Systemic Lupus Erythematosus ACR Criteria

1. Serositis: Pleuritis (inflammation of the membrane around the lungs) or pericarditis (inflammation of the membrane around the heart); sensitivity = 56%; specificity = 86% (pleural is more sensitive; cardiac is more specific).

2. Oral ulcers (includes oral or nasopharyngeal ulcers).

3. Arthritis: nonerosive arthritis of two or more peripheral joints, with tenderness, swelling, or effusion; sensitivity = 86%; specificity = 37%.

4. Photosensitivity (exposure to ultraviolet light causes skin rash, or other symptoms of SLE flareups); sensitivity = 43%; specificity = 96%.

5. Blood—hematologic disorder—hemolytic anemia (low red blood cell count) or leukopenia (white blood cell count<4000/µl), class=”mw-redirect”>lymphopenia (<1500/µl) sensitivity =” 59%;” specificity =”">

6. Renal disorder: More than 0.5g per day protein in urine or cellular casts seen in urine under a microscope; sensitivity = 51%; specificity = 94%.

7. Antinuclear antibody test positive; sensitivity = 99%; specificity = 49%.

8. Immunologic disorder: Positive anti-Smith, anti-ds DNA, antiphospholipid antibody, and/or false positive serological test for syphilis; sensitivity = 85%; specificity = 93%. Presence of anti-ss DNA in 70% of cases (though also positive with rheumatic disease and healthy persons)

9. Neurologic disorder: Seizures or psychosis; sensitivity = 20%; specificity = 98%.

10. Malar rash (rash on cheeks); sensitivity = 57%; specificity = 96%.

The mnemonic to remember the 11 symptoms is ‘SOAP BRAIN MD’.

Some people, especially those with antiphospholipid syndrome, may have SLE without four criteria, and also SLE may present with features other than those listed in the criteria.

Aedes - dengue fever

Two cases of dengue fever have been found in Kathmandu. Dengue is caused by dengue virus (DenV), a mosquito-borne flavivirus. It is transmitted by Aedes mosquitos.

“This is the first discovery of dengue fever in the Kathmandu Valley even though the disease was detected in the Tarai and inner-Tarai districts some five years ago,” according Sukraraj Tropical and Infectious Disease Hospital, Teku.

“Aedes mosquitos are found in cold water, freeze, cooler houses and other cold places and rich people are vulnerable to dengue fever,” said Dr Bashu Dev Pandey at Teku Hospital on Monday.

He said the disease is communicable from one person to another and its symptoms are high fever, bleeding and unconsciousness. “If an infected person is not treated on time, the patient may die,” he said.

Aedes mosquitos also breed on water collections in artificial containers such as plastic cups, used tires, broken bottles, flower pots, etc. Dr Pandey advised people to keep their freezes and cooler houses clean and treated water to remain safe from the disease.

Dengue fever is acute febrile disease which normally occurs in the tropics. It is also known as break-bone fever and can be life-threatening. There is no tested and approved vaccine for the dengue flavivirus. Prevention of dengue mainly resides in mosquito control. Dengue may also be transmitted via infected blood products including blood transfusions, plasma, and platelets.

Source : www.thehimalayantimes.com

From Nepalnews.com

Cases of dengue fever and Leptospirosis have been detected in various parts of the country including Kathmandu, Chitwan, Dhangadi, Nepalgunj, Kanchanpur, Bhairahawa, Tanahu and Dhading in the recent days, Kantipur daily reported.

The disease is spread from a kind of mosquito that breeds in fresh water. Tests have shown the two diseases are spreading fast in Chitwan.

Out of 72 samples of patients suffering from viral fever sent from Chitwan for special tests at the central laboratory in Kathmandu, ten samples tested positive for Leptospirosis, three for Dengue and one for both.

“Of the samples we found Leptosporis in ten, dengue in three and both in one,” said Dr Geeta Shakya, director of the central laboratory. “There is a need to investigate further on these diseases.”

Dr Basuedev Pande, a specialist doctor at Shahid Shukraraj Tropical and Contagious Diseases Hospital in Teku, warned of an epidemic if preventive measures are not taken soon.

“The cases of dengue has been found in many places of the country,” said Dr Pande. “It will invite an epidemic if it is not controlled on time.”

Dr Pande claimed two persons from Kathmandu were undergoing treatment for Dengue at Tribhuvan University Teaching Hospital (TUTH) and two Japanese nationals had also contracted the disease in Chitwan.

Dr Pande further said, 40 percent of the patients who are undergoing treatment for Typhoid in Teku hospital have also suffered from Leptospirosis.

Director at Epidemiology and Disease Control Division, Dr GD Thakur, takes the occurrences as sporadic. “There are few cases of Lepto and Dengue in Chitwan,” he said. “It can’t be termed an outbreak.”

www.nepalnews.com

Lecture notes

Obesity , as known from various Studies, is an associated cause for increase in morbidity and mortality. There is  50–100% increase in risk of death from all causes compared to normal weight people, mostly due to cardiovascular causes. Mortality rates rise as obesity increases, particularly when obesity is associated with increased intraabdominal fat . Life expectancy of a moderately obese individual could be shortened by 2–5 years, and a 20- to 30-year-old male with a BMI > 45 may lose 13 years of life. It is also apparent that the degree to which obesity affects particular organ systems is influenced by susceptibility genes that vary in the population.

Insulin Resistance and Type 2 Diabetes Mellitus

Obesity  is a major risk factor for diabetes, and as many as 80% of patients with type 2 diabetes mellitus are obese.

Hyperinsulinemia and insulin resistance are pervasive features of obesity, increasing with weight gain and diminishing with weight loss . Insulin resistance is more strongly linked to intraabdominal fat than to fat in other depots. The molecular link between obesity and insulin resistance in tissues such as fat, muscle, and liver has been sought for many years.

Major factors under investigation include:

(1) insulin itself, by inducing receptor downregulation;

(2) free fatty acids, known to be increased and capable of impairing insulin action;

(3) intracellular lipid accumulation; and

(4) various circulating peptides produced by adipocytes, including the cytokines TNF- and IL-6, RBP4, and the “adipokines” adiponectin and resistin, which are produced by adipocytes, have altered expression in obese adipocytes, and are capable of modifying insulin action.

Weight loss and exercise, even of modest degree, are associated with increased insulin sensitivity and often improve glucose control in diabetes.
Also read Dieting for weight control : good or bad

Reproductive Disorders

Males-

• Male hypogonadism is associated with increased adipose tissue, often distributed in a pattern more typical of females.
• In men >160% ideal body weight, plasma testosterone and sex hormone–binding globulin (SHBG) are often reduced, and estrogen levels  are increased.
• Gynecomastia.

Females-

• menstrual abnormalities in women, particularly in women with upper body obesity.
• increased androgen production, decreased SHBG, and increased peripheral conversion of androgen to estrogen.
• may be associated with polycystic ovarian syndrome (PCOS), with its associated anovulation and ovarian hyperandrogenism; 40% of women with PCOS are obese.
• lower body obesity  may contribute to the increased incidence of uterine cancer in postmenopausal women with obesity.

Cardiovascular Disease

• coronary disease – Read on Acute MI
• stroke
• and congestive heart failure (CHF).

The waist/hip ratio may be the best predictor of these risks.

• Obesity-induced hypertension is associated with increased peripheral resistance and cardiac output, increased sympathetic nervous system tone, increased salt sensitivity, and insulin-mediated salt retention; it is often responsive to modest weight loss.

Pulmonary Disease

• Reduced chest wall compliance,
• increased work of breathing,
• increased minute ventilation due to increased metabolic rate,
• and decreased functional residual capacity and expiratory reserve volume
• Severe obesity may be associated with obstructive sleep apnea and the “obesity hypoventilation syndrome” with attenuated hypoxic and hypercapnic ventilatory responses

Gallstones

higher incidence of gallstones, particularly cholesterol gallstones

Cancer

• Males-

cancer of the esophagus,colon,rectum,pancreas,liver, and prostate

• Females -

cancer of the gallbladder, bile ducts, breasts, endometrium, cervix, and ovaries.

Bone, Joint, and Cutaneous Disease

• Obesity is associated with an increased risk of osteoarthritis, no doubt partly due to the trauma of added weight bearing and joint malalignment.
• The prevalence of gout may also be increased
• Among the skin problems associated with obesity is acanthosis nigricans, manifested by darkening and thickening of the skin folds on the neck, elbows, and dorsal interphalangeal spaces. Acanthosis reflects the severity of underlying insulin resistance and diminishes with weight loss.
• Friability of skin may be increased, especially in skin folds, enhancing the risk of fungal and yeast infections. Finally, venous stasis is increased in the obese.

Source: Harrison’s Internal Medicine Book

The posterior inferior cerebellar artery also known as PICA is the largest branch of the vertebral artery, passes on an irregular course between Medulla and Cerebellum.  It is one of the 3 major arteries supplying  the cerebellum. It supplies the posterior part of inferior surface of Vermis, Central nucleii of Cerebellum and undersurface of Cerebellar hemisphere.It also supplies  Medulla ( branches of PICA along with medullary branches of Vertebral artery) and Choroid Plexus of 4 th ventricle.

Cause :-

• It results from thrombosis of Posterior Inferior Cerebellar Artery.
• Causing lateral part of the medulla oblongata to infarct.
• The most commonly affected artery is the vertebral artery, followed by the PICA, superior middle and inferior medullary arteries.

Lateral Medullary syndrome of Wallenberg

Signs and Symptoms that are Characteristic of Wallenberg Syndrome are-

1. Dysphagia and Dysarthria ( Due to paralysis of Ipsilateral palatal and laryngeal muscles- Innervated by Nucleus Ambiguus)
2. Analgesia and Thermaesthesia on the Ispsilateral side of the face ( Due to lesion of Nucleus and Spinal tract of Trigeminal nerve)
3. Vertigo, Nausea, Vomiting and Nystagmus. ( Lesion of Vestibular nucleii)
4. Ipsilateral Horner Syndrome ( due to lesion of Descending Sympathetic fibres)   Mnemonic- “Horny PAMELa” for Ptosis, Anhydrosis, Miosis, Enophthalmos and Loss of ciliospinal reflex
5. Cerebellar Symptoms and Signs-

• • Cerebellar Ataxic/ Drunken Gait
  • Dysdiadochokinesia ( unable to perform quick alternative repeated actions like pronation/supination)
  • Pendular knee jerk
  • Nystagmus
  • Dysmetria
  • Intention Tremor ( Tremor increases as fingers arrive the target)
  • Hypotonia
  • Rebound phenomenon
  • Scanning speech

are the most popularly used antibiotics. They are  any antibiotic agent that contains a β-lactam chain in the molecular structure. Penicillin is the prototype drug and once was a cure for almost anything. Sir Alexander Fleming discovered Penicillin. It was a miracle discovery in history of Mankind.

Sir Alexander Fleming Discovered Penicillin

Mechanism of Action:

-          Interfere with the synthesis of bacterial cell wall

-          Inhibit transpeptidases so that cross linking does not take place

-          When susceptible bacteria divide in the presence of it- cell wall deficient forms are produced resulting in the lysis of bacterial cell

-          Peptidoglycan cell wall is unique to bacteria and it is non toxic to man

-          Gram positive bacteria have higher susceptibility to PnG

Penicillin G (Benzyl Penicillin):

-          Narrow spectrum; gram positive

-          Majority of gram negative bacilli, M.tuberculosis, ricketsiae, chlamydiae, virus insensitive

-          Resistance:

1. Inherent: PBPs located deeper under lipoprotein where PnG is unable to penetrate
2. Penicillinase: opens the beta lactam ring
3. Penicillin tolerant but not penicillin destroying like pneumococci

-          Pharmacokinetics:

1. Acid labile: gastric acid
2. Low oral absorption and rapid and complete absorption from i.m site
3. Plasma t1/2  30 minutes
4. Poor CSF  and serous cavity penetration but increased in inflammation
5. Rapid renal excretion (GFR-10 % and rest tubular secretion)
6. Tubular secretion blocked by Probenecid: higher and longer lasting plasma concentration

-          Preparation and Dose:

1. Sodium Penicillin G injection
2. Repository Penicillin G injection
   1. Procaine Penicillin G
   2. Benzathine Penicillin G

-          Adverse Effects:

1. Local irritancy and direct toxicity: pain at im site, nausea, thrombophlebitis, mental confusion, muscular twitchings, convulsions, bleeding, hallucinations, CNS stimulation
2. Hypersensitivity: Urticaria, fever, wheezing, edema, serum sickness
3. Superinfections
4. Jarisch Herxheimer reaction

Semisynthetic Penicillins:

1. Acid resistant alternative: Phenoxymethyl penicillin (Penicillin V)
2. Penicillinase Resistant: Methicillin, Cloxacillin
3. Extended Spectrum:
   1. Aminopenicillin: Amoxycillin, Ampicillin, Bacampicillin
   2. Carboxypenicillin: Carbenicillin, Tircarcillin
   3. Ureidopenicillin: Poperacillin, Mezlocillin
   4. Beta- lactamase inhibitor: Clavulanic acid, Sulbactam, Tazobactam

Opioids are among the commonly misused substance by drug abusers around the world. Opioids come in various forms – Heroin , Morphine, Methadone, Coedine, Pethidine, Dihydrocoedeine.

Opioids are a class of drugs derived from the extracts of plant- opium poppy. Used as Analgesics but  most opiates give a feeling of euphoria and a degree of sedation. These side effects are the cause of Abuse of Opioids.

Opioid overdose can be lethal

Clinical Features Of Opiod Intake in body are-
Rapid, intensely presurable experience
Heightened sexual arousal
Increase dose required for same experience within weeks

Withdrawl Symptoms include-
Intense craving , Rhinorrhea, Lacrimation, Yawning, Perspiration, Shivering, Piloerection, Vomiting and diarrhea, abdominal cramps.
Tachycardia, hypertension, mydriasis ( dilation of Pupil ) and facial flushing.

Hallmark Of Opioid Poisoning are-
Respiratory depression – may lead to death
Pin-point Pupil
CNS depression- decresed level of consciousness.
Signs of IV drug misuse like needle tract marks, tattoo.

Severe –
Respiratory depression
Hypotension
Non-cardiogenic pulmonary edema
Hypothermia
Death due to Respiratory arrest and Gastric aspiration
Others- Ventricular Arrhythmia, Conduction defects and heart blocks

Lab Diagnosis Criteria ( CDC)

• Biologic: A case in which opioids are detected in urine, as determined by hospital or commercial laboratory tests. Fentanyl derivatives and certain other synthetic opioids (e.g., oxycodone) might not be detected by routine toxicologic screens.

- OR-

• Environmental: Detection of opioids in environmental samples, as determined by FDA

Management-
1. Clear Airway and provide Respiratory support
2. Supplement increase flow Oxygen administration
- Severe cases Endotrachel intubation may be required.
3. Antidote- Naloxone is the anti-dote for Opioids. Naloxone is given in dose of 0.8-2 mg bolus IV and repeated every 2 minutes until pupil dilates. Opioid overdose is a challenging condition that requires a difficult balancing act between over and under treatment with naloxone. Nalorphine is an alternative. Literature : Naloxone in Opioid Overdose
4. O2 saturation must be monitored .
5. Management of Hypotension.
6. CPAP/ PEEP for ventilator support.

SAY NO TO DRUGS- Medchrome Against Drug Abuse
Warning- Do not take drug without physician’s prescription.

Syndrome in which hepatic encephalopathy , characterized by mental changes progressing from confusion to stupor and coma, results from a sudden severe impairment of hepatic function. According to emedicine/medscape.com Acute liver failure is a broad term and encompasses both fulminant hepatic failure  and subfulminant hepatic failure.

Fulminant hepatic failure (FHF)  which is  defined as the severe impairment of hepatic functions or severe necrosis of hepatocytes in the absence of preexisting liver disease.( encephalopathy within 8 weeks of the onset of symptoms in a previously healthy liver).

Defined originally further as-

• occurring withion 8 weeks of onset of precipitating illness.
• In the absence of evidence of pre-existing liver disease

Classified as-

1. Hyperacute – occurring in less than 7 days. Cerebral edema is common. Commonly caused by viral hepatitis and paracetamol poisoning .

2. Acute- Occuring between 1 week to 4 weeks. Cerebral edema is common.  Follows Drug toxicity and cryptogenic causes.

3. Sub-acute- Occuring between 4 weeks to 12 weeks. Cerebral edema is uncommon. Cryptogenic causes and drugs are main causes.

   
   
   Causes Of Acute liver Failure-
   Enlarge the picture

Causes of acute liver failure

Clinical Assessment-

• Mild episodic symptoms may progress up to hepatic encephalopathy later causing severe cerebral disturbances.
• Reduced alertness, poor concentration
• Behavioural changes- aggressive and restless.
• Altered sensorium
• Flapping tremor or Asterexis
• Fetor hepaticus ( typical smell breath in liver disease)
• Abnormal pupilary reaction
• Hypertension, Bradycardia, hyperventilation
• Profuse sweating, Myoclonus, focal fits, decerebrate posturing and late- Papilloedema

General Symptoms are-

Weakness, nausea and vomiting, right hypochondrial discomfort

Examination may reveal-Jaundice, Reye’s Syndrome

• Fetor hepaticus
• Hepatomegaly is unusual
• Sudden onset ascites
• Normal spleen size

Investigation useful for assessing the problem are-

1. Toxicology Screen of blood and urine for drugs and toxins
2. Hepatitis Virus Antibody screening and test to detect CMV, EBV, HSV etc
3. Liver function test
4. Serum Caeruloplasmin level,  Serum copper, Urinary copper, Slit lamp eye examination to rule out Wilson’s Disease
5. Auto-antibodies like ANF, ASMA, LKM
6. Utrasonography – Liver and Doppler of Hepatic veins

Management-

1. Patient is critical and need ICU care
2. Monitor – Neurological, Cardiorespiratory functions
3. Fluid balance- maintainance and input/output charting
4. Blood Analysis- Arterial Blood Gas Analysis, Peripheral blood count, Electrolytes,Glucose-2 hourly
5. Kidney function test
6. Prothrombin time
7. Infection Survillence-
8. Culture Blood, urie throat, sputum, cannula sites
9. Chest x-ray

Treatment-

1. Conservative treatrment is Dialysis for removal of toxins and drugs
2. Paracetamol Poisoning-NAC (Read Paracetamol poisoning in children)
3. Liver transplant

Monitor the adverse prognostic criteria.

Complications – ( HERMIM – Mnemonic)

• Hypoglycemia
• Encephalopathy and cerebral edema
• Renal failure
• Metabolic acidosis
• Infection
• MODS

Survival – 1 yr =60%

“ Akinetic Rigid Syndrome’ or Idiopathic Parkinson Disease-Are a number of degenerative diseases affecting Basal Ganglia which present with differing combinations of

• Bradykinesia
• Rigidity
• Tremor
• Loss of postural reflex

Epidemiology-

• 90% cases are above 45 years
• Male  and Female have equal risk
• Cigarette smoking is known to be protective.

Cause or Etiology-

• Unknown but toxin called MPTP ( Methyl-Phenyl-Tetrahydropyridine) suspected if disease starts in Young.

Pathology-

Symptoms are the result of depletion of Pigmented Dopaminergic neurons in Substancia Nigra causing impairment in dopaminergic transmission through the NigroStriatal pathway. Lewy Bodies are seen in Nigral cells. Atrophic changes in S. nigra and decrease neurons in Locus Cerulous.

Clinical Features-

source: Brainmind.com

Initial symptoms include- Tiredness, Aching limbs, Mental slowness, Depression and Micrographia ( small handwriting)

General features-

• Expressionless face ( Hypomimia)
• Greasy skin
• Soft Rapid indistinct speech
• Flexed posture
• Impaired postural reflexes

Gait- Festinate Gait is typical of Parkinsonism.  Slow to start walking, short strides, reduced arm swing and loss of balance on turning can occur.

Tremors-

• Resting tremor is typical for Parkinsonism. Coarse tremors usually thumb and fingers ‘ Pill Rolling motion’ , later whole body may have tremors.
• Postural tremors are less obviously noticed but are present

Rigidity-

• Cog Wheel Rigidity- Rigidity with Tremor. Movement become like turning of Cog-wheel .
• Lead Pipe or Plastic Rigidity

Bradykinesia -

• Slowness in Initiating and repeating movements
• Poor fine-movements

Investigations-

Diagnosis is made Clinically

CT, MRI to rule out other causes of tremor like Wilsons Disease.

Management:

LevoDopa ( Dopamine Precursor) + Carbidopa / Benserazide ( Peripheral Dopa Decarboxylase Inhibitor) Is Best combination for treatment of Parkinsonism.

Others- Trihexiphenidyl ( Benzhexol) Or Orphenadrine help to cope with Cholinergic Side-effects of above drugs.

Amantadine ( anti-flu drug) has no effect on Bradykinesia but worksfor Rigidity and Tremor

Entacapone- ( COMT Inhibitor)

Selegiline ( MAO-B Inhibitor)

Dopamine Receptor Agonists like – Apomorphine, Domperidome, Bromocriptine, Pergolide, Ropinirole and Pramipexole are sometimes used.

Surgery-

• Sterotactic Thalamotomy
• Pallidotomy
• Implantation Of fetal midbrain cells in basal ganglia is under experiment.

Speech Therapy and Physiotherapy

Warning- Do not take drug without Physicians Prescription.

Source- Davidson’s Medicine, Lecture Notes.

Details Reading and latest researches on PD – Interested readers http://en.wikipedia.org/wiki/Parkinson’s_disease

MS is one of the most common neurological causes of long term disability. MS has been elaborated in terrific and realistic manner even in movies. Many well-known persons have fallen for this disease and many have set examples for other people living with Multiple sclerosis.

More common among Females with Female : Male 2:1 ratio.

It is more common in the Temperate zones of the Earth’s latitude.

Etiology or Cause:

MS is caused by interplay of multiple genetic and environmental factors. Occurrence is higher in temperate zones, although no specific environmental factors have so far been co-related.

Myelin producing of CNS are target of recurrent Cell-mediated Autoimmune attack. Associated with Class II MHC alleles and genes related to TNF- Alfa and HLA haplotypes.

Familial recurrence rate is 15%

Concordance in Monozygotic twins is 35%

PATHOLOGY- Entry of Activated T Lymphocytes through Blood-Brain-Barrier

Recognition of Myelin derived Ag on surface of CNS’s Ag-presenting microglia

Clonal proliferation

Activation of Cascade of Cytokines

Initiation of Destruction of Oligodendrocyte-myelin Unit by Macrophage .

CLINICAL FEATURES:

Common Presentations:

Optic Neuritis

1. Relapsing and remitting sensory symptoms
2. Subacute painless Spinal Cord Lesions
3. Acute Brain Stem Syndrome
4. 6^th Cranial Nerve palsy or Abducens palsy

Other Signs and symptoms of CNS demyelination:-

1. RAPD and Optic Atrophy
2. Lhermitte’s syndrome
3. Progressive non-compressive paraparesis
4. Partial Brown-sequard syndrome
5. Intranulear Ophthalmoplegia with Ataxia
6. Postural or Rubral Holmes tremor
7. Trigeminal Neuralgia
8. Recurrent Facial Palsy

Onset and Courses:

Rarely before puberty or after 50s

Peak incidence is in the 4^th decades

Symptoms come over days to week and resolve over weeks to months

4 patterns of Course has been seen in Multiple Sclerosis

1. I.            Relapsing and Remitting course-80% cases
2. II.            Fulminant couse- 10% cases, In this type death occurs early
3. III.            Primary progressive -10-20%
4. IV.            Secondary Progressive

Diagnosis

Demonstration of Lesion in more than 1 site at more than 1 time for which there is no other explanation.

Macdonald’s Criteria  has been used for diagnosis

INVESTIGATIONS

MRI, Myelography  to exclude other structural disease

Multiple Sclerosis

Visual Evoked Potential and other Evoked Potentials

CSF examination- Cell count is high, Protein Electrophoresis o CSF- Oligoclonal bands

To Exclude other diseases- Chest x ray, Serum ACE ( Sarcoidosis) , Antiphospholipid antibody and ANA ( SLE) and Serum B12 ( for B12 Deficiency)

Management:

Acute Phase:  High Dose of Methylprednisolone IV 1 gm for 3 days or

Orally 500mg OD for 5 days

Pulse Steroid can be given 3 times in a year

Treatment shortens the course and early  prevention of relapse.

Preventing Relapse:

Immunosuppressive agents – Azathioprine, Cyclophosphamide, Mitoxanthrone

Immuno Modulators- Glatimer Acetate, IV Ig, Natalizumab ( Monoclonal Ab to B-intergrins)

Plasmapheresis

Treatment Of Complications:

Disability

Spasticity- Physiotherapy, Musle relaxants

Ataxia- Isoniazid , Clonazepam

Bladder Symptoms- CISC

Dysaesthesia : Antidepressants, Phenytoin, Methyldopa

Impotence: Sildenafil

Fatigue- Amantadine, Modafinil, Amitriptylline

Prognosis- 50% are disabled by 15 years of Onset of the Disease

Hematemesis : Peptic ulcer

When blood is present in the vomitus it is called Hematemesis. The color may be red when profuse. Often Black to coffee ground color when less sever – acid degraded due to formation of acid-hematin.

It usually indicated Bleeding proximal to Ligament of Teitz.

It should be differentiated from Malena and Hematochezia which present as blood in stool.

Causes of Hematemesis

• Peptic Ulcer 35-50%
• Gastric erosion 10-20%
• Esophagitis- 10%
• Mallory-Weiss Tear 5%
• Vascular Malformations 5%
• Variceal bleeding 2-4%
• Cancer of Stomach and esophagus 2%
• Aorto-enteric fistula 1%

Management

1. IV access
2. Initial Assessment- History, examination, Vitals, Comorbidities.
3. Blood tests- CBC, KFT,bleeding profiles, Blood grouping and matching
4. Resuscitation with Crystalloids, colloids or Blood transfusion
5. Monitor Central Venous Pressure.
6. Oxygen to all shocked patients
7. Endoscopy followed by Electrocautery, Sclerotherapy  etc
8. Visceral Angiography
9. Drug therapy- PPI, H2 blockers, Somatostatin or Octreotide, Vasopressin
10. Surgery