2k17 BATCH GM 1ST INTERNAL ASSESSMENT : OCT-2021

1. Define bone density, how is it measured? What are the causes, clinical features, diagnosis and management of osteoporosis?  (1+2+2+2+3)

A measure of the amount of minerals (mostly calcium and phosphorous) contained in a certain volume of bone. Bone density measurements are used to diagnose osteoporosis (a condition marked by decreased bone mass), to see how well osteoporosis treatments are working, and to predict how likely the bones are to break.

The test can identify osteoporosis, determine your risk for fractures (broken bones), and measure your response to osteoporosis treatment. The most commonly used BMD test is called a central dual-energy x-ray absorptiometry, or central DXA test. 

Causes:

  • Sex. Your chances of developing osteoporosis are greater if you are a woman. Women have lower peak bone mass and smaller bones than men. However, men are still at risk, especially after the age of 70.
  • Age. As you age, bone loss happens more quickly, and new bone growth is slower. Over time, your bones can weaken and your risk for osteoporosis increases.
  • Body size. Slender, thin-boned women and men are at greater risk to develop osteoporosis because they have less bone to lose compared to larger boned women and men.
  • Race. White and Asian women are at highest risk. African American and Mexican American women have a lower risk. White men are at higher risk than African American and Mexican American men.
  • Family history. Researchers are finding that your risk for osteoporosis and fractures may increase if one of your parents has a history of osteoporosis or hip fracture.
  • Changes to hormones. Low levels of certain hormones can increase your chances of developing osteoporosis. For example:
    • Low estrogen levels in women after menopause.
    • Low levels of estrogen from the abnormal absence of menstrual periods in premenopausal women due to hormone disorders or extreme levels of physical activity.
    • Low levels of testosterone in men. Men with conditions that cause low testosterone are at risk for osteoporosis. However, the gradual decrease of testosterone with aging is probably not a major reason for loss of bone.
    • Diet. Beginning in childhood and into old age, a diet low in calcium and vitamin D can increase your risk for osteoporosis and fractures. Excessive dieting or poor protein intake may increase your risk for bone loss and osteoporosis.
    • Other medical conditions. Some medical conditions that you may be able to treat or manage can increase the risk of osteoporosis, such as other endocrine and hormonal diseases, gastrointestinal diseases, rheumatoid arthritis, certain types of cancer, HIV/AIDS, and anorexia nervosa.
    • Medications. Long-term use of certain medications may make you more likely to develop bone loss and osteoporosis, such as:
      • Glucocorticoids and adrenocorticotropic hormone, which treat various conditions, such as asthma and rheumatoid arthritis.
      • Antiepileptic medicines, which treat seizures and other neurological disorders.
      • Cancer medications, which use hormones to treat breast and prostate cancer.
      • Proton pump inhibitors, which lower stomach acid.
      • Selective serotonin reuptake inhibitors, which treat depression and anxiety.
      • Thiazolidinediones, which treat type II diabetes.
      • Lifestyle. A healthy lifestyle can be important for keeping bones strong. Factors that contribute to bone loss include:
        • Low levels of physical activity and prolonged periods of inactivity 
        • Chronic heavy drinking of alcohol  is a significant risk factor for osteoporosis.
        • Studies indicate that smoking is a risk factor for osteoporosis and fracture. 
Clinical features:

Bones affected by osteoporosis may become so fragile that fractures occur spontaneously or as the result of:

  • Minor falls, such as a fall from standing height that would not normally cause a break in a healthy bone.
  • Normal stresses such as bending, lifting, or even coughing.
Diagnosis:

The most common test for measuring bone mineral density is dual-energy x-ray absorptiometry (DXA). 

Treatment:

The goals for treating osteoporosis are to slow or stop bone loss and to prevent fractures. Your health care provider may recommend:

  • Proper nutrition.
  • Lifestyle changes.
  • Exercise.
  • Fall prevention to help prevent fractures.
  • Medications.


2. What is myxedema coma? Describe its clinical features, diagnosis and treatment of myxedema coma?  (2+2+2+4)

Myxedema coma is a rare fatal condition as a result of long-standing hypothyroidism with loss of the adaptive mechanism to maintain homeostasis. Hypothyroidism due to any cause,, including autoimmune disease, iodine deficiency, congenital abnormalities, or medications like lithium and amiodarone, can precipitate myxedema coma if left untreated.

Its a misnomer as patient may present with a spectrum ranging from depression psychosis to coma.


Clinical features:

CVS : Common cardiovascular symptoms include hypotension, shock, arrhythmia, and heart block. Myxedema causes decreased myocardial contractility (bradycardia) and reduced cardiac output, which leads to hypotension.


CNS: depression, disorientation, decrease deep tendon reflexes, psychosis, slow mentation, paranoia, and poor recall.One case describes a rare presentation of a patient with status epilepticus.


RESPIRATORY: Hypoventilation in myxedema coma is due to impaired hypoxic and hypercapnic ventilatory response and the associated diaphragmatic muscle weakness


GIT: Myxedema coma commonly causes abdominal pain, nausea, vomiting, ileus, anorexia, and constipation. Ileus is of particular importance as it can lead to megacolon. Ascites has also been seen in cases of myxedema 


RENAL : Typical findings in myxedema coma are hyponatremia and decreased glomerular filtration rate. Hyponatremia occurs mainly due to decreased water transport to the distal nephron. Other causes can be an increase in antidiuretic hormone (ADH). Hyponatremia is also a key factor in the patient’s altered mental status and development of  coma


Diagnosis:

Clinically : Altered mental status with hypothermia

Lab investigation:

• Septic workup to rule out infection, including cultures and chest X-ray, etc.

• EKG (can show bradycardia with non-specific changes, decrease voltage, variable block, or prolong QT interval)

• Arterial blood gases can show hypoxia, hypercapnia, and respiratory acidosis.

• If cardiomegaly is present on imaging studies, further investigations to rule out pericardial effusion are necessary (echocardiogram is a necessary follow-up)

• Thyroid profile : severely low or undetected low serum total T4, free T4, free T3, and elevated TSH. 


Treatment:

The identification of the precipitating factor is essential. Respiratory and airway management is a critical component in the management of the patient. Frequent monitoring of the arterial blood gas should be performed to monitor the hypercapnia and hypoxemia. Most will require mechanical ventilation as the altered mental status does leave patients more prone to aspiration, and airway obstruction could occur due to the myxedema of the larynx.

According to the most recent American Thyroid Association (ATA) guidelines, the recommended initial dose is 200 to 400 mcg IV once (lower dose for elderly, or underlying cardiac disease or arrhythmia with some reports up to 500 mcg). Subsequently, dosing is 1.6 mcg/kg/day, reduced to 75% when given IV as a preferred route, for patients may not be able to tolerate PO, and the absorption could be impaired secondary to intestinal impaired motility and edema. 

Hyponatremia : 3% NaCl infusion

Cardiac temponade : pericardiocentasis

Adrenal insuffienciency : Hydrocortisone 100 mg iv TID

https://www.ncbi.nlm.nih.gov/books/NBK545193/


3. What is the diagnostic approach of young onset hypertension, its manifestations and treatment?

Hypertension among young people is common, affecting 1 in 8 adults aged between 20 and 40 years.
young people with raised BP should be investigated for secondary causes of hypertension. 
the presence of hypertension at a young age increases the risk of cardiovascular events in middle age.2 It contributes to an earlier onset of coronary heart disease, heart failure, stroke, and transient ischemic attacks

The ACC/AHA lowered the diagnostic threshold for stage 1 hypertension in the 2017 Guidelines from 140/90 to 130/80 mm Hg across all age categories

Primary hypertension:

Primary hypertension (also called essential hypertension) has no specific cause, although genetic and environmental factors play an important role.[9] More than 90% of young people with hypertension have primary hypertension.[7,10] It is often associated with a family history of hypertension and frequently accompanied by obesity or the metabolic syndrome. International population surveys show an increase in obesity in children and adolescents, which parallels an increase in the prevalence of hypertension in the same age groups.[11] Hypertensive children and adolescents go on to become hypertensive adults – a phenomenon known as ‘BP tracking’.

Secondary hypertension:

This form of hypertension affects approximately 10% of young hypertensives.The probability of secondary hypertension is inverse­ ly proportional to the age of the patient (i.e. higher in a school­going child, but lower in a young adult).The importance of identifying secondary hypertension lies in the potential for cure with appropriate treatment.
The causes of secondary hypertension can be further divided as follows:
• renal parenchymal disease (e.g. glomerulonephritis)
• renovascular disease (e.g. renal artery stenosis)
• mineralocorticoid­mediated hypertension (e.g. primary hyper­
aldosteronism)
• catecholamine­mediated hypertension (e.g. phaeochromocytomas) • medication (e.g. the oral contraceptive pill)
• abuse of cocaine or amphetamines
• coarctation of the aorta
• rarer causes.

Clinical features:

The examination is focused on establishing if there is target­organ damage or whether there are features that suggest a secondary cause. The presence of target­organ damage should prompt the institution of pharmacotherapy and closer follow­up.[4] The clinician should look for:
• an elevated body mass index (BMI) and increased waist circum­ ference
• features of insulin resistance (e.g. acanthosis nigricans)
• urinary dipsticks to detect primary renal disease (e.g. glomerulo­
nephritis) or renal damage
• a pressure overloaded apex in keeping with LVH
• fundoscopy to check for retinal hypertensive changes.
Features that point to a secondary cause include:
• pulse discrepancies (this may suggest a vasculopathy, such as
Takayasu’s arteritis)
• radiofemoral delay (this suggests coarctation of the aorta)
• abdominal bruits (these are suggestive of renal artery stenosis)

Investigations :

serum potassium (hypokalaemia may suggest primary hyperaldos­ teronism)
• serum creatinine and determination of estimated glomerular fil­ tration rate
• urine microalbumin­to­creatinine ratio
• fasting blood glucose and lipogram
• 12­lead electrocardiogram (ECG). The clinician should note that the
ECG is not validated for diagnosis of LVH in individuals <30 years,
and should be interpreted with caution.[16]
• Where resources allow, an echocardiogram to evaluate for LVH
may be performed, which is the gold standard for diagnosis.
Specific tests for a secondary cause should only be performed if there is a clinical suspicion. These include:
• plasma renin and aldosterone for suspected primary hyper­
aldosteronism
• urinary catecholamines for suspected phaeochromocytoma
• renal sonography for suspected renal disease
• computed tomography angiography of the renal vessels for
suspected renal artery stenosis
• urine screening for amphetamines and cocaine.

Treatment:

All patients should be encouraged to lose weight by eliminating refined carbohydrate from their diet, reducing saturated fat intake and undertaking an exercise programme or joining an organised sports programme. Fresh fruit and vegetables in the diet should be encouraged and salt intake must be reduced. Avoidance of junk food is strongly recommended. Alcohol use needs to be moderated and all tobacco product use discontinued. If substance abuse is detected, the patient should be referred for appropriate treatment.
The three front­line classes of antihypertensive agents are thiazide or thiazide­like diuretics, calcium channel blockers, and either an angiotensin­converting enzyme (ACE) inhibitor or angiotensin receptor blocker.




4. Localization of spinal cord lesion.




5. Causes,diagnosis and treatment of atrial fibrillation.

Causes of atrial fibrillation:

Problems with the heart's structure are the most common cause of atrial fibrillation. Possible causes of atrial fibrillation include:

Coronary artery disease
Heart attack
Heart defect that you're born with (congenital heart defect)
Heart valve problems
High blood pressure
Lung diseases
Physical stress due to surgery, pneumonia or other illnesses
Previous heart surgery
Problem with the heart's natural pacemaker (sick sinus syndrome)
Sleep apnea
Thyroid disease such as an overactive thyroid (hyperthyroidism) and other metabolic imbalances
Use of stimulants, including certain medications, caffeine, tobacco and alcohol
Viral infections

Diagnosis:

On ECG, atrial fibrillation presents with the typical narrow complex "irregularly irregular" pattern with no distinguishable p-waves. fibrillary waves may be seen or they may be absent. The ventricular rate usually ranges between 80 and 180/min.
Laboratory work is required to evaluate for the causes of atrial fibrillation, for example, a complete blood count (CBC) for infection,for electrolyte abnormalities, thyroid function tests to evaluate for hyperthyroidism, and a chest x-ray to evaluate the thorax for any abnormality.
echocardiogram should be done for these patients to evaluate for atrial thrombus secondary to atrial fibrillation and heart structure.
to evaluate the patient for pulmonary embolism (with the d-dimers test or spiral CT scan) because the right heart strain can lead to atrial malfunctioning and atrial fibrillation

Treatment:

In cases where the patient is hemodynamically unstable, it is recommended to carry out immediate cardioversion with anticoagulant therapy. Although TEE is recommended before any cardioversion; however, if the patient is hemodynamically unstable due to a rapid ventricular response, cardioversion may be indicated without prior TEE.
If pt is hemodynamically stable and evidence of rapid ventricular response, a beta-blocker or calcium-channel blocker should be commenced for rate control. These options can be used in the intravenous (IV) form for rapid response. Usually, a bolus is administered to the patient and then started on a drip if symptoms do not resolve. 

Amiodarone can also be given as a rhythm control agent but is also not a first-line option in the acute setting

In the case of preexisting atrial fibrillation, the patient should be risk-stratified using the CHADs-2-Vasc score, which is helpful in estimating the risk of stroke per year.



6. MEGALOBLASTIC ANEMIA.

Megaloblastic anemia (MA) encompasses a heterogeneous group of anemias characterized by the presence in the bone marrow of large red blood cell precursors called megaloblasts. This condition is due to impaired DNA synthesis, which inhibits nuclear division.

Etiology:

Folic acid deficiency may be related to decreased intake in the case of alcoholism or malnutrition (elderly, institutions, poverty, special diets, etc.), increased demand particularly in case of pregnancy, hemolysis and hemodialysis and malabsorption (tropical sprue, celiac disease, jejunal resection, Crohn disease, etc.). 

Vegan diets are low in vitamin B12.

Autoimmune gastric atrophy, leading to intrinsic factor production reduction.

May also develop following gastrectomy, ileal resection, or ileitis of any cause. Other causes of impaired vitamin B12 absorption include Zollinger-Ellison syndrome, blind loop syndrome, fish tapeworm infestation, and pancreatic insufficiency.

Pathophysiology:

Ineffective erythropoiesis secondary to intramedullary apoptosis of hematopoietic cell precursors, which results from DNA synthesis abnormalities. Both vitamin B12 and folate deficiencies may cause defective DNA synthesis. 

Diagnosis:

In peripheral blood smear (PBS), megaloblasts, while not pathognomic, are highly suggestive of megaloblastic anemia. The changes are not limited to red blood cells, and hypersegmented neutrophils, with six or more lobes, may be present. Other findings include Howell-Jolly bodies, anisocytosis, and poikilocytosis.

If there are megaloblasts on PBS with a high reticulocyte count, the first-line investigation includes an assay of vitamin B12 and folate red blood cell levels. Levels of less than 200 pg/ml of vitamin B12 indicate a deficiency.

Treatment:

patients receive 1000 ug of vitamin B12 daily in their first week of treatment. In the following month, they receive weekly and then monthly injections.

Usually, reticulocytosis occurs within 3 to 5 days. By the tenth day, hemoglobin starts to increase, and a total resolution of anemia normally occurs after 2 months of treatment. 

https://www.ncbi.nlm.nih.gov/books/NBK537254/


7. Acute pancreatitis.
Acute pancreatitis is an inflammatory condition of the pancreas that is painful and at times deadly.
Etiology:
  • Alcohol use
  • Gallstones
  • Hypertriglyceridemia
  • Idiopathic
  • Drug-induced pancreatitis
  • Post-procedural (endoscopic retrograde cholangiopancreatography or abdominal surgery)
  • Ampullary stenosis is formerly known as sphincter of Oddi dysfunction type I
  • Autoimmune pancreatitis, type I (systemic IgG4 disease-related), and type II
  • Viral infection (Coxsackie, Cytomegalovirus, Echovirus, Epstein-Barr virus, Hepatitis A/B/C, HIV, Mumps, Rubella, Varicella)
  • Bacterial infection (Campylobacter jejuni, Legionella, Leptospirosis, Mycobacterium avium, Mycobacterium tuberculosis, Mycoplasma)
  • Trauma
  • Smoking
  • Congenital anomalies (annular pancreas) 
  • Genetic disorders (hereditary pancreatitis, cystic fibrosis, alpha 1-antitrypsin deficiency) 
  • Hypercalcemia
  • Parasitic infections (Ascaris lumbricoides, Cryptosporidium, Clonorchis sinensis, Microsporidia)
  • Renal disease (Hemodialysis)
Pathophysiology:

The release of damage associated molecular patterns causes the recruitment of neutrophils and the initiation of the inflammatory cascade. This inflammatory cascade is responsible for the systemic manifestations of acute pancreatitis and can ultimately lead to increase capillary permeability and damage of endothelium with microvascular thrombosis that causes multiorgan dysfunction syndrome (MODS), the main cause of morbidity and mortality in acute pancreatitis.

Evaluation:

The diagnosis of acute pancreatitis has been defined by the Revised Atlanta Classification and requires at least 2 of 3 criteria be met: 1) a lipase or amylase level that is three times the upper limit of normal 2) abdominal pain that is consistent with pancreatitis 3) abdominal imaging consistent with acute pancreatitis.
 An abdominal ultrasound is recommended in all the patients to assess for choledocholithiasis and bile duct dilatation.
 A chest radiograph is also often obtained in moderate to severe cases to evaluate for pleural effusions, which is an indication of the higher severity of disease with elevated mortality.
 In cases where the diagnosis is equivocal but pancreatitis is still suspected, computed tomography (CT) with intravenous contrast is obtained to establish or rule out the diagnosis. 
CT is also recommended in cases where the patient has failed to improve or to worsen despite appropriate fluid resuscitation over 48 hours to determine the presence of necrosis.
MRCP is non-invasive, doesn’t require contrast but lacks sensitivity for detection of biliary stones less than 3 mm, and chronic pancreatitis and  is preferred. 
Diagnostic endoscopic retrograde cholangiopancreatography (ERCP) is reserved for recurrent episodes of acute pancreatitis.

Treatment:

Management for acute pancreatitis remains early aggressive fluid resuscitation. Lactated Ringer's solution is the recommended fluid with an initial bolus of 15 to 20 mL/kg and following rates of 3 mL/kg per hour (usually approximately 250 to 500 mL per hour) for the first 24 hours if no other contraindications are present. 
The fluid resuscitation is monitored with a combination of blood urea nitrogen, hematocrit, and urine output, monitoring every 4 to 6 hours in the first 24 hours of resuscitation to adjust the fluid rate.
Prophylactic antibiotics are not needed. If an infection is suspected, empiric antibiotics are appropriate until cultures results are finalized. Indication for antibiotics is limited to the presence of infected necrosis. 



8. Ascites


http://www.primagem.org/draining-fluid-from-liver-disease/

pathophysiology:

The first abnormality that develops is portal hypertension in the case of cirrhosis. Portal pressure increases above a critical threshold and circulating nitric oxide levels increase, leading to vasodilatation. As the state of vasodilatation becomes worse, the plasma levels of vasoconstrictor sodium-retentive hormones elevate, renal function declines, and ascitic fluid forms, resulting in hepatic decompensation.

Through the production of proteinous fluid by tumor cells lining the peritoneum, peritoneal carcinomatosis also can cause ascites. In high-output or low-output heart failure or nephrotic syndrome, effective arterial blood volume is decreased, and the vasopressin, renin-aldosterone, and sympathetic nervous systems are activated, leading to renal vasoconstriction and sodium and water retention.

Differential diagnosis:

The initial tests that should be performed on the ascitic fluid include a blood cell count, with both a total nucleated cell count and polymorphonuclear neutrophils (PMN) count, and a bacterial culture by bedside inoculation of blood culture bottles.

Ascitic fluid protein and albumin are measured simultaneously with the serum albumin level to calculate the serum-ascites albumin gradient (SAAG).

The presence of a gradient greater or equal to 1.1 g/dL (greater or equal to 11 g/L) predicts that the patient has portal hypertension with 97% accuracy. This is seen in cirrhosis, alcoholic hepatitis, heart failure, massive hepatic metastases, heart failure/pericarditis, Budd-Chiari syndrome, portal vein thrombosis, and idiopathic portal fibrosis. A gradient less than 1.1 g/dL (less than 11 g/L) indicates that the patient does not have portal hypertension and occurs in peritoneal carcinomatosis, peritoneal tuberculosis, pancreatitis, serositis, and nephrotic syndrome.

 LDH and glucose level should be determined in suspected cases of secondary peritonitis.

 Other tests to consider include amylase (greater than 1000 U/L suggests pancreatic ascites).

CT scan can also be used to detect ascites and may also help determine for presence of any masses.


9. Mention the differences in findings between UMN and LMN lesion?



https://www.google.com/amp/s/www.researchgate.net/figure/Differentiating-features-of-upper-and-lower-motor-neuron-lesions_tbl3_258253205/amp



10. Indications of hemodialysis?

Renal Indications
    • Oliguria/Anuria with volume overload
      • Uremia with symptoms
        • Refractory Hyperkalemia ( K+ over 6.0)
          • Refractory Metabolic acidosis due to renal failure (pH < 7.2)
            • Acute pulmonary edema
            Non-renal Indications
              • Removal of dialysable toxins, i.e. ones which aren’t very lipophilic or protein-bound
                • Lithium
                • Methanol
                • Ethylene glycol
                • Salicylates
                • Theophylline
                • Valproate
                • Pretty much any drug with a volume of distribution less than 0.5L/kg

              • Removal of contrast agent
              • Clearance of cytokines to decrease severity of sepsis
              Still controversial. May be of use in patients with renal failure and sepsis.
              No evidence that it helps in patients with sepsis who don’t have renal failure.
                • Control of body temperature
                An extracorporeal circuit can help control hypo or hyperthermia which is resistant to other methods of control.
                • Control of otherwise uncontrollable electrolytes
                Hypercalcemia refractory to pamidronate, for one example.




                11. Role of sucralfate in treatment of erosive gastritis?

                Sucralfate is a cytoprotective drug widely used in clinical practice to prevent or treat several gastrointestinal diseases such as gastro-esophageal reflux, gastritis, peptic ulcer, stress ulcer and dyspepsia. 
                The drug is actually able to form a physical barrier between epithelium and damaging agents (-bile salts, drugs, refluxate.). 
                Moreover, sucralfate increases the local levels of fibroblast growth factors and induces a rise in the mucosal concentration of prostaglandins which are considered important factors in mucosal healing. 



                12. Mention the renal manifestations of snake bite?

                Bites by haemotoxic snakes and myotoxic snakes are the common causes of renal involvement especially acute renal failure. 
                clinical renal manifestations vary from mild proteinuria, haematuria, pigmenturia to acute renal failure.
                Therefore, renal failure is often associated with haemorrhagic diathesis, intravascular haemolysis and rhabdomyolysis.
                Renal pathological changes include mesangiolysis, glomerulonephritis, vasculitis, tubular necrosis, interstitial nephritis and cortical necrosis. 
                Tubular necrosis is an important pathological counterpart of acute renal failure.

                Haemodynamic alterations induced by cytokines and vasoactive mediators leading to renal ischaemia are important in the pathogenesis of acute renal failure. Haemolysis, intravascular coagulation and rhabdomyolysis are important contributing factors. Direct nephrotoxicity can be induced by the venom through metalloproteases and phosphilipase A2. Immunologic mechanism plays a minor role in the pathogenesis of the renal lesion.



                13. Causes of portal hypertension?

                Portal hypertension occurs when there is an obstruction of blood flow through the liver, and pressure rises within the portal vein. This obstruction can be intrahepatic (intra=within +hepatic=liver), pre-hepatic (pre=before) or post- hepatic (post=after).

                Intrahepatic causes of portal hypertension

                Intrahepatic causes of portal hypertension include cirrhosis and hepatic fibrosis or scarring. A wide variety of illnesses are implicated as the cause of portal hypertension. Examples include the following:

                Pre-hepatic causes of portal hypertension

                Portal vein thrombosis or blood clots within the portal vein
                Congenital portal vein atresia or failure of the portal vein to develop

                Post-hepatic causes of portal hypertension

                Post-hepatic causes are due to obstruction of blood flow from the liver to the heart and can include:

                • Hepatic vein thrombosis
                • Inferior vena cava thrombosis
                • Restrictive pericarditis, where the lining of the heart stiffens and does not allow the heart to relax and expand when blood returns to it. Causes may include tuberculosis, fungal infections, tumors, connective tissue disorders (for example, scleroderma), and complications from radiation therapy.



                14. Clinical features of Down’s syndrome?

                • Flattened face
                • Small head
                • Short neck
                • Protruding tongue
                • Upward slanting eye lids (palpebral fissures)
                • Unusually shaped or small ears
                • Poor muscle tone
                • Broad, short hands with a single crease in the palm - simian crease
                • Relatively short fingers and small hands and feet
                • Excessive flexibility
                • Tiny white spots on the colored part (iris) of the eye called Brushfield's spots
                • Short height
                • Intellectual disability : mild to moderate cognitive impairment. Language is delayed, and both short and long-term memory is affected.



                15. Complications of post streptococcal glomerulonephritis?

                During the acute phase:
                • Congestive heart failure
                • Azotemia 
                Delayed complications:
                • Chronic kidney disease
                • Nephrotic syndrome.


                16. Causes of cervical myelopathy?

                • Congenital spinal stenosis
                • Bulging or herniated discs and bone spurs in the neck.
                • Ossification (hardening) of the ligaments surrounding the spinal cord, such as posterior longitudinal ligament and ligamentum flavum.
                • Rheumatoid arthritis of the neck
                • Whiplash injury or other cervical spine trauma
                • Spinal infections
                • Spinal tumors and cancers

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