wall ruptures forming a pericystitic swelling.. It points below and to outer side of the sac.
3. Stage of fistula formation... When lacrimal abscess is left un attende it discharges spontaneously leaving external fistula. Abscess may open up into nasal cavity forming an internal fistula ..
COMPLICATION.....
1. Acute conjunctiva 2. Corneal abrasion 3. Lid abscess 4.orbital cellulitis.

TREATMENT......
1. During cellulitis stage... Systemic topical antibiotics, analgesic drugs ,hot fomentation to relieve pain and swelling..
2. During stage of lacrimal abscess ... When pus starts coming out on skin it should be drained with small incision.. It should be squeezed out and dress it with betadine guaze .
        Later on DCT OR DCR is done..
3. Treatment of external lacrimal fistula..... After controlling the acute infection with systemic anti biotics fistulactomy along with DCT or DCR  operation is performed..
SURGICAL TECHNIQUE of DCR  conventional external approach DCR.
1. Anaesthesia... General
2.skin incision... Curved incision along lacrimal crest or straight incision medial to medial canthus.
3. Exposure of medial palpebral ligament and anterior lacrimal crest..
4.dissection of lacrimal sac..  Periosteum is separated from anterior lacrimal crest.  5.exposure of nasal mucosa.. Bony osteum is made exposing nasal mucosa.
6. Preparation of flaps of sac.. A probe is introduced into sac through lower canaliculus and sac is incised vertically.. To prepare flaps this incision is coverted got H shape..
7. Fashioning of nasal flaps  is also done by vertical incision converted into H shape..
8. Suturing of flaps..  Posterior flap of nasal mucosa is sutured with posterior flap of sac using 6 vicryl.
9. Closure...  

Acute glomerulonephritis

Acute glomerulonephritis

 it is glomerular inflammation in which there is an immunological mediated injury to the glomeruli
AETIOLOGY
1.INFECTIOUS DISEASE
post streptococcal glomerulonephritis, infective endocarditis ,syphilis , mumps,nearles
hepatitis b ,infectious mono nucleosis,epstein barr virus .
2.MULTI SYSTEM DISEASE



SLE, GOOD PASTURES SYNDROME ,Henoch schonlein purpura, sickle cell  nephropathy.
3.Primary glomerular disease
Diffuse proliferative glomerulonephritis ,Iga nephropathy ,mesangiocapillary glomerulonephritis ,crescentib glomerulonephritis ,membranous  glomerulonephritis, focal segmental  glomerulonephritis.
4.miscellaneous -malignancy
 eclampsia, penicilamine.
PATHOGENESIS
TWO mechanism are involved
-deposition of antigen -antibody complexes in glomeruli resulting in glomerular disease.
-deposition of an antibody in the glomerular basement membrane which them reacts with  an antigen in the basement membrane causing gloodrtlitis

Normally the immune complexes formed in the body are removed an the host reticulodndithelial system. This impaired ability for this results in their deposition in the glomerular basillary walls.
-the antigen may be exogenous  or endogenous.
-
mechanism for immune complexes and antibodies against glomerular injury are
-complement activation
-fibrin deposition
- platelet aggregation
-release of cytokine and free oxygen radical.
CLINICAL FEATURES
ACUTE NEPHRITIC SYNDROME
-hematuria
-RED blood cell
-oligouria
-odema
-hypertension
- proteinuria
-uraemia
INVESTIGATION
-URINE MICROSCOPY red cell cast -cultures throat shows group A beta haemolytic streptococci

-anti streptolysin elevated
-a3level may be reduced
-urinary protein increased
-urea and creatinine elevated
-renal biopsy features of glomerulonephritis

TREATMENT
IT INCLUDES REST , SALT RESTRICTION ,DIURETICS, BOTH HYPERTENSIVES AND ANTIBODIES .
,-DIALYSIS is required in severe oligouria-fluid overload -and hyperlalaemia.
-steroids and cytotoxic drugs are of no value.
-complications include pulmonary oedema-,hypertensive encephalopathy , and renal failure.
   

  

Acute myocardial infarction

Acute myocardial infarction

 - Myocardial infarction is myocardial necrosis occuring as a result of a critical imbalance betn coronary blood supply and myocardial demand
   - Usualy due to atheromatous thrombus in coronary artery.
   - Hypercoagulable state in youngs result in MI
   - Use of cocain is another cause of MI. Cocain produces
hypercoagulable state an dvasospasm of coronay arteries




Clinical features:
Syptoms:
1) chest pain is cardinal symptom. It is at the left chest and medial aspect of the left arm. severe and prolonged, described as tightness, heaviness or constriction.
2) other are breathlessness, syncope, vomiting and extream tiredness
  - pain may b absent in some pts

Signs:
Mild fever
Pallor, sweating
Tachycardia or bradycardia
Arrythmias
Narrow pusle pressure
Raised JVP
Diffuse apical impulse
Soft first h sound
Third h sound
Pericardial friction rib
Systolic murmur
Basal crepitations

Complications:
 A) arrythmias
     - sinus bradycardia, sinus tachycardia
     - atrial trachycardia, atrial fibrillation
     - ventricular ectopic beats
     - ventricular tachycardia, ventricula fibrillation
     - heart blocks
     - acclerated idioventricular rhythm
 B) cardiogenic shock
     - may b caused by arrythmias, excessive               diuretic therapy
     - may b due to extensive myocardial damge
 C) other
     - cardiac failure
     - infarction papillary muscle--mitral regurgitation
     - pulmonary oedema
     - interventricular septum rupture
     - cardiac tamponade
     - cerebral and peripheral embolism
     - deep vein thrombosis
     - ventricular aneurysm
     - Dressler's syndrome--autoimmine reaction to necrosed muscles--fever, pericarditis, pleurisy--Rx is NSAIDs and corticosteroids

Investigations:
1) electrocardiogram
     -typical changes seen
     - ST elevation > 1-2 cm
     - pathological Q waves
     - rarely MI T waves may become tall and               peaked. These r transient.
     - appearance of a new left bundle branch block

2) plasma enzymes
  - creatinine kinase (CK)
  - aspartate aminotransferase (AST)
  - lactate dehydrogenase (LDH)
  - myoglobin
  - troponins (cardiac specific)
* CK starts to rise at 4-6 hrs, peak at 12 hrs, fall     to normal by 48-72 hrs
* AST rise by 12 hrs, peak on 1st or 2nd day
* LDH rise aft 12 hrs, peak by 2-3 days, remain        elevated for a week
* myoglobin rises within 2-6 hrs and remains for       7-12 hrs
* cardia troponins remains elevated for 100-200 hrs
   Useful in pts presenting late

3) other investigations
    -leucocytosis
    -raised ESR
    -elevated C reactive protein
    -chest radiography- pul oedema
    -radionucleotite scanning
    - echocardiography

Management
1) initial rx:
  - attach a cardia monitor
  - iv line
  - oxygen
  - sublingual nitrate
  - iv morphine 3-5 mg along with antiemits
  - aspirin 150 mg, clopidogrel 300 mg
2) confirm diagnosis
  - ECG
3) specific rx
  - thrombolysis
  - iv beta blocker
  - rx complication like arrythmia, ccf, shock
  - admit in icu

Oxygen:
    Admister oxygen in suspected MI
Nitrates
    Nirates reduce o2 demand of myocarium.
    Iv nitrogycerine is given
Control of pain
    Morphine 3-5 mg iv every 10-15 min along with        antiemitics
    Morphine also reduce preload
Antiplatelet agents
    Aspirine and clopidogrel
Beta blocker
    Decreases O2 demand by decreasing bld              pressure and heart rate
    Given orally or iv, metoprolol and esmolol
Calcium chaneel blocker r not recommanded
ACE inhibitor
    Improves myocardial fucn by reducin myocardial     remodeling
    Givn within 24 hrs
    Intially short acting captopril 12.5 mg given
    Dose may be increase upto 25 mg 8 hrly
Thrombolytic theorapy
    Steptokinase, urokinase and recombinant plasma     activator (altiplase)
    Leads to generation of plasmin which lyses clot

Prophylactic anticoagulants:
   - low dose heparine 5000 units twice daily SC to prevent DVT and pulmonary embolism

per cutaneous coronary interventions
   - angioplasy or stent placement in coronary           artery
   - indicated in cardiogenic shock and presence of containdications to thrombolytic therapy

Coronary artery bypass grafting:
   - benifit in pts with acute MI with persistant pain or deteriorating haemodynamic status

Management of RV infarction
  - volm expansion is the initial rx
  - inotropic vasodilators may b required

Management of complications
 (1) arrythmia
      - pain relief, reassurance, rest
      - correction of hypocalemia
      - manage CCF
      - lignocain aftr resuscitation
      - DC cordivesion is Rx for ventricular                   fibrillation
      - varapamil, diltiazem, ismolol or digoxin is used to treat atrial trachycardia, fibrillation and flutter
      - atropin used to rx symptomatic sinus bradycardia and heart block
      - temporary pacemaker in heart block complicating inferior wall MI

 (2) cardiogenic shock
      - treated by iv fluids

 (3) aftercare and rehabilitation
     - contol of obeysity
     - exercise
     - cesation of smoking
     - control of lipids by diet and drugs

 (4) medications
     - aspirin 75-100 mg daily
     - clopudogrel 75 mg daily upto 12 months
     - beta blockes unless contraindicated continued indefinately
     - ACE inhibitors given early aft acute coronary syndrome
     - statin therapy for all pts of CHD
     - nitrates for chest pain
     - warfarin for those at high risk of thromboembolism
                                    - by Mâk

Acute pancratitis

Acute pancratitis

Etiology
 Alcohol ingestion
 Biliary calculus
 Post operative
 Post ERCP
 Trauma to abdomen
 Metabolic  renal failure, hyprcal
 Penetrating peptic ulcr
 Connective tissue disease SLE
 polyarteritis nodasa
 Infections mumps,roundwrm ,vir
  hepatitis
 Drugs sulphonamds
,oestrogen,thiazide ,frusemide,steroids.



 Hereditery pancratitis
 OP posng
PATHOLOGY
 Oedematous pancratitis
 necrotic    "
 haemorrhgic   "
CLINICAL FEATURES
SYMPTMS
 Cardinal s PAIN mild to severe
 intensity. Dull, boring ,sudden in onset gradually increases in severity usually located in epigastric radiates to back.
 Nausea n vomiting
 Anorexia.
SIGNS
 FEVER ,TACHYCARDIA,TACHYPNEA
 HYPOTEN, JAUNDICE,
 Abd tendrns ,guardng disten.
 LUNGS cynosis,pleural effusion
 SKIN erythematous modules
 Cullens sign (bluish dis arnd umbilics.)
 Turners sign (bluish dis in flnk)
OTHE$ Hemetmesis ,malaena,ischemic injry to retina.
INVESTIGATIONS
1)Serum amylase  Increase for 72 hours them decline to normal in 1to2 weeks.
2)Hypertriglyceridemia in 15to20%
3)serum Lipase  Preferable n more specific.
Marked increase in pleural n peritoneal fluid..
4)Blood picture
5)plain x ray and chest .to exclud othere cause of acute abdominal pain.
6)ultrasound abdomen to evaluate gallblader and billary tree. It can detect acute pancreatitis
7)CT abdomen show mass swollen pancreas.
PROGNOSTIC FEATURES
 RANSON CRITERIA
According to this if
0-2=mortality 2%
3-4=mortality 15%
5-6=mortality 40%
>6  mortality 100%
DD
Intestinal perforatin
Acute MI
Acute cholecystitis
Pneumonia
Acute appendicitis
COMPLICATIONS
LOCAL
 Necrosis
 Pseudocyst
 pancreatic abscess
 Pancreatic ascites
 Intraperitoneal hemorrhage
 obstructive laundice
 intestinal obstruction
SYSTEMIC
Hypovoldmic shock
Acute respiratory distess syn.
Multiple organ failure
Renal failure
DIC
Gstroint hemrge
Fat necrosis
Pleural effusion
TREATMENT
1) NBM
2)IV Fluids
3)analgesics
4)Nasogastric tube if pain ,vmtng
obstrn
5)Moniter TPR BP Urine bld
6)Antibiotics carbapenems or ceftazidime.
7)protön pmp inhb,glucagon ,octreotide,aprotonin.
8)Surgery if
 infected necrosis
 complicn
9)ERCP Wthn 36-48hr wtih gallstn pancreatitis.

Acute peritonitis

Acute peritonitis

Def=inflammation of peritoneum is called peritonitis

CAUSES
A)PRIMARY PERITONITIS
1)spontaneous peritonitis of childhood
2)spontaneous peritonitis of adults
3)tuberculous peritonitis
4)peritonitis a/w dialysis

B)SECONDARY PERITONITIS
peritonitis due to intra abdominal
source



1)perforation of hollow viscus
*perforated duodenal ulcer,gastric ulcer
*perforated enteric ulcer,tubercular ulcer
*perforated Meckel's diverticulum
*perforated colonic ulcer

2)direct spread post inflammatory
*acute cholecystitis
*acute appendicitis
3)penetrating injuries to abdo.
4)post operative peritonitis=due to introduction of inf during surgery
*improper suerilization technique
*foreign body in abdo.
5)parturition peritonitis

PATHOGENESIS
1)Gram negative organisms=E coli,proteus,klebsiella
2)enterococci=streptococci faecalis.Present in urinary tract,genital tract,intestine.
3)bacteroids=anaerobic organisms,present mainly in lower intestine
4)bacteria from outside alimentary tract=gonococci,pneumococci,tubercular orgamism
5)these organisms proliferate in perotoneal cavity resulting in peritonitis
6)this result in large amt of fluid secretion in peritoneal cavity which leads to hypovolaemic shock
7)fluid is rich in fibrinogen which form fibrin n localises inf.
8)peritoneum becomes reddish n oedematous covered with thick fibrous exudate.

C/F =
1)severe abd pain=cutting in nature,become worse on movement of abd wall
2)persistant vomiting due to irritation of parietal peritoneum
3)pulse rate incrsd
4)high grade fever with chills n rigor
5)cough tenderness indicates parietal peritoneum inflammation
6)rebound tenderness/Blumbergs sign=abd is pressed 4 few sec.Pt experiences pain.Sudden release of press causes severe pain due to sudden movement of sensitive parietal peritoneum
7)guarding n rigidity
8)bowel sounds r absent
9)end stage disease=Hippocratic facies

INVESTIGATION
1)complete bld pict shows high total count with predominant neutrophils
2)urine n bld 4 sugar
3)plain X ray abd erect
*gas under diaphragm=perforation
*ground glass appearance due to fluid
*obliteration of psoas shadow
4)abd usg to detect fluid in abd
5)4 quadrant abdominal tap
*aspiration of bld indicates haemoperitoneum n gangrene of bowel
*aspiration of bile=biliary peritonitis
*aspiration of frank pus=peritonitis due to gm -ve bacteria
*amylase estimation should b done to rule out pancreatitis
6)diagnostic laparoscopy
*used to confirm peritonitis
*can diagnose pancreatitis
*peritoneal toilet can b done

MANAGEMENT
1)Aspiration=nasogastric aspiration decreases git secretion thus reduces abd distension.Prevent vomiting n give rest to guj
2)bowel care n bld=purgatives should not b given
3)charts=temp,pulse rate,rr
4)drugs=against gm +ve,-ve n anaerobes
5)exploratory laparotomy
6)iv fluids before,during n after surgery

COMPLICATIONS OF PERITONITIS
1)severe hypovolemic shock
2)septic shock,multi organ failure
3)subacue intestinal obstruction
4)pelvic abscess
5)subphrenic abscess 

Acute pancreatis

Acute pancreatis

Causes
1>alcohol-it stimulate pancreatic secretion rich in protein,form protein plug,result in obstruction 2 pancretic duct.It stimulates trypsiogen
2>biliary tract disease-stone in biliary tree
3>collagen vascular disorder-polyarteritis nodosa
4>drug-corticosteroid,estrogen,diuretics
5>endoscopic procedure-sphicterectomy,cannulation of CBD or pancreatic duct or basketing of stones from CBD



6>genetic
7>hyperparathyroidism
8>hyperlipidemia
9>hypothermia n hypotension
10>injury 2 pancreas
11>infection-mumps
PSEUOCYST of pancreas-
invertigation-
1>USG-can detect size,location of cyst
2>barium meal follow through
3>ERCP
Treatment-
1>coservative line of treatment
a>majority resolve by itself within 3-4 weeks
b>regular usg 2 observe pseudocyst
2>surgery
a>increase in size of cyst,severe pain,no response 2 conservative line of treatment r indication 4 surgery
A>cystogartrostomy-
indication-pseudocyst in relation 2 head n body of pancreas
timing-after 6 weeks
size-6 cm
procedure-ant gastrotomy is done n incision in post wall of stomach opens in2 cyst cauity.Content r drained.Opening is emlarged n cut end of stomach in post wall is sutured 2 cut edge of cyst wall.After 1 week cyst colapses
B>cyst confined 2 tail of pancreas-distal pancreatectomy wth removal of tail n cyst
C>large cyst:cystojejunostomy by roux-en-Y loop done,by suturing jejunal loop

Acute renal failure

Acute renal failure

DEF.

Rapid Reversible deterioration in renal function sufficient to result in accumulation of nitrogenous waste in body.

ETIOPATHOLOGY.

1 At rest 25% of co to kidney

2 in prerenal :- inadequate perfusion lead to decrease GFR lead to oliguria




3 post renal: obstruction of urine out flow


CAUSES.

A) prerenal
     1) hypovolumeia
:-hemorrhage
-sever vomiting
-diarrhne
- los of plasma
:-burn
:-pancreatitis
:- excess of diuretics
:- diabetic ketoacidosis

      2 reduce co
:-heart failure septic shock

     3 renal vessel disease
 :- renal artery occlusion

     4drug
:-ace inhibitor

B) renal
   1 glomular. -GN
   2 interstitial- drug infection
   3 act tubular necrosis
        --malaria.
        INJURY
        heavy metal.
        septic Abortion
    4 vascular
        vasculitis
        Renal artery occlusion

C) post renal
        1 extrarenal obstruction
        prostatic enlargement
       urethral stenosis

        2 intrarenal obstruction
          uric acid crystal

          slough papilla

C/F

1 Low blood Pressure

2 falling urine output

3 acute tubular necrosis is  most imp cause of it .it consist
    a) oliguric phase
         1 wit fluid overload n azotaemia .
         2 Elevation of JVP
         3 Pedal edema
         4 ascitis
         5 pulmonary edma.
         6 HyperK

    b) maintainance  phase:-
          1 low urine output

    c ) diuretic phase.:-
        1 polyuria lead to dehydration and hypoNa hypoK



4 40% of ATN develop NON OLIGURIC RENAL FAILURE

5 GN typically hav HT proteinuria hematuria

6 obstruction hav loin pain hematuria.

7 Sym of uremia:-
vomiting
pluritius
asterix
pericardial rub.



Investigation.:-

1 elevated blood urea

2 elevated blood creatin

3 hypoNa

4 hyperK hypoCa

5 hyperPo4

6 urine show
red cel cast.
Proteinuria .
Graularcast.

7 ECG

8 chest x ray

9 kidney biospy

10 USG


aMANAGEMENT

1 CORRECTING fluid  and electro imbalance

2 underlying cause

3 hyperK TREATMENT

4 acidosis by NaHCO3

5 loop diuretic. Mannitol

6 hemodialysis

        Indication. 1symptomatic uremia
           2 Sr.Creatinin > 8 mg/dl
            3 resistant hyperK
           4refractoy pulmonary edema

7 dietary protein restriction

8 salt restriction

9 energy in form CHO

10 RPGN is treated by corticosteroid

  

ADAMANTINOMA

ADAMANTINOMA

Arises from ameloblasts
  Benign tumour, grows slowly, behaves like a basal cell carcinoma.
   Inadequate Rx results in local recurrence & metastasis. Hence Rx like malignant tumour
    * SITES
  mandible ( most common) , tibia, pgtuitary
    * C/f
- 4th or 5th decade
- it undergoes cystic degeneration
 resulting in multiple cystic spaces.Hence called multilocular cystic disease



- causes expansion of outer table of mandible & causes fracture mandible
- complains of falling teeth
    * Diagnosis
 -X ray - honey comb appearance
    * Surgical Rx
  - Wide excision with 1 cm of healthy normal tissue should be removed  

Addisons disease

Addisons disease

Addisons disease=  primary causes        1 addisons disease
 2 congenital or acquired enzyme defects                        secondary causes  1. hypothalamic or pituitary 2.witgdrawal of glucocorticoid therapy.
Addisons disease-
causes-
1.Autoimmune adrenalitis-infectious adrenalitis,TB,fungal
2.Adrenal haemorrhage:-waterhouse-friderichsen syndrome,anticoagulation therapy,trauma.



3.Adrenal infarctiön-SLE,polyarteritis nodosa,antiphospholipid syndrom,trauma.
4.metastases in the adrenal-lung,breast,stomach carcinoma,lymphoma.
5.drug iduced-adrenolytic therapy.
6.congenital adrenal hyperplasia
7.bilateral adrenalectomy
8.amyloidosis
9.haemochromatosis
10.sarcoidosis
clinical features:-
1.clinical featurest results from glucocorticoid,mineralocorticoid,androgen deficiency & ACTH excess
2.cardinal features-hypotension,pigmentation,previous history of acute adrenal crisis
3.glucocorticoid deficiency result in malaise,weakness,weight loss,anorexia,nausea,vomitting.
4.mineralocorticoid deficiency manifest as hypotention
5.ACTH excess results in pigmentation of exposed areas,pressure area like elbows,knees&knuckle
6.androgen deficiency result in diminution of body hair especially in female and usually occurs with a secondary cause of adrenal insufficiency.
6.a number of autoimmune disease may be associated
7.the association of two or more of these endocrinopathies is known as type || polyglandular autoimmune syndrom.
9.the combination of adrenal insufficiency,hypoparathyroidism and chronic mucocutaneous candidiasis constitutes type l polyglandular autoimmune syndrom.
Investigation:-
1.elevated blood urea,hyponatraemia and hyperkalaemia
2.low blood sugar level
3.mild anemia,mild eosinophilia.
4.plasma cortisol measured between 8 and 9 am < 3 mg/dl suggets adrenal insufficiency while a level >19 ug/dl exclude it.
5.ACTH Stimulation test -there is failure of plasma cortisol to rise following adminstration of 250 ug of sythetic ACTH.
6.plasma ACTH Level are elevated(>100pg/dl) in primary adrenal insufficiency
7.plasma renin activity is high &plasma aldesteron level low or normal.
8.in tuberculous adrenalitis, chest radiograph may show evidancy of pulmonary TB.
9.adrenal and other specific antibody may be detected in the serum in autoimmune adrenalitis.
Manegment -
1.pt with disease require life löng glucorticoid & mineralocorticoid replacement therapy
2.cortison given at dose of 20mg on getting up in the morning and 10mg in the evening at 6 pm. Alternativly , prednisolone-5mg in am and 2.5mg at evening
3.fludrocortisone 0.05-0.1mg daily in pt with primary adrenal insufficiency
4.disease due to tuberculous adrenalitis treated with anti TB Chemotherapy.
5.during stress and infection-additional dose of prednisolone. 

Adenomyosis

Adenomyosis

*Def:
Adenomyosis is condition characterized by the presence of ectopic endometrial tissue  within the myometrium..
The condition is typically found in women between the ages of 35 and 50..
The disease coexist with uterine  fibromyoma and endomdtrial carcinoma.

*Grossly :
 uterus appears symmetricaly enlarged to not more than 14 weeks size.



*Cut section :it shows only localized nodular enlargement . The affected areas reveals peculiar ..diffuse.. Striated and non capsulated involvement of myometrium ..with tiny dark haemorrhagic areas interspersed in between .

*Histological examination :
reveals island of endomdtrial gland surrounded by stroma

*Clinical examination
symmetrical enlargement of uterus he the adenomyosis gigs diffuse and the uterus is tender.
Painful symmetrical enlargement of uterus should suggest the correct diagnosis.
Treatment:
NSAIDS& hormonal suppression for symptomatic relief, withhysterectomythe only permanent cure option.

ADHD

ATTENTION DEFICIT HYPERACTIVITY DISORDER

It is defined cp age inappropriate hyperactivity ,impulsiveness , and inattention .
It is divide into three classes
class1, all three symptoms
class2 first two only
class3 mainly the third

DIAGNOSIS
diagnosis is mainly based on clinical symptoms
INATTENTION :



Six or more of the following symptoms of inattention have been present for at least 6 months to a point that is disruptive and inappropriate for developmental level:
1.Often does not give close attention to details or makes careless mistakes in schoolwork, work, or other activities. 2.Often has trouble keeping attention on tasks or play activities.
3.Often does not seem to listen when spoken to directly.
4.Often does not follow instructions and fails to finish schoolwork, chores, or duties in the workplace (not due to oppositional behavior or failure to understand instructions).
5.Often has trouble organizing activities. 6.Often avoids, dislikes, or doesn't want to do things that take a lot of mental effort for a long period of time (such as schoolwork or homework).
7.Often loses things needed for tasks and activities (e.g. toys, school assignments, pencils, books, or tools).
8.Is often easily distracted.
9.Often forgetful in daily activities

HYPERACTIVITY- IMPULSIVITY.
B. Six or more of the following symptoms of hyperactivity-impulsivity have been present for at least 6 months to an extent that is disruptive and inappropriate for developmental level: *.Hyperactivity:
1.Often fidgets with hands or feet or squirms in seat.
2.Often gets up from seat when remaining in seat is expected.
3.Often runs about or climbs when and where it is not appropriate (adolescents or adults may feel very restless). 4.Often has trouble playing or enjoying leisure activities quietly.
5.Is often "on the go" or often acts as if "driven by a motor".
6.Often talks excessively.
*7.mpulsiveness:
8.Often blurts out answers before questions have been finished.
9..Often has trouble waiting one's turn. 10..Often interrupts or intrudes on others

#Pervasive Developmental Disorder,Schizophrenia, or other Psychotic Disorder should be excluded.

Management:
 It inclede behvoir and drug therapy
(a) behavior therapy:
       In this parents shud stay calm
       Child shud be rewarded for routines
       Study period shuld b brief with constant feedback
     
B) drug therapy:
       Drugs which stimulate frontal lobe dominance and helps modulate behavior can b used
 1) stimulants:
      Methyl phenidate, dextroamphitamine and pemoline
 2) tricyclic antidepressants:
       Rhis can b used in case with unsuccessful respone to stimilant drugs
       Clonidine,
 3) low dose of antipsychotic drugs: thyoridazine, resperidole, fluoxetine

Alcoholic liver disease

Alcoholic liver disease

Etiopathogenesis=
.Alcohol intake..
Alcohol is metabolised by liver to acetaldehyde by mitochondrial enzyme,ADH.
Acetaldehyde forms adducts with cellular proteins in hepatocytes which activate immune system,leading to cell injury.
Acetaldehyde then metabolised to acetyl coA nd acetate by ALD,this generate NADH,which changes redox pontential of cell



 Cytochrome CYP2E1 is induced by alcohol,which generates microsomal peroxidation leading to oxygen free radicals formatn leading to mitochondrial damage
.PATHOLOGY=
.Alcoholic hepatitis
.Lipogranuloma
.Neutrophil infiltratn
.Mallory hyaline
.Pericellular fibrosis
.Macrovesicular steatosis
.Fibrosis nd cirrhosis
.Central hyaline sclerosis
.C/F=
.Clinical syndrome of alcoholic liver disease=
.1..Fatty liver=
abnormal liver biochemistry ,normal/large liver
.2..Alcoholic hepatitis=
.Jaundice
.Malnutritn
.Hepatomegaly
.Portal hypertension features like ascites ,encephalopathy
.3..Cirrhosis=
.Stigmata of chr liver disease
.Large/normal liver
.Ascites
.Encephalopathy
.Hepatocellular carcinoma
INVESTIGATION =
.Clinical history frm pt abt alcohol misuse,duratn ,severity
.Biological markers in absense of anemia
.Raised GGT wil b elevated in hepatic steatosis nd fibrosis
.Unexplained rib fracture on chest x ray suggest alcohol misuse
.Presence jaundice suggest alcoholic hepatitis
.Liver biopsy
.Maddreys score by prothrombin time nd bilirubin give discriminant function
.MANAGEMENT=
.Cessatn of alcohol consumptn.Life long abstinence is best advice
.Treatment of complicatn of cirrhosis such as variceal bleeding ,ecephalopathy nd ascites
.Nutrition is imp nd enteral feeding via fine bore nasogastric tube needed.
.Corticosteroids r of valve in pt with severe alcoholic hepatitis
.Pentoxifylline,a weak anti TNFaction beneficial in sever alcoholic hepatitis
.Liver transplantation.

Alopecia

Alopecia

It mean loss of hair n is a sign rather than diagnosis.
 - detail history, cair ful scalp exam^ n complete physical exam^ shud enable a confident diagnosis to b made.

CLASSIFICATION
LOCALISED
1 Non scarring
 - Tinea capitis
 - alopecia areata
 - androgenetic alopecia



 - traumatic
 - syphilis.

2 scarring
 - idiopathic
 - developmental defects
 - harpes zoster
 - pseudopelade
 - radiotheropy

DIFFUSE
 - androgenetic alopecia
 - Telogen effluvium
 - metabolic
 - hypo n hyperthyroidism
 - hypopituitarism
 - DM
 - HIV
 - nutritional deficiency.

INVESTIGATION
 - Complete bld picture
 - ESR
 - Urea n electrolytes
 - LFT n TFT
 - treponema pallidum haemagluitination
   test.
 - hair pluck test.
 - scalp biopsy.

MANAGEMENT
 - tretment is difficult
 - alopecia areata is responds to topical steroid.
 - androgetic alopecia is treated wit systemic steroid.
 - wig may b the most appropriae treatment for extensive alopecia
 - scalp surgery n autologous hair transplants r expensive but sometine  effective in androgenetic alopecia.

                          -by pam  

Alzheimers disease

Alzheimers disease

Is a progressive neurodegenerative disease resulting in decline in congnitive functions and behavioural disturbances.It is the most common cause of cognitive impairment in elderly persons

c/f:

1. Insidious onset disease

2. There is a gradual decline in activities of daily living which ultimetly leads to profound disability and depandance on others




3. The patient has disturbed memory,language n visual skills:
 a)there is an impaired ability to learn new things and recall previously learnt information
 b)a decline in language function n increased difficulty with names n understanding what is being said
 c)an impaired ability to carry out motor activities,despite intact motor function
 d)failure to recognise or identify objects despite intact sensory function

4. Other features include behavioural problems,psychotic symptoms n depression.Persecutory delusions occur in nealy 50% of patients

5. It is important to differentiate b/w alyheimers disease n other treatable causes of demantia

laboratory investigations-

1. There r carried out to exclude a treatable cause of dementia

2. Common investigations r blood chemistry,a complete blood count,tests for syphilis n thyroid functions,a CT head is usually done to exclude an intracranial pathology.An MRI may be necessary to detect presence of white ischaemic lesions

management

cognitive deficits
 1. Cholinesterase inhibitors provide modest improvement in symptoms n reduction in the rate of cognitive decline.These drugs include donepezil,rivastigming,galantamine n tacrine

 2. Other agents include vit E n NSAIDS though their exact role is not clear

co morbid conditions
 optimal management should be provided for any co morbid conditions including visual or hearing deficits,dental problems n other common medical illnesses

behavioural problems
 treatment of associated behavioural problems by non pharmacological n pharmacological interventions should be prescribed

Amenorrhia

Amenorrhoea :

absence of menstruatino two types Primary secondary
primary amenorrhoea :failure of onset of menstruatino beyond age of 16 years regardless of development of secondary sexual character .
Classification it is made on basis of serum FSHlevel
! Hyper gonadotropic 2 eu gonadotropic 3 hypo gonadotropic
etiology: 1delayed puberty 2 cerebral stress emotional



disturbane infection trauma tumor 3 hypothalamus kallmans syndrome vigorous exercise weight loss 4 pituitary gland  empty sella turcica cushings syndrome frohlich syndrome 5 ovary turner syndrome savage syndrome PCOD genital tract absent uterus refractory endometrium obstruction in lower genital tract 7 chromosomal 8 drugs anti hyper tensive 9 nutrition
MANAGEMEnt A hyper gonadotropic : there is gonadal failure or dys genesis  FSH > 4o miu/ml  chromosomal 45 xo 1 GONADECTOMY in pt of testicular feminizing syndrome 2 OOCYTE  donation 3 cyclic oestrogen and progesterone
EU gonado tropic : FSH normal  testicular feminizing syndrome with 46 xy 1 prophylactic GONADECtomy 2 oestrogen therapy 3 vagino plasty 4 creation of functional vagina for coitus 5 simple cruciate incision of hymen
c hypo gonado tropic : FSH < 4O due to hypothalamic dys function pituitory dys fun 1 GnRH therapy
General therapy 1 HRT 2 nutrition 3 psychogenic therapy  

AML

AML

OAML also termed as acute non lymphoblastic leukemia accounts for 15-20% of childhood leukemia.AML is much more complex and resistant disease than acute lymphoalartic leukemia.progress has been slower therapy more complicated.but with intensive myelosuppressive induction and further post remission therapy abt 40% of such patients can now achieve long term survival and probably cure.

Biology...



AML can be divided into several sub groups according to the french american british morphological classification system (M0 to M7).
M0-immature
M1-acute myeloblastic leukemia with minimal maturation
M2-acute myeloblastic leukemia with maturation
M3-acute promyelocytic leukemia
M4-acute myelomonocytic leukemia
M5-acute monoblastic leukemia
M6-erythroblastic L.
M7-acute megakaryoblastic L.
   Abt 30-40% are M1 and M2.same %age of M4 and M5.M3 constitutes 5-10%.M7 strongly associated with downs syndrome.trans location between chromosome 8 and 21 is found almost exclusively in M1 and M2.all patients with M3 carry translocation t(15;17) and M5 is asso. With t(9;11).

Clinical presentation
Most patients with presents with pallor.fatigue.bleeding or fever as manifestations of their under lying anemia.thrombocytopenia and neutropenia as a result of bone marrow failure.unlike ALL,bulky lymphadenopathy and massive hepatosplenomegaly is not very common.however infants and toddlers may have more organomegly.high WBC count and CNS disease at diagnosis. They are mostly M4 and M5 sub types.

Disseminated intravascular coagulation may occur with any sub group but common in M3.

Chloromas are localised collections of leukemia cells seen almost exclusively in patients with AML.They may occur at any site including CNS, bones typically orbit and skin.gingival hyper trophy may be present.

Diagnosis must be confirmed by bone marrow exam.morphological cytochemical immunophenotypic and genetic characteristics of the leukemia blast should be determined if possible.sometimes the diagnosis is preceded by prolonged pre leukemia phase lasting several weeks or months.usually this is characterised by a lack of one of the normal blood cell lineages resulting in either a refractory anemia a moderate degree of neutropenia or thrombocytopenia.the condition is often referred to as myelodysplastic syndrome.some children may be seen with hypo plastic marrow that may develop later into an acute leukemia.

Treatment
The main drug used for induction therapy are combination of cytosine arabinose and an anthracycline(doxorubicin or daunorubicin).the induction regimen most commonly used is 100 mg/m2/day of cytosine given as continuous infusion for 7 days plus daunomycin at 45 mg/m2/daw for 3 days with or without additional drugs.other drugs like etoposide n thioguanine have been added.with the current regimen remission could be induced in about 70 to 80% of children.however without further therapy most children relapse within 1 year.
Post remission therapy include high ford chemo therapy hocke Ara C and etoposide or bone marrow trans plantation.
allogenic bone marrow trans. is superior to intensive chemo therapy alone.
The subset acute pro myelocytic L. which accounts for about 10-15% of children with AML should be treated separately.best therapy to induce remission by All transretinoic acid as a single agent and then the remission is consolidated with post remission intensive chemo therapy.
Children also require platelets and broad spectrum antibiotics for control of severe infections.   

Amoebic liver abscess

Amebic liver abscess.

Liver involv by E. hirtolytica produce ALA.

Pathogenesis.
Trophozoit of E.his carid as emboli by portal vein.capilarys of lever as filter n hold parasites.larg no.cause coagulaton necrosis n absces formatiA?n. Absces is single n at postsup of rt lobe of liver.

Clinical manifestations.



 Fever swat wt los chils rigor. Pain in rt hypochondrium. Diaphram irretaton refer pain in rt shoulder. Tenderness of liver.

Complicatom.

Granuloma cutis. Abses rupture in bronchus. Anchovy sauce pus. Peritonitis. Pericarditis n rarely cardiac tamponade. Metastatic brain abses n slenic abses.

Investigation.

Polymorphonucler leucocytosis.
Alkaline phosphatase elevaton.
SGOT reflect severty of disease.
Raised dome of diafragm in radio.
rt sided pl efusion n implis basal pneumonitis.
Floroscopy,
diminis moment of diafram on rt side.
Ultrasonic scanig locaton of abses.
Isotop liver scan.
Serology test.
Aspiration.

Tretment

Metronidazole 800mg thrice daily. Chloroquine 300mg twice daily.  Ementine or dehydroementine. Chemotherapy is not prompt.   Furamide at a dose of 500mg thrice a day.?