Menu

 

  • Pyogenic abscess, accounts for 80% of abscess.
  • Amebic abscess due to Entamoeba histolytica, accounts for 10%.
  • Fungal abscess, accounts for < 10%.
  • 50% of solitary liver abscesses occur in the right Liver lobe.
  • Right hepatic lobe (~75%), less commonly left (20%) or caudate (5%) lobes.
  • Pyogenic abscesses are usually polymicrobial.
  • 50% of the bacterial cases develop by cholangitis. 
  • Pyogenic Abscess- initial manifestation of an occult intra‐abdominal malignancy (up to 15%).
  • Positive blood cultures in up to 50%.
  • Most common organisms: E. coli, Klebsiella, Streptococcus, Staphylococcus, & anaerobes.
  • K pneumoniae thought to be associated with colorectal cancer.
  • Fever in 90% & abdominal pain in about 50-75%.
  • In-hospital mortality estimated at 2.5% -19%

       Drainage of the abscess & antibiotic treatment are the cornerstones of treatment.

  • Antibiotic Therapy: 
        If the size of the abscess < 3-5 cm
        Oral antibiotics are given after intravenous antibiotics are first administered. 
  • Percutaneous Drainage: 
         Abscess > 5 cm
         Continuous fever despite 48-72 hours of ABX therapy
         Indications that the abscess may rupture
         U/S or CT-guided aspiration & drainage- first-line treatment. 
  • Surgery:
          Where percutaneous drainage is impractical.
          When there are complications like rupture or numerous abscesses. 
          Open surgery or laparoscopic surgery.



Significant electrolyte depletion can result in serious complications. These guidelines are meant to assist with empiric dosing of electrolytes for inpatients. Doses may need to be adjusted based on patient-specific factors, including creatine & cardiac status; & responses to initial doses.

  • Goal serum potassium concentration 4.0 – 5.0 mEq/L
  • Goal serum ionized calcium concentration 1.12 – 1.3 mmol/L
  • Goal serum magnesium concentration 2.0 – 2.4 mg/dL
  • Goal serum phosphorus concentration 2.7 – 4.6 mg/dL

IV electrolyte replacement can produce life-threatening complications, serious arrhythmias & phlebitis; therefore, supplementation must be carefully monitored.  There are multiple underlying factors for electrolyte disorders in adult inpatients, including alterations in absorption, distribution, hormonal, and/or homeostatic mechanisms that can all cause disturbances. Treating the underlying cause and prescribing adequate therapy is essential for repletion. In addition, the intracellular vs. extracellular electrolyte concentrations must be considered. Due to distribution variances, labs may not directly correlate with true electrolyte levels. Therefore, continuous monitoring is essential to properly replete patients.

 

A systematic approach to the analysis of the fluid in conjunction with the clinical presentation helps to understand the etiology, narrow the differential diagnoses, & design a management plan. Includes biochemistry, microscopic examinations & infectious disease tests.


 

 Chronic, constantly progressive disease. Initially, it affects the muscle tissues of the face, then spreads to the trunk. The following types of MG are distinguished:
  • Ocular – the nerve endings in the cranial region are affected, and the eyelids fall asymmetrically. The patient complains of double vision and deterioration in visual acuity. Gradually focusing on one subject becomes difficult.
  • Bulbar – the lesion extends to the masticatory muscles and tissues of the larynx. The patient’s voice changes, speech becomes quieter and nasal. Some consonants are very difficult to pronounce, and stuttering develops. Due to the penetration of fluid into the respiratory tract, the risk of pneumonia increases.
  • Lambert-Eaton – the muscles of the arms, legs, and neck do not receive nerve impulses. It is difficult for the patient to coordinate these areas of the body. This form is diagnosed in the elderly and is characterized by rapid progression.
  • Generalized – the muscles of the eyes are immediately affected, then the process spreads to the larynx, arms, legs, and hips. The main danger of this form is that the respiratory muscles are affected over time.
The disease is characterized by constant progression. 

Plasma exchange (PLEX) is first-line for severe exacerbation & usually causes improvement in a few days. It directly removes anti-acetylcholine receptor antibody from the body. May be more effective in MuSK+ patients.

IVIG may be useful for less severe exacerbations; takes longer to work (e.g., 2-3 weeks), but the efficacy may be more sustained. The dose of IVIG is 2 grams/kg, usually divided over 2 or 5 days.


  1. Immune-mediated: Some drugs can trigger an immune response in the body, leading to the production of antibodies that attack and destroy platelets. This immune-mediated destruction of platelets is one of the common mechanisms in drug-induced thrombocytopenia. Examples of drugs associated with immune-mediated DITP include certain antibiotics (such as penicillin and sulfonamides), anti-inflammatory drugs (such as nonsteroidal anti-inflammatory drugs, or NSAIDs), and anticonvulsants.

  2. Non-immune-mediated: Other drugs can cause thrombocytopenia through non-immune mechanisms, such as direct toxicity to the bone marrow where platelets are produced. Chemotherapy drugs, for example, can suppress bone marrow function and lead to a decrease in platelet production.


Average arterial pressure throughout one cardiac cycle, systole, and diastole. 
Surrogate indicator of blood flow and believed to be a better indicator of tissue perfusion.
To perfuse vital organs requires the maintenance of a minimum MAP of 60 mmHg. 
MAP = [Cardiac Output (CO) x Systemic Vascular Resistance (SVR)] + Central Venous Pressure (CVP)
MAP = (CO × SVR) + CVP
Because CVP is usually at or near 0 mmHg, this relationship is often simplified to:
MAP ≈ CO × SVR.
Cardiac output (CO) = Heart Rate (HR) X Stroke Volume (SV).

Stroke Volume is by ventricular inotropy and preload. 
Preload is affected by blood volume and the compliance of veins. 
Increasing the blood volume increases the preload, increasing the stroke volume and therefore increasing cardiac output. 
Afterload also affects the stroke volume in that an increase in afterload will decrease stroke volume. 
Heart rate is affected by the chronotropy, dromotropy, and lusitropy of the myocardium. 
Systemic vascular resistance is determined primarily by the radius of the blood vessels. 
Decreasing the radius of the vessels increases vascular resistance. 
Increasing the radius of the vessels would have the opposite effect. 
Blood viscosity can also affect systemic vascular resistance. 
An increase in hematocrit will increase blood viscosity and increase systemic vascular resistance. 
Viscosity, however, is considered only to play a minor role in systemic vascular resistance.


Common formula:
MAP = Diastolic blood pressure + 1/3 (Systolic Blood pressure – Diastolic Blood Pressure)
          = DBP + 1/3(SBP – DBP) or 
MAP = DBP + 1/3(Pulse Pressure)
MAP = [Systolic Blood Pressure + (2 x Diastolic Blood Pressure)]
                                                      3
Example, if blood pressure is 82 mm Hg/50 mm Hg,

MAP = SBP + 2 (DBP) = 82 +2 (50) = 182 = 60.67 mmHg; or
                3                              3              3
MAP = 1/3 (SBP – DBP) + DBP = 1/3 (82-50) + 50 = 10.67 + 50 = 60.67 mmHg


In sepsis, vasopressors are often titrated based on the MAP. 
In the guidelines of the Surviving Sepsis Campaign, it is recommended that MAP be maintained ≥ 65 mm Hg.

Chronotropy = Heart Rate
Dromotropy = Speed of electrical conduction in the Heart
Lusitropy = Rate of myocardial relaxation
Inotropy = Contractility

Mean Arterial Pressure (MAP) = 70-100 mmHg

Cardiac Index (CI) = Cardiac Output (CO)/ Body Surface Area (BSA) 
                               = 2.5-4 L/min/m2.

Stroke volume (SV) = Cardiac output / Heart Rate 
                                 = 60-120 mL/beat.

Systemic vascular resistance (SVR) = (MAP – Mean Right Atrial Pressure) x 80 / CO 
                                                          = 800-1200 dynes x sec/cm3.
Pulmonary Vascular Resistance = (Mean Pulmonary Artery Pressure – Mean Pulmonary Capillary Wedge Pressure) X 80 / Cardiac Output 
                                                 =125-250 dynes X sec/cm3.


Pulse Pressure (PP)
Pulse Pressure (PP) = Systolic Blood Pressure – Diastolic Blood Pressure
Normal pulse pressure, approximately 40 mmHg.
Change in pulse pressure (Delta Pp) = Volume change (Delta-V) = Stroke volume (SV)
                                                                 Arterial compliance (C)     Arterial compliance (C)
                                                                         
                                                            = Approximately 80 mL = Approximately 40 mm Hg
                                                                       2 mL/mm Hg
Arterial compliance (C) = Delta V/Delta P
Because the aorta is the most compliant portion of the human arterial system, the pulse pressure is the lowest. Compliance progressively decreases until it reaches a minimum in the femoral and saphenous arteries, and then it begins to increase again. 

Narrowed PP (Low) < 25% of the SBP.
Widened PP (High) > 100 % of SBP.

Widened (High) Pulse Pressure (PP)
> 100 % of SBP
Indicative of a noncompliant stiff aorta with a reduced ability to distend and recoil.
With age there is a decrease in compliance of the aorta & small arteries.
In majority, SBP increase while DBP remain near normal. 
In aortic regurgitation (AR), backward, or regurgitant flow, increase SBP and decrease DBP, and therefore increased PP.
Heart valve conditions (Aortic regurgitation, Aortic sclerosis)
Reduced blood viscosity (Severe Iron deficiency anemia)
Increased systolic pressure (Hyperthyroidism), 
Less compliant arteries (Arteriosclerosis)

Narrow (Low) Pulse Pressures (PP)
< 25% of the SBP
Decreased pumping (Heart failure), 
Decreased Stroke Volume (Aortic Stenosis)
Decreased Blood Volume (Blood loss), 
Decreased Filling Time (Cardiac Tamponade/Pericarditis). 
Dysautonomia/postural orthostatic tachycardia syndrome (POTS)

  • RA-associated interstitial lung disease (RA-ILD).
  • Pleural disease (pleural thickening/effusions).
  • Airway disease (Both upper & lower airway).
  • Rheumatoid nodules
  • Drug-induced lung toxicity (i.e., Methotrexate-induced lung injury)
  • Fibro-bullous disease
  • Thoracic cage immobility
  • Venous thromboembolic disease
  • Vasculitis
  • Pneumonia.
RHEUMATOID EFFUSION:
  • WCC <5000/mm3
  • Fluid glucose <60 mg/Dl
  • Pleural fluid to serum glucose ratio < 0.5
  • pH < 7.3
  • High pleural LDH level (ie, > 700 IU/L)
  • Cytology: Slender or elongated multinucleated macrophages, round giant multinucleated macrophages, and necrotic background debris.
Pulmonary function testing in ILD (PFT):
  • Reduced VC, lung volumes, & DLCO.
  • Oxygen desaturation during exercise.
  • Restrictive abnormalities common (poor muscle strength or kyphosis due to osteoporosis rather than ILD).


 

  • Indicator of kidney damage and / or a biomarker of systemic diseases dates back to 1969, when elevated albumin levels were first demonstrated in the urine of patients with newly diagnosed diabetes.
  • Urine dipstick is a relatively insensitive marker for albuminuria, not becoming positive until albumin excretion exceeds 300-500 mg/day. 
  • Normal rate of albumin excretion is < 30 mg/day (20 mcg/min).
  • Persistent albumin excretion between 30-300 mg/day (20 to 200 mcg/min) is called moderately increased albuminuria (formerly called "microalbuminuria").
  • Excretion > 300 mg/day (200 mcg/min) represents overt or dipstick positive proteinuria (severely increased albuminuria [formerly called "macroalbuminuria"].
  • Albuminuria reflects functional and / or structural changes in the glomerular filtration membrane that allow increased leakage of albumin into primary urine in amounts exceeding the reabsorption capacity of the proximal nephron tubules. 
  • Albuminuria considered as an indicator of early damage (dysfunction) of the vascular endothelium (including the glomerular vessels), which leads to increased permeability of the vascular wall. 
  • Relationship between albuminuria and cardiovascular risk has been shown in studies of the general population. 
  • It is linear and risk is independent of eGFR. 
  • Associated with arterial stiffness assessed by the pulse wave velocity measurement







  • Cytoplasmic enzymes present in tissues throughout the body.
  • Oxidoreductase, enzyme of the anaerobic metabolic pathway.
  • Heart, muscle, kidney, lung, and RBC’s have the highest concentration.
  • Upon tissue damage, the cells release LDH in the bloodstream.
  • Drugs that can increase LDH include alcohol, aspirin, fluorides, narcotics, anesthetics, clofibrate, mithramycin, and procainamide.
  • Cancer cells employ LDH to increase their aerobic metabolism (glycolysis, ATP production, & lactate production): Warburg effect.
  • CSF LDH increases in bacterial meningitis (normal in viral meningitis).
  • Cancer cells undergo LDH mediated energy production to fulfill the demand for fast cellular growth (marker of metastases, prognosis, survival rates., and radiosensitivity).
  • LDH serves as a general indicator of acute and chronic diseases.
  • LDH helps in distinguishing exudate from transudate effusions.
  • Isozymes, named LDH-1 through LDH-5, have differential expression in different tissues.

 

Role of Bile acids

  • Bile acids play a key role in the absorption of lipids in the small intestine. 
  • Contribute to cholesterol metabolism by promoting the excretion of cholesterol. 
  • Denature dietary proteins, thereby accelerating their breakdown by pancreatic proteases. 
  • Direct and indirect antimicrobial effects. In this capacity, recent evidence suggests bile acids are mediators of high-fat diet-induced changes in the gut microbiota. 
  • Act as signaling molecules outside of the gastrointestinal tract.

The primary bile acids—cholic acid and cheno-deoxycholic acid—are synthesized from cholesterol in the liver.

The maximal rate of bile acid synthesis is on the order of 4 to 6 g/day.



Horseshoe kidneys are often asymptomatic with incidence of approximately 1 in 500 in the normal population with a male preponderance of 2:1.

The isthmus connecting the two renal masses may be positioned in the midline or laterally resulting in an asymmetric horseshoe kidney, 70% of which are left dominant.

The isthmus consists of renal parenchyma in about 80% of cases with the remainder being composed of a fibrous band.

In more than 90% of cases, fusion occurs at the lower pole, although fusion may occur at the upper pole in a small minority of cases.

Higher incidence of UPJ obstructions, nephrolithiasis, and reflux compared to the general population. Increased frequency of some common renal cancers including transitional cell tumors (three to four times more common), Wilms tumor (twice as frequently), and an extremely large increase in very rare tumors such as carcinoid (62 to 82 times).






Autosomal Dominant, M = F, by 60 yrs-50% need renal replacement therapy

Multisystem & progressive disease with cysts formation

Kidney enlargement with other organ involvement (liver∼ 80%, pancreas 7-36%, spleen)

Intracranial aneurysms in ∼6% of pts without family history & ∼20% with a family history (rupture in 65-75%, usually before age 50)

Cardiac Valve abnormalities in 25-30%








  • First sensation of bladder filling at 100–150ml in an adult.
  • Feeling of need to pee at 200 - 350 ml of urine
  • Can comfortably hold between 300 - 450 ml
  • Wall pressure of 5 - 15 mm Hg creates a sensation of bladder fullness while 30 mm Hg & beyond is painful.
  • Most people pee 6 or 7 times/ 24 hours (4 -10 times daily is healthy).
  • Normal 24-hour Urine output is 800 - 2000 ml/day (at normal fluid intake of about 2 liters/day).





Calot's triangle is a small (potential) triangular space at the porta hepatis of surgical importance as it is dissected during cholecystectomy. Its contents, the cystic artery and cystic duct must be identified before ligation and division to avoid intraoperative injury.

Borders

  • Medial – common hepatic duct.
  • Inferior – cystic duct.
  • Superior – inferior surface of the liver.

The above differ from the original description of Calot’s triangle in 1891 – where the cystic artery is given as the superior border of the triangle. The modern definition gives a more consistent border (the cystic artery has considerable variation in its anatomical course and origin).

Contents

  • Right hepatic artery
  • Cystic artery
  • Cystic lymph node (of Lund)
  • Connective tissue

  • Lymphatics
  • Occasionally accessory hepatic ducts and arteries

Significance

  • Cystic artery arises from Right Hepatic Artery in the Calot's triangle in 75%
  • Cystic artery origin & course vary in 25% of population.

IV/IM admin of cosyntropin (250 μg), with collection of serum & measurement of cortisol at baseline & 30–60 min post stimulation.

Supra-physiological dose stimulates the pituitary & releases cortisol from the adrenal cortex, as long as the adrenal cortex has a functional reserve.

Factors affecting ACTH stim test interpretation:

  • Falsely negative or normal in mild disease or disease of recent onset.
  • Most common- false-positive test is seen in recent use of corticosteroids
  • Exogenous steroids lead to both baselines &adrenal responsiveness to cosyntropin.
  • Propofol impairs adrenal steroidogenesis
  • Midazolam, morphine, and fentanyl blunt the HPA axis, thereby interfering with corticosteroid metabolism.
  • Metyrapone, etomidate, ketoconazole, megesterol, & mitotate interfere with cosyntropin function.
  • Rifampin & phenytoin may increase cortisol metabolism.

In females, response to ACTH may be affected OCs which increase CBG levels.

  • Salivary cortisol response can be useful as their measurement is a surrogate for serum free cortisol & are not affected by OCs
  • Opioid receptors are present in the pituitary gland & hypothalamus, & opioids may impact HPA function.
  • Nenke et al studied 17 pts treated with long-term opioids. Five of the 17 (29%) were found to have evidence of AI, with cortisol levels of <5 μg/dL.




 

In patients ≥65 years of age treated with medication for type 2 diabetes, hemoglobin A1c values of 7%–8% have shown the greatest reduction in mortality in multiple studies. The specific hemoglobin A1c target between 7% and 8% should be based on shared decision-making and the overall condition of the patient at that specific age, with goals in the lower 7% range for those with good to excellent functional status. It is suggested that lower hemoglobin A1c values are associated with frequent hypoglycemia, which presents a greater risk than a higher hemoglobin A1c value alone. Hemoglobin A1c values over 9% are associated with greater mortality. Thus, while the risk of complications increases linearly with hemoglobin A1c, mortality has a U-shaped curve. Management of blood pressure and treatment with statins improves mortality in these patients as well and is important in addressing overall cardiovascular risk.



 

Xanthogranulomatous pyelonephritis is an uncommon, severe, subacute, or chronic suppurative process characterized by destruction and replacement of the renal parenchyma by granulomatous tissue containing histocytes and foamy cells. It is most often associated with chronic obstruction and stones with ongoing infection. It is also referred to as a pseudotumor due to an enlarged kidney resembling a tumor and the ability of local invasion and destruction.

The etiology remains unknown. However, most of the cases result from chronic urinary obstruction and infection. The organisms most commonly associated with XGP are Escherichia coli, Proteus mirabilis, Pseudomonas, Enterococcus faecalis, and Klebsiella, etc. Urinary obstruction occurs as a result of calculus, most commonly, staghorn calculus (in almost 80% of patients), which serves as a nidus for infection resulting in the destruction of the renal parenchyma.




 

Defined as neoplastic lesion in the periumbilical region arising as a primary tumor or representing as a site of metastasis from visceral organ malignancies such as from the gastrointestinal tract and the reproductive organs. The overall incidence is 1-3% in general population with malignancies. The primary site of malignancy associated is significantly different in men and women. The most common primary site in men is the stomach followed by the colon and pancreas, whereas in women, the most common site is the ovary followed by endometrium, colorectal, and pancreas.

The prognosis of patients presenting with Sister Mary Joseph’s nodule is generally poor as it is a sign of advanced malignancy. Management of the disease should consider patient preference, the clinical state of the patient, and the etiology of the primary malignancy.






Term porcelain gallbladder (PGB) is often used to describe calcification of the gallbladder wall. When infiltrated by extensive calcium deposits, the gallbladder wall can become fragile, brittle and bluish in appearance, resulting in a ‘porcelain’ appearance.

The true incidence of porcelain gallbladder is unknown, but it is reported to be 0.6-0.8%, with a male-to-female ratio of 1:5. Most porcelain gallbladders (90-95%) are associated with gallstone.  Mean age at diagnosis is 32 to 70 years.

Patients with porcelain gallbladder are usually asymptomatic, and the condition is usually found incidentally on plain abdominal radiographs, sonograms, or CT images.

Based on early studies which revealed a high association between porcelain gallbladder and gallbladder adenocarcinoma (22-30% of porcelain gallbladders developing gallbladder adenocarcinoma), cholecystectomy has been routinely performed when a porcelain gallbladder is identified.

More recent studies have cast some doubt on the association, and the risk of gallbladder cancer associated with calcification of the wall may be as low as 5-7%. There is no accepted follow-up interval, but the annual incidence of developing gallbladder cancer is likely to be <1% per year.






Dupuytren’s contracture is predominantly a myo-fibroblastic disease that affects the palmar and digital fascia of the hand and results in contracture deformities. The most commonly affected digits are the fourth and fifth digits. It is a genetic disorder that often is inherited in an autosomal dominant fashion, but is most frequently seen with a multifactorial etiology. There are a number of factors that are believed to contribute to the development or worsening of this disease.

These include:

  • Men are more likely to develop the condition than women.
  • People of northern European (English, Irish, Scottish, French, and Dutch) and Scandinavian (Swedish, Norwegian, and Finnish) ancestry are more likely to develop the condition.
  • Dupuytren's often runs in families.
  • Drinking alcohol may be associated with Dupuytren's.
  • Diabetes, HIV, Vascular disease, smoking and seizure disorders are more likely to have Dupuytren's.
  • Incidence of the condition increases with age.



  1. Uses x-rays at two energy levels to determine the bone mineral content.
  2. Major role in diagnosis of osteoporosis, the assessment of patients' risk of fracture, and monitoring response to treatment.
  3. T-score is a number of standard deviations between the patient’s mean BMD and the mean of the population compared with reference populations matched in gender and race.
  4. Z-score is the number of standard deviations above or below the mean of age-matched controls.
  5. DEXA could be used to measure bone density at many skeletal sites, two sites are typically measured: the first four vertebrae of the lumbar spine posteroanterior, and the proximal femur (“hip”), including the femoral neck and the trochanteric areas and total hip measurement. Femoral neck and lumbar spine are the gold standard for evaluating osteoporosis, with good accuracy and high precision.
  6. All women 65 years and older and men 70 years and older should be screened for asymptomatic osteoporosis.

The World Health Organization (WHO) defines T-scores as:

  • Greater than or equal to -1.0: normal
  • Less than -1.0 to greater than -2.5: osteopenia
  • Less than or equal to -2.5: osteoporosis
  • Less than or equal to -2.5 plus fragility fracture: severe osteoporosis

Clinical risk factors included in WHO fracture algorithm

  • Age
  • Low body mass index
  • Prior fracture after age 50
  • Parental history of hip fracture
  • Current smoking habit
  • Current or past use of systemic corticosteroids
  • Alcohol intake >2 units daily
  • Rheumatoid arthritis 






 

  • Patients who undergo splenectomy are at increased risk of infections secondary to encapsulated organisms: H Influenzae, Streptococcus pneumoniae & Neisseria meningitidis. 
  • Vaccinations against these organisms are highly recommended in patients who have undergone splenectomy. 
  • Careful attention must be paid to post-splenectomy patients presenting with febrile illnesses as they may require more aggressive, empiric antibiotic therapy.
  • Palpation of spleen ---see below



Distinctive dark red rash appears on the hands, feet, calves, neck, and face, and the tongue and mouth turn dark red.

Many people with niacin deficiency also have deficiencies of protein, riboflavin (a B vitamin), and vitamin B6.

Pellagra develops only if diet is deficient in niacin & tryptophan (body can convert tryptophan to niacin).

Affects the skin, digestive tract, & brain.

Also develops in:

Hartnup disease (absorption of tryptophan is impaired), & Carcinoid syndrome (tryptophan is not converted to niacin).

Alcoholism & isoniazid can lead to a deficiency of niacin.

The diagnosis of niacin deficiency is based on the diet history and symptoms. Measuring a by-product of niacin in urine can help establish the diagnosis, but this test is not always available. The diagnosis is confirmed if niacin relieves symptoms.

Treatment: Nicotinamide, unlike nicotinic acid, does not cause flushing, itching, burning, or tingling sensations.



Disclaimer

The contents of this website, such as text, images and other information, are "NOT" a substitute for medical decisions or medical advice. This website is for informational and educational purposes only and not for rendering medical advice. The opinions expressed on this site are our own and do not represent the views of any affiliated organization. Images, text and graphics will be taken from research articles published online and from Google Images/Academic. Although we strive to keep the medical information on our website up to date, we cannot guarantee that the information on our website reflects the latest research. In case of emergency, call 911 immediately. Please consult your doctor for personalized treatment. Always seek the advice of a physician or other qualified healthcare professional with any questions you may have regarding the disease. Never disregard or delay seeking professional medical advice or treatment because of something you have read on this website. This website does not endorse or recommend any specific test, doctor, product, procedure, opinion or other information contained on the website.

Search This Site

Copy Right @DharSaty

'O' My Dear LORD! Lead us, guide us, inspire us, and remind us to believe in possibilities.