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Medical-infopedia - by Dr. Ali Shahzad Malik, Karachi (2026)

27/11/2025

Have a skin issue? Here’s a handy image to use to assess the problem.

The skin, our body’s largest organ, can be affected by a wide variety of conditions—some mild, others more serious.

Common skin issues include acne, which results from clogged pores and can lead to pimples and cysts, and eczema, a chronic condition marked by itchy, inflamed rashes. Other frequently seen problems are psoriasis, which causes red, scaly patches; rosacea, known for facial redness and bumps; and hives, sudden raised welts triggered by allergies or stress.

These conditions often appear with symptoms like rashes, flaking, or bumps, and while some are temporary, others may require long-term care.

Beyond these, infections also affect the skin. Bacterial infections like cellulitis involve painful swelling and warmth; fungal infections such as ringworm or athlete’s foot thrive in moist areas; and viral infections like shingles cause painful rashes from dormant viruses. More serious concerns include skin cancer, where abnormal cells grow and may spread, and autoimmune-related issues like alopecia areata, which causes patchy hair loss, and vitiligo, where skin loses pigment. Recognizing the symptoms and seeking early medical attention is key to managing these diverse skin conditions effectively.

07/11/2025

ASD and Eisenmenger

An Atrial Septal Defect (ASD) patient can develop tachycardia due to chronic volume overload and electrical remodeling of the heart chambers, and desaturation (low oxygen saturation) due to the reversal of the normal left-to-right blood flow (right-to-left shunting), often in the setting of developing pulmonary hypertension or during specific arrhythmias.

●Tachycardia
The primary cause of tachycardia (rapid heart rate, often experienced as palpitations) in ASD patients is the long-standing volume and pressure overload, primarily on the right side of the heart, resulting from the left-to-right shunt.

Chamber Remodeling: The extra blood flow to the right atrium and right ventricle causes them to dilate and stretch over time.

Electrical Instability: This chronic stretching and associated cellular changes, such as interstitial fibrosis, alter the heart's electrical properties (electrical remodeling).

Arrhythmias: These changes create an unstable electrical substrate, predisposing the patient to various atrial tachyarrhythmias, such as atrial fibrillation, atrial flutter, and supraventricular tachycardia (SVT). Tachycardia can also be a general response to heart failure or reduced cardiac output, which can occur in advanced stages of ASD.

●Desaturation (Low Oxygen)
Normally, an ASD causes a left-to-right shunt, meaning oxygenated blood from the left atrium flows into the right atrium, increasing blood flow to the lungs and generally maintaining normal systemic oxygen saturation (a cyanotic defect).

However, desaturation can occur through several mechanisms:

Pulmonary Hypertension and Shunt Reversal: The chronic, excessive blood flow to the lungs can damage the pulmonary arteries, leading to increased pressure in the lungs (pulmonary hypertension). Eventually, the pressure in the right atrium and pulmonary circulation can equal or exceed the pressure in the left atrium. When this happens, the blood flow reverses (right-to-left shunt), allowing deoxygenated blood to bypass the lungs and enter the systemic circulation, leading to cyanosis and desaturation (Eisenmenger syndrome).

Atrial Arrhythmias: Tachycardia itself, such as atrial flutter or fibrillation, can disrupt the normal hemodynamics of the heart. The rapid and uncoordinated contractions can cause a temporary functional increase in right atrial pressure relative to the left, leading to a transient right-to-left shunt and sudden desaturation, even in patients without established pulmonary hypertension.

Paradoxical Embolism: In a patient with an ASD, a blood clot (embolus) from the venous system (e.g., in the legs) can cross the defect into the left circulation and travel to the brain or other organs (stroke or other arterial occlusion). While this is not a direct cause of general desaturation, it is a related serious complication involving the abnormal blood flow pathway.

In summary, tachycardia in ASD is an arrythmic consequence of long-term cardiac remodeling, while desaturation typically indicates a significant increase in pulmonary pressures leading to shunt reversal or an acute hemodynamic change caused by the arrhythmia itself.

28/10/2025

Primary hyperparathyroidism and surgery

Parathyroidectomy is indicated for all patients with symptomatic hyperparathyroidism. Parathyroidectomy is recommended in patients with asymptomatic hyperparathyroidism with evidence of subclinical target organ complications such as bone disease (osteoporosis/fractures) or renal involvement (reduced kidney function, occult stones) and in those at risk of disease progression

Indications for surgery in asymptomatic patients with primaryhyperparathyroidism, according to some authorities, include:

○Age 0.25 mmol/L (>1 mg/dL) above normal range
○Creatinine clearance 300 mg/day in men
○Presence of nephrolithiasis or nephrocalcinosis by x-ray, ultrasound, or CT.

BP

24/10/2025

PE, Pregnant patients and the D-Dimer

》Request D-dimer testing in all pregnant patients with suspected PE.

●Use the D-dimer result in combination with the YEARS criteria to assess the clinical probability of PE. The YEARS criteria are:

a. Clinical signs of DVT

b. Haemoptysis

c. PE is the most likely diagnosis.

●PE can be safely ruled out if:

▪︎None of the YEARS criteria are met and the D-dimer level is

22/08/2025

Drugs to avoid in Myasthenia Gravis pts

31/05/2024

Lown-Ganong-Levine syndrome.

What is Lown-Ganong-Levine syndrome?
The Lown-Ganong-Levine (LGL) syndrome is one of the pre-excitation syndromes of which Wolff-Parkinson-White (WPW) syndrome is the best known. In WPW syndrome there is an accessory pathway for conduction, called the Bundle of Kent, that bypasses the atrioventricular (AV) node. No such pathway has been identified for LGL. Theories to explain the condition have suggested possible accessory fibres that bypass all, or part of, the AV node.1 In some cases there may be a congenitally malfunctioning AV node.2 Whatever the pathophysiology, conduction is passed from the atria to the bundle of His without the delay usually incurred at the AV node.

Diagnostic criteria include PR interval of no more than 120 ms, normal QRS complex duration, a normal or inverted P wave, and paroxysmal supraventricular tachycardia (PSVT) but not atrial fibrillation or flutter.

The condition was first described in 1952 before the advent of electrophysiological testing, and some people dispute its existence as an entity.3 Where there is a short PR interval but no history of supraventricular tachycardia (SVT), it is probably just a variation of normal. Where arrhythmias have been investigated in people with the diagnostic criteria, another cause has often been found.

Sometimes the duration of conduction through the AV node is fast and this is called enhanced atrioventricular nodal conduction (EAVNC).1

Although tachycardia, along with increased stroke volume, enables cardiac output to meet demands in exercise, a very fast tachycardia is inefficient and may cause compromise. The ventricles do not have adequate time to fill in diastole and this may reduce cardiac output. Tachycardia reduces the duration of both systole and diastole but it is diastole that is reduced more. Around 75% of the blood flow to the right ventricle and 100% of the blood flow to the left ventricle occur during diastole. Hence, there is less time to perfuse the myocardium at a time of increased metabolic need.

How common is Lown-Ganong-Levine syndrome? (Epidemiology)
The initial retrospective study by Lown found nearly 200 electrocardiograms (ECGs) of 13,500 had a short PR interval and a normal QRS complex, giving a prevalence of just over 1% in a selected population.4 Further evaluation has determined that the incidence of paroxysmal supraventricular tachycardia in Lown-Ganong-Levine patients is significantly higher, nearing 11%.. In the general population however, it is very rare, with prevalence estimated to be less than one in a million.5

Continue reading below

Symptoms of Lown-Ganong-Levine syndrome (presentation)4
History
The history is of bouts of tachycardia that may present as rapid palpitations. It most often starts in early adulthood but can present in childhood. It tends to get less frequent with passing years. In the otherwise healthy person there is probably no other feature but, where the heart and circulation are already compromised, perhaps from coronary heart disease, this can produce angina pectoris, shortness of breath and heart failure. There may well be light-headedness and dizziness due to hypotension.

Examination
There is usually no abnormality to be found between attacks, although some people have a resting sinus tachycardia. During an attack the pulse rate may be 200 beats per minute or sometimes even higher.

Diagnosing Lown-Ganong-Levine syndrome (investigations)
A 12-lead ECG is required. The PR interval should be less than 120 ms and with no delta wave. A normal QRS is essential for diagnosis and a delta wave suggests an accessory pathway and a diagnosis of WPW syndrome.

If possible, try to encourage the patient to come in during an attack so that an ECG can be recorded when symptomatic.

Check U&E, calcium and magnesium. Check TFTs.

A Holter monitor may be used to record the heart rate. Ask the patient to note the time that an attack starts and stops. A longer recording of a week increases the chances of recording an episode.

Management of Lown-Ganong-Levine syndrome4
Referral to a cardiologist is required to try to obtain a definite diagnosis.

Echocardiogram and electrophysiological studies may be performed in an attempt made to find a cause for the SVT and assess the risk of sudden cardiac death.

There is no aberrant bundle to ablate as in WPW syndrome.

Beta-blockers such as metoprolol or atenolol may be useful and slow AV conduction.

Non-dihydropyridine calcium-channel blockers such as verapamil may slow AV conduction and can be used to treat an acute PSVT. Verapamil plus a beta-blocker may produce complete heart block and so they should not be used together.

Digoxin can also decrease conduction in the AV node. It has been used to control symptoms in pregnancy.6

In cases refractory to medical therapy, as with other supraventricular tachycardias or accessory pathways, radiofrequency catheter ablation has become a preferred treatment.7

Dual AV sequential demand pacemakers have been used for this condition where medication has failed to give control.8

People with LGL syndrome need special care and management during anaesthesia as they are at high risk of peri-operative arrhythmias which may be life-threatening.2 Certain drugs and anaesthetic agents should be avoided, and specialist cardiology input is helpful.

Prognosis
The syndrome can produce ventricular fibrillation and sudden death.9 However, this is unusual, and it is normally far more benign and can be controlled by pharmacological means.

History
LGL is named after three American cardiologists. Bernard Lown was born in 1921, William Ganong was born 1924 and died in 2007, and Samuel Albert Levine was born in 1891 and died in 1966. The occurrence of frequent paroxysms of tachycardia in patients with a short PR interval and normal QRS duration had been described by Clerc et al in 1938 but it was the Americans who achieved the immortality of an eponym. Bernard Lown was a founder of International Physicians for the Prevention of Nuclear War and, in 1985, the group was awarded the Nobel Prize for Peace. He developed the direct current defibrillator.

02/04/2024

Primary Hyperparathyroidism:

Most common cause is parathyroid single adenoma. Less than 15% are due to adenomas in multiple glands or hyperplasia or ectopic PTH production. 1% or less is due to parathyroid carcinoma.

Familial or genetic cases should be considered in patients younger than 30, more than one parathyroid glands involved, or when part of MEN syndrome (MEN 1.2 or 4).

Mostly cases have hypercalcemia which is mild to moderate which is often clinically not symptomatic due to slow onset. However, patient can have renal &/or bone diseases despite being clinically not having symptoms of high calcium. Like the hypercalcemia, these changes of the bone or kidneys are also detected on testing.

Less commonly, primary hyperparathyroidism can have normal serum calcium. Such cases should be differentiated from secondary hyperparathyroidism due to low Vit D or calcium. High PTH level in these cases can compensate for low calcium and the calcium level may become normal. However, such cases don’t have bone or renal involvement which is seen in primary Hyperparathyroidism.

Renal involvement in primary Hyperparathyroidism include:
Calcium excretion >250 mg/24 hour
Renal failure (especially CLD with eGFR0.02 in primary Hyperparathyroidism. However, this ratio may be b/w 0.01-0.02 in both disease. Rarely FHH can have high ratio and Hyperparathyroidism can have low ratio as well. Parathyroid adenoma isn’t there in FHH. Parathyroid Surgery is contraindicated in FHH.

Tertiary hyperparathyroidism develops after long-standing Vit D or calcium deficiency (CKD, chronic malabsorption, chronic malnutrition etc.). This also has high calcium and high PTH. But the disease course is very obvious.

All other cause of hypercalcemia (Dietry intake, vitamin D intoxication, granulomatous disease, malignancies, etc.) have low PTH.

Investigations are:
Serum calcium (total) & albumin. Ionised calcium is also available.
24 hour urinary calcium to exclude FHH. Also to quantify urinary calcium excretion.
PTH level
Renal functions and Renal imaging for stones or nephrocalcinosis.
Bone density at radius, lumbosacral spine and hip.
X-ray hands, radius and spine.
Prolactin and blood glucose, etc. to exclude MEN-1
Genetic studies in selected cases (see above).

Parathyroid imaging :

It’s done if the patient is candidate for surgery or cancer is suspected. It helps plan less invasive surgical approach.

USS is poor if there are thyroid nodules, neck fibrosis due to surgery, ectopic gland, more than one gland is involved. It’s 80% sensitive for single adenoma.

Technetium-sestaMIBI has sensitivity of 88-90% for single adenoma and can also detect ectopic. It’s also poor if multiple glands are involved.

CT with contrast (4-D) or PET with fluorocholine are very useful if available and if not contraindicated.

MRI of the neck is also very useful.

Surgery is indicated for the following cases of primary Hyperparathyroidism after exclusion of FHH;
1): Age 250 mg/24 hour in females (>300 mg/24 hours in males).
5): Bone changes as stated above
6): High risk of malignancy such as those in MEN syndrome, etc.

If patient can’t have surgery, then medical therapy is option.

Bisphosphonates if not contraindicated such as CKD, denture issues, severe GORD, swallowing issues, etc.

Denosumab if bisphosphonates can’t be used for any reason.

Cinacalcet stimulates CaSR on parathyroid cells and reduces PTH. But it does not improve bone density, etc. Also it’s costly and GI upset is common.

Calcium or vitamin D supplements are not usually stopped. Risk of rising calcium level is low but risk of increasing PTH level due to low calcium intake is there.
A.H

21/02/2024

Vitamin D Deficiency in Pregnancy

Background:

The NICE Guideline in 2008 and British Scientific Advisory Committee on Nutrition (SACN) in 2007 provided somewhat contradictory advice reviewed below.

The NICE Guideline2 advises that all women should be informed at the booking appointment about the importance for their own and their baby’s health of maintaining adequate vitamin D stores during pregnancy and whilst breastfeeding. NICE also advises that the safe upper intake for supplementary vitamin D is 25 micrograms/day (1000units/day).

NICE defines a cohort of women who are particularly at risk of Vitamin D deficiency and who would benefit from 400units/day Vitamin D.

‘At risk’ women include:
• Women in low-income households
• Women 19–24 years of age
• Women of South Asian, African, Caribbean or Middle Eastern family origin
• Women who have limited exposure to sunlight, such as women who are predominantly housebound, or usually remain covered when outdoors
• Women who eat a diet particularly low in vitamin D, such as women who consume no oily fish, eggs, meat, vitamin D-fortified margarine or breakfast cereal
• Women with a pre-pregnancy body mass index above 30 Kg/m2

In addition:
• Women with malabsorption (coeliac, small bowel resection etc.).
• Women on bone modifying drugs: steroids, anti-epileptics, anti-retrovirals.
• Women at risk of osteoporosis: inflammatory disease, immobilization, liver or kidney disease.

SACN does not define an at risk group but highlights that all pregnant and breastfeeding women should consider taking a daily supplement of vitamin D in order to ensure their own requirement for vitamin D is met and to build adequate fetal stores for early infancy and recommends 10micrograms a day (400units/day).

Evidence and the subsequent Endocrine Society guideline in 20115 suggests that pregnant and lactating women require at least 600units/day of vitamin D and recognise that at least 1,500–2,000units/day of vitamin D may be needed to maintain a target blood level of 25(OH)D above 75nmol/L.

In April 2013 the Vitamin D guidance from the National Osteoporosis Society highlighted that all pregnant and lactating women are at risk of Vitamin D deficiency and all should receive 400 units/day to ensure mother’s requirements are met and to build adequate fetal stores for early infancy.

A randomised mixed ethnicity UK trial of women recruited at 27/40 gestation and treated with daily 800units Vitamin D or single dose 200,000units Vitamin D showed that the entire cohort remained deficient with median Vitamin D levels of 42nmol/l (daily dose) and 34nmols/l (stat dose) versus 27nmol/l (no supplementation).

A further randomised controlled trial with 350 women of diverse racial and ethnic backgrounds in the US (baseline total Vitamin D ~60nmols/l) showed that doses of up to 4,000units Vitamin D/day starting at 12–16 weeks of gestation are effective in improving the vitamin D status of pregnant women without causing any adverse effects.

The concern about high dose vitamin D is that there are reports in the literature of hypercalcaemia and fetal malformations, but it should be noted that these have been noted with the active metabolites of vitamin D and not when treated with native vitamin D itself. These active metabolites should therefore be avoided. *Data is not available for the use of high dose Vitamin D in the first trimester.

The rationale behind correcting severe Vitamin D deficiency in pregnancy is to optimise both maternal and fetal well-being. The fetus at birth (cord blood) will contain ~50–60% of the maternal circulating concentrations of 25(OH) vitamin D9. This relation appears to be linear. Without correction, Vitamin-D deficiency in the fetus may result in hypocalcaemia with associated risks of rickets and hypocalcaemic seizures. The long-term benefit to bone health in the child/adult remains controversial. The evidence for preventing adverse pregnancy outcomes such as pre-eclampsia, small for gestational age, low birth-weight, gestational diabetes etc remain controversial.

Human breast milk and unfortified cows milk contain very little Vitamin D. Data suggest that only after lactating women were given 4,000-6,000 units/day was enough transferred to breast milk to meet the infant’s requirements.

Therapy:

Essentially many of the national recommendations for low dose Vitamin D are in place in order to supplement normal levels since requirements increase during pregnancy. However, when you have a woman with severe vitamin D deficiency (30
Malabsorption syndromes
Women on bone modifying drugs
Women with high osteoporosis risk

Treatment options could include:
1. Colecalciferol 20,000 units (Dekristol®;see above) once a week for two months
OR
2. Colecalciferol 1,600 units (Fultium-D3®;see above) daily for two months
OR
3. Colecalciferol oily solution 3,000units in 1mL daily for 8 weeks. Derived from wool fat of (slaughtered) sheep and may be unacceptable to some individuals.
4. Ergocalciferol 150,000 units by intramuscular injection. This is a red drug in the formulary and therefore for hospital use only. Suitable for vegetarians and vegans. Ideally only to be used if strictly vegetarian/vegan or significant concordance issues with medication. There is some evidence to suggest that an oral dosage is more likely to achieve target levels but this must be balanced against concordance issues etc.

Total vitamin D levels should ideally be reassessed after 6 months of treatment but an earlier repeat at 3 months may be considered in the context of pregnancy if concerns remain regarding on-going severe deficiency to help guide a further treatment course.

Maintenance therapy should be introduced at the end of the course of treatment (once total Vitamin D >50nmol/l). Appropriate maintenance would typically be 1,000 units per day.

21/02/2024

Vitamin D Deficiency in Primary Hyperparathyroidism (PHPT):

Vitamin D deficiency appears to be more common in patients with PHPT and Vitamin D deficiency appears to make PHPT more severe1. There is a theoretical risk of exacerbating hypercalcaemia with Vitamin D replacement but some studies suggest that it can be done reasonably safely without any impact on the serum calcium when the corrected calcium is 50nmol/L then please continue with maintenance Vitamin D. The frequency of serum calcium monitoring will depend upon the individual case and guidance will be given via the required endocrine out-patient review.

21/02/2024

Risk factors for Vitamin D deficiency:

Aging : Reduced synthesis in the skin

Season : Reduced exposure to UV radiation October-April

Latitude : Reduced exposure to UV radiation

Sunblock use : Reduced exposure to UV radiation

Clothing : Reduced exposure to UV radiation

Institutionalization : Reduced exposure to UV radiation

Skin pigmentation : Absorption of UV radiation by melanin

Malabsorption : e.g. pancreatic insufficiency, inflammatory bowel disease, coeliac disease, bariatric surgery, medications such as cholestyramine and orlistat

Obesity : Sequestration of Vitamin D in fat

Drugs : Induced metabolism of Vitamin D to inactive calcitroic acid e.g. rifampicin, phenytoin, glucocorticoids, HAART for HIV, transplant medications

Severe liver failure : Failure to 25-hydroxylate vitamin D

Nephrotic syndrome : Loss of Vitamin D in urine

Chronic kidney disease : Hyperphosphataemia suppresses 1-hydroxylation

23/01/2024

Role of SGLT-2 inhibitors and GLP-1 Agonists in type II Diabetes:

Type II Diabetes patients with any of the followings should be on SGLT-2 inhibitor &/or GLP-1 agonists (with proven CVS benefits) regardless of Metformin, with or without Metformin, and regardless of HBA1c value.

1): Heart failure (systolic or diastolic)
2): eGFR

Medical-infopedia - by Dr. Ali Shahzad Malik

27/11/2025

07/11/2025

28/10/2025

24/10/2025

22/08/2025

31/05/2024

02/04/2024

21/02/2024

21/02/2024

21/02/2024

23/01/2024

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