#can pancreatitis cause elevated liver enzymes

[gastroenterologyucgconferences]

Unraveling the Complexity: Exploring Pancreatic and Biliary Diseases

Introduction:

The pancreas and biliary system are integral components of the digestive system, playing crucial roles in digestion, nutrient absorption, and waste elimination. However, diseases affecting these organs can lead to significant morbidity and mortality if left untreated. In this blog, we will delve into the intricacies of pancreatic and biliary diseases, their causes, symptoms, diagnosis, and treatment modalities.

Pancreatitis:

Pancreatitis, inflammation of the pancreas, can be acute or chronic and is often triggered by factors such as gallstones, alcohol consumption, medications, or genetic predisposition. Acute pancreatitis manifests with sudden onset severe abdominal pain, nausea, vomiting, and elevated pancreatic enzymes. Chronic pancreatitis is characterized by recurrent episodes of abdominal pain, weight loss, and pancreatic insufficiency. Diagnosis involves clinical evaluation, imaging studies such as CT scans, and laboratory tests. Treatment aims to relieve symptoms, prevent complications, and address underlying causes through pain management, dietary modifications, enzyme replacement therapy, and, in severe cases, surgery.

Gallstone Disease:

Gallstone disease, one of the most common biliary disorders, occurs when gallstones form in the gallbladder or bile ducts. These stones can obstruct the flow of bile, leading to symptoms such as abdominal pain (biliary colic), nausea, vomiting, and jaundice. Diagnosis is typically made through imaging studies such as ultrasound or CT scans. Treatment options include lifestyle modifications, medications to dissolve stones, and surgical removal of the gallbladder (cholecystectomy) in symptomatic cases.

Biliary Obstruction:

Biliary obstruction occurs when the flow of bile from the liver to the small intestine is impaired, leading to jaundice, dark urine, pale stools, abdominal pain, and itching. Common causes of biliary obstruction include gallstones, tumors (benign or malignant), strictures, or inflammation of the bile ducts. Diagnosis involves imaging studies such as MRCP (magnetic resonance cholangiopancreatography) or ERCP (endoscopic retrograde cholangiopancreatography) to visualize the biliary tract. Treatment depends on the underlying cause and may include endoscopic interventions, surgical procedures, or palliative measures to relieve symptoms.

Pancreatic Cancer:

Pancreatic cancer is a highly aggressive malignancy with a poor prognosis, often diagnosed at an advanced stage due to nonspecific symptoms and lack of effective screening tools. Common symptoms include abdominal pain, jaundice, weight loss, and new-onset diabetes. Diagnosis involves imaging studies such as CT scans, MRI, and endoscopic ultrasound (EUS), followed by tissue biopsy for confirmation. Treatment options may include surgery, chemotherapy, radiation therapy, and targeted therapies, depending on the stage and extent of the disease.

Pancreatic and biliary diseases encompass a range of conditions affecting the pancreas and the biliary system, including the gallbladder, bile ducts, and associated structures. These diseases can be complex and challenging to diagnose and manage due to their often nonspecific symptoms and potential for severe complications.

Pancreatic Diseases

Acute Pancreatitis:

Definition: A sudden inflammation of the pancreas that can be mild or life-threatening.

Causes: Gallstones, chronic alcohol use, certain medications, and high triglyceride levels.

Symptoms: Severe abdominal pain, nausea, vomiting, fever, and a swollen abdomen.

Diagnosis: Elevated serum amylase and lipase levels, abdominal ultrasound, CT scan.

Treatment: Hospitalization for fasting, IV fluids, pain management, and treating the underlying cause​ (MDLinx)​​ (MGMA Homepage)​.

Chronic Pancreatitis:

Definition: Long-term inflammation of the pancreas that leads to permanent damage.

Causes: Chronic alcohol consumption, genetic predisposition, and autoimmune conditions.

Symptoms: Chronic abdominal pain, malabsorption, weight loss, and diabetes.

Diagnosis: Imaging studies (CT, MRI), pancreatic function tests, and endoscopic ultrasound.

Treatment: Pain management, enzyme supplements, dietary changes, and addressing complications like diabetes​ (MDLinx)​​ (MGMA Homepage)​.

Pancreatic Cancer:

Definition: Malignant tumor of the pancreas, often with poor prognosis.

Symptoms: Jaundice, weight loss, diabetes, and upper abdominal pain.

Diagnosis: Imaging (CT, MRI, endoscopic ultrasound), biopsy, and blood tests (CA 19-9).

Treatment: Surgery (Whipple procedure), chemotherapy, radiation therapy, and palliative care​ (MDLinx)​​ (MGMA Homepage)​.

Biliary Diseases

Cholelithiasis (Gallstones):

Definition: Formation of stones within the gallbladder.

Symptoms: Often asymptomatic; can cause biliary colic, nausea, and vomiting if stones block ducts.

Diagnosis: Ultrasound, CT scan, and sometimes MRCP (magnetic resonance cholangiopancreatography).

Treatment: Dietary changes, pain management, and possibly cholecystectomy (surgical removal of the gallbladder)​ (MDLinx)​​ (MGMA Homepage)​.

Cholecystitis:

Definition: Inflammation of the gallbladder, often due to gallstones blocking the cystic duct.

Symptoms: Severe right upper abdominal pain, fever, nausea, and vomiting.

Diagnosis: Ultrasound, HIDA scan, and blood tests showing elevated white blood cells.

Treatment: Hospitalization, antibiotics, fasting, IV fluids, and cholecystectomy​ (MDLinx)​​ (MGMA Homepage)​.

Choledocholithiasis:

Definition: Presence of gallstones in the common bile duct.

Symptoms: Jaundice, dark urine, pale stools, and biliary colic.

Diagnosis: MRCP, ERCP (endoscopic retrograde cholangiopancreatography), and ultrasound.

Treatment: ERCP to remove stones, and possibly cholecystectomy to prevent recurrence​ (MDLinx)​​ (MGMA Homepage)​.

Primary Sclerosing Cholangitis (PSC):

Definition: Chronic disease causing inflammation and scarring of the bile ducts.

Symptoms: Jaundice, itching, fatigue, and episodes of cholangitis.

Diagnosis: MRCP, ERCP, liver biopsy, and blood tests showing elevated liver enzymes.

Treatment: Symptom management, bile acid therapy, and eventually liver transplantation in advanced cases​ (MDLinx)​​ (MGMA Homepage)​.

Diagnostic Techniques

Imaging: Ultrasound, CT scan, MRI, MRCP, and ERCP are crucial for visualizing the pancreas and biliary system.

Laboratory Tests: Blood tests to check liver function, pancreatic enzymes (amylase, lipase), and tumor markers (e.g., CA 19-9).

Biopsy: Fine-needle aspiration or surgical biopsy for histological examination.

Conclusion:

Understanding pancreatic and biliary diseases requires a multidisciplinary approach involving gastroenterologists, radiologists, and surgeons. Timely diagnosis and appropriate treatment are crucial to manage these conditions effectively and prevent complications.

For further reading and detailed information, you can explore the following resources:

MDLinx on Gastroenterology

Gastroenterology & Hepatology Journal

Medical Group Management Association (MGMA)

Pancreatic and biliary diseases pose significant challenges in clinical practice, requiring a multidisciplinary approach for effective management. Early recognition of symptoms, timely diagnosis, and appropriate treatment interventions are essential for improving outcomes and quality of life for patients affected by these conditions. Through ongoing research, advances in diagnostic techniques, and therapeutic innovations, healthcare providers continue to strive towards better understanding, prevention, and treatment of pancreatic and biliary diseases, offering hope to patients and their families facing these complex challenges.

Important Information:

Conference Name: 14th World Gastroenterology, IBD & Hepatology Conference Short Name: 14GHUCG2024 Dates: December 17-19, 2024 Venue: Dubai, UAE Email:  gastroenterology@ucgcmeconference.com Visit: https://gastroenterology.universeconferences.com/ Call for Papers: https://gastroenterology.universeconferences.com/submit-abstract/ Register here: https://gastroenterology.universeconferences.com/registration/ Exhibitor/Sponsor: https://gastroenterology.universeconferences.com/exhibit-sponsor-opportunities/ Call Us: +12073070027 WhatsApp Us: +442033222718

[newslime]

15 Ways Sugar is Making You Sick

In a world where sugar-laden treats tempt us at every turn, it's essential to heed the warnings about its detrimental effects on our health. While celebrities and influencers advocate for steering clear of sugar, the truth about its harmful impacts often gets buried beneath its sweet allure. Here are 15 ways sugar may be wreaking havoc on your well-being:

Risk to Your Heart: Excessive sugar consumption can elevate blood pressure and cholesterol levels, increasing the risk of heart disease. Renowned cardiologist Dr. KK Talwar emphasizes how traditional Indian diets high in carbohydrates contribute to cardiac problems.

Link to Dementia: Research suggests a strong connection between blood sugar levels and Alzheimer's disease, with excessive glucose potentially harming enzymes critical in combating inflammation associated with early Alzheimer's stages.

Children's Health at Risk: Excess sugar intake in children can lead to short-term energy spikes, behavioral changes, and tooth decay. Long-term risks include obesity, nutrient deficiencies, and cognitive function impacts.

Cholesterol Concerns: High sugar consumption correlates with lower levels of good cholesterol (HDL-C), as indicated by a study published in the Journal of the American Medical Association.

Fueling Cancer Cells: Cancer cells thrive on glucose, exhibiting increased demand compared to normal cells. This heightened glucose requirement fuels tumor growth, especially in lung squamous cell tumors.

Skin Aging Acceleration: Sugar accelerates skin aging by promoting glycation, triggering inflammation, disrupting gut bacteria balance, and stimulating excess oil production, contributing to conditions like acne and rosacea.

Liver Damage: Excessive sugar, particularly fructose, is linked to non-alcoholic fatty liver disease (NAFLD), with the liver metabolizing fructose into fat, leading to liver disease development.

Gum Health Complications: A high-sugar diet inflames gums and increases the risk of periodontal disease, causing serious gum infections and potential jawbone damage.

Premature Aging: Sugar contributes to the formation of Advanced Glycation End-products (AGEs), leading to wrinkles, sagging skin, and other signs of premature aging.

Blood Pressure Concerns: A high-fructose diet can elevate blood pressure levels, emphasizing the need to monitor sugar intake alongside salt consumption.

Kidney Strain: Excess sugar places strain on the kidneys, potentially leading to kidney disease as the organs work overtime to filter blood sugar.

Energy Instability: Relying on sugary snacks for energy boosts leads to short-lived energy spikes followed by crashes, leaving individuals feeling more exhausted than before.

Pancreatic Strain: Chronic sugar exposure can lead to pancreatic inflammation, contributing to pancreatitis and long-term pancreatic damage.

Inflammation: Excessive sugar consumption contributes to chronic inflammation, increasing the risk of various diseases, including arthritis and autoimmune disorders.

Sugar Addiction: Sugar can be addictive, leading to cravings and dependency similar to alcohol and drugs. Breaking free from sugar addiction requires mindfulness and persistence.

In conclusion, understanding the detrimental effects of sugar empowers individuals to make informed dietary choices. While the allure of sugary treats may be strong, prioritizing health and well-being is paramount. By recognizing the profound impact sugar can have on our bodies, we can take proactive steps towards cultivating healthier lifestyles. So, the next time sugar beckons, remember the toll it takes on your health and opt for nourishing alternatives instead. Your body will thank you in the long run.

[superdupernutrition]

Amylase

By: Paul Claybrook, MS, MBA

Amylase, a pivotal enzyme crucial in the digestive process, serves as the linchpin for breaking down carbohydrates into more manageable molecules within the human body. Its primary function lies in the breakdown of complex carbohydrates into simpler compounds that the body can readily absorb and utilize for energy. This article delves into the multifaceted realm of amylase, exploring its significance in health, its mechanisms within the body, and factors that influence its levels.

Understanding Amylase:

Amylase is an enzyme classified under three main types: alpha, beta, and gamma. Each type, secreted by different glands such as saliva, pancreatic juice, and intestinal juice, serves a distinct yet interrelated function in the digestive process. These enzymes primarily target carbohydrates, catalyzing their breakdown into smaller, more easily digestible molecules.

Importance in Health:

The paramount importance of amylase in maintaining health stems from its pivotal role in carbohydrate digestion and subsequent absorption. Carbohydrates, alongside proteins and fats, constitute the fundamental macronutrients necessary for the body's proper functionality. Proper breakdown of carbohydrates prevents potential digestive complications, including bloating, gas, and diarrhea, that may arise from inefficient processing.

Moreover, recent studies have hinted at the potential broader health benefits of amylase. Some research suggests its role in managing blood sugar levels among individuals with diabetes. Additionally, indications have surfaced regarding its possible anti-inflammatory properties, potentially contributing to a lowered risk of chronic diseases like heart disease and certain forms of cancer.

Mechanisms in the Body:

The digestive journey of amylase initiates in the mouth, where alpha-amylase, present in saliva, commences the breakdown of carbohydrates the moment food is chewed. However, upon reaching the stomach, the acidic environment briefly halts this enzymatic activity. Subsequently, as the food progresses to the small intestine, pancreatic amylase, released by the pancreas, resumes the breakdown process.

Here, complex carbohydrates are fragmented into glucose and maltose. While glucose is promptly absorbed into the bloodstream, maltose undergoes further disintegration by the enzyme maltase, forming two glucose molecules. These simplest forms of carbohydrates are then absorbed into the bloodstream, traversing to the liver, where they're either utilized immediately as energy or stored as glycogen for future requirements.

Factors Influencing Amylase Levels:

Numerous factors intricately influence the levels of amylase within the body. Dietary choices play a significant role, as a high-carbohydrate diet often prompts the body to produce increased amounts of this enzyme. Medications, such as diuretics and steroids, can also impact its production.

Moreover, various medical conditions like pancreatitis, salivary gland disorders, and kidney disease can either elevate or diminish amylase levels depending on the underlying health issue. Disturbances in these levels can serve as indicators of certain health conditions, aiding in diagnosis and treatment.

Medical conditions such as pancreatitis, an inflammation of the pancreas, can significantly elevate amylase levels due to the leakage of the enzyme into the bloodstream. Salivary gland disorders, which impede the normal release of amylase in saliva, can lead to decreased levels. Similarly, kidney diseases might cause fluctuations in amylase levels due to impaired excretion or altered production within the body.

Maintaining an optimal balance of amylase levels is crucial for the smooth functioning of the digestive system and overall health. Monitoring and understanding these levels in the context of various conditions are fundamental in diagnosing and treating underlying health issues.

Products Containing Amylase:

Many health supplements and digestive aids contain amylase due to its essential role in breaking down carbohydrates. These products, often in the form of digestive enzyme supplements, aim to support the body's digestive processes, especially for individuals who may have deficiencies or difficulties in naturally producing adequate amounts of amylase.

The inclusion of amylase in these products is to aid in the digestion of carbohydrates, supporting individuals with conditions that might compromise their natural enzyme production, such as pancreatic disorders or certain digestive system disorders.

Conclusion:

Amylase stands as a cornerstone in the intricate process of carbohydrate digestion and absorption within the human body. Its significance in maintaining digestive health and potential broader health benefits make it a subject of ongoing research and exploration in the medical and nutritional fields.

Understanding the factors influencing its levels, the role it plays in different bodily functions, and its inclusion in various health products highlights the importance of amylase in supporting overall health and well-being.

As ongoing research unveils more about the diverse functions and potential benefits of amylase, it continues to be an integral component in comprehending human physiology, digestion, and exploring therapeutic interventions for various health conditions.

#protease #lipase #enzymes #whichvitaminsyoushouldtake.com

[lustgarten22]

What Cancers Can Cause Elevated Liver Enzymes?

Elevated liver enzymes are a common sign of liver damage, irritation, or inflammation. However, they can also be a sign of other serious health conditions, including pancreatic cancer.

Pancreatic cancer is a rare but deadly cancer that begins in the pancreas, a small organ located in the abdomen. The pancreas produces enzymes that help with digestion and hormones that help regulate blood sugar.

There is no definitive blood test for pancreatic cancer. However, elevated liver enzymes can be a sign of the disease. Other symptoms of pancreatic cancer include:

Abdominal pain

Jaundice

Weight loss

Fatigue

Nausea and vomiting

Dark urine

Pale stools

If you have elevated liver enzymes and any of the other symptoms of pancreatic cancer, it is important to see a doctor right away. Early diagnosis and treatment can improve the chances of survival for pancreatic cancer.

Pancreatic Cancer Blood Test

There are a number of blood tests that can be used to screen for pancreatic cancer. These tests include:

CA 19-9: This is a tumor marker that is often elevated in people with pancreatic cancer. However, it can also be elevated in people with other conditions, such as liver disease.

CEA: This is another tumor marker that can be elevated in people with pancreatic cancer. However, it is not as specific as CA 19-9.

Lipase: This enzyme is produced by the pancreas. Elevated levels of lipase can be a sign of pancreatic cancer, but it can also be elevated in people with other conditions, such as pancreatitis.

If you have elevated liver enzymes or any of the other symptoms of pancreatic cancer, your doctor may order a combination of blood tests to help diagnose the condition.

If you are concerned about what cancers cause elevated liver enzymes, it is important to talk to your doctor. They can help you determine the cause of your elevated enzymes and recommend the appropriate treatment.

[drforambhuta]

The development of organ failure has a significant impact on the outcomes of acute pancreatitis patients. Organ failure can affect multiple organs, with the most commonly involved being the lungs, kidneys, heart, and gastrointestinal tract.

a. Respiratory Failure: Severe acute pancreatitis often leads to lung complications, resulting in acute respiratory distress syndrome (ARDS). ARDS is characterized by severe lung inflammation and fluid accumulation, leading to impaired oxygen exchange and respiratory failure.

b. Renal Failure: Another common consequence of severe acute pancreatitis is acute kidney injury. Reduced blood flow to the kidneys and the release of inflammatory mediators can lead to kidney dysfunction.

c. Cardiovascular Complications: Severe pancreatitis can also cause cardiovascular instability, which includes hypotension, tachycardia, and arrhythmias. These complications can further worsen organ failure.

d. Gastrointestinal Complications: The gastrointestinal tract may experience motility disturbances and ischemic damage, potentially resulting in paralytic ileus or bowel ischemia.

e. Hepatic Dysfunction: The liver can also be affected, leading to hepatic dysfunction, which may present as elevated liver enzymes and jaundice.

f. Coagulation Abnormalities: Severe acute pancreatitis can disrupt the normal coagulation process, leading to disseminated intravascular coagulation (DIC) and bleeding complications.

Pancreatitis can lead to severe digestive problems which may include symptoms like blood in stools, constipation, diarrhea, fatigue, stomach pain, and stomach bleeding. It is important to consult a good gastroenterologist like Dr. Amit Maydeo to get an early diagnosis and appropriate pancreatitis treatment plan for pancreatitis before it can lead to complications like organ failure.

[medtalksblog]

Understanding SGOT and SGPT Tests

SGOT and SGPT are vital examinations in the medical realm for evaluating liver functionality. Representing Serum Glutamic Oxaloacetic Transaminase and Serum Glutamic Pyruvic Transaminase, they are also known as AST (Aspartate Transaminase) and ALT (Alanine Transaminase). These tests gauge the levels of two enzymes in the body—SGOT in the heart, skeletal muscles, and kidneys, and SGPT in the liver.

Significance of SGOT and SGPT Tests

The liver, a crucial organ, plays a pivotal role in the body's metabolic processes. Its primary task is blood detoxification by processing and filtering harmful waste through enzyme production and secretion, ensuring a smooth and efficient process.

SGPT and SGOT, common liver enzymes, elevate in the blood when the liver undergoes damage or inflammation, disrupting the equilibrium. These markers aid in diagnosing various liver ailments, including hepatitis, cirrhosis, liver cancer, and other conditions affecting liver function. They also monitor the effectiveness of specific medications or treatments for liver diseases.

Levels and Causes of Elevated SGOT and SGPT Levels

Normal SGPT and SGOT ranges in a patient's serum should typically be between 7-56 units/liter and 8-45 units/liter, respectively. Levels exceeding 56 units/liter for SGPT and 50 units/liter for men or 45 units/liter for women for SGOT indicate serious concerns, suggesting an underlying chronic condition.

Increased SGPT and SGOT levels often point to liver damage due to conditions like acute viral hepatitis, alcoholic liver disease, non-alcoholic fatty liver disease, cirrhosis, and liver cancer. Other clinical situations like kidney disease, celiac disease, heart attack, diabetes, obesity, infectious mononucleosis, gallbladder inflammation, inflammation of skin and muscles, pancreatitis, etc., can also contribute to SGOT/SGPT imbalance.

Moreover, factors such as alcohol abuse, specific medications, intense exercise, or muscle damage may lead to elevated levels. Seeking healthcare guidance is crucial to determine the cause and receive proper treatment. Regular monitoring of liver enzymes aids in early liver disease detection, preventing long-term damage.

Symptoms of High SGOT & SGPT Levels

While elevated SGOT and SGPT levels usually show no noticeable symptoms, some individuals may experience mild indications like constant fatigue, nausea, vomiting, and abdominal discomfort. Severe cases of liver disease may manifest symptoms such as jaundice, breathlessness, leg and abdomen swelling, dark-colored urine, and pale stools.

Experiencing any symptoms necessitates immediate medical attention. If elevated SGOT and SGPT levels are detected, further testing or necessary treatment is decided by the physician.

[doctorfoxtor]

post ain't long it's wrong, can't study till dawn? yawn

100 days of productivity

day 44 + 45

CVS/RS

rheumatoid pleural effusions closely mimic complicated parapneumonic effusion on analysis, w/ ph <7.2, marked ↑LDH and notably glucose <30 (in fact glucose >30 almost rules out rheumatoid effusion)

in afib, digoxin will slow ventricular rate but is unlikely to cardiovert the rhythm

itraconazole in ABPA causes a 50% reduction in steroid dose and 25% reduction in anti-aspergillus IgE, and either partial or complete resolution of CXR infiltrates or improvement in PFTs/exercise tolerance

TRALI can happen as early as 15 minutes into the transfusion apparently?????

mesothelioma is an abject death sentence. The most you can do for patients beyond stage 1 is chemotherapy (limited survival benefit with platinics), radiotherapy to biopsy/thoracoscopy tracts only and surgery (lung-sparing debulking ± pleurodesis for recurrent effusions; radical surgery has shown no survival benefit)

mild tachy + broad qRs in haemodynamically stable pt s/p PCI for MI → likely to be LBBB developing; watch and wait

CNS/Ophthal/Psych

PSP looks similar to parkinson's bc it affects the opposite pathway as parkinsons (striatonigral vs nigrostriatal)

the best response you can get from deep brain stimulation for parkinsons = the best response you got from medication; DBS will NOT add a greater response compared to maximum medical therapy

without any other information, parkinson's ssx w/ dementia WITHIN 1 year of onset, it's Lewy body dementia; if it's more than 1 year, it's parkinson's w/ 2° dementia

choroidal neovascularisation with NO OTHER fundal signs: wet mac degen > diabetic retinopathy

focal dystonias are better treated with botox than with medication

SAH is unlikely to cause cranial nerve palsies other than III and maybe VI; pituitary apoplexy presents similarly with very severe headache/projectile vomiting/AMS, while affecting nerves III, IV, V-1 and VI

MS relapse: 500 mg PO or 1 g IV methylpred x5 days

there is no difference in risk of progression to Korsakoff when Wernicke is treated w/ glucose first vs w/ thiamine first

Endocrine/Repro

hyperaldosteronism: hyperplasia > adenoma

acute alcohol consumption can trigger hypoglycaemic events as the liver uses up NAD+ for each step of the alcohol detox pathway, where NAD+ is an important cofactor for the malate-oxalate shuttle used in gluconeogenesis

cinacalcet's major indication is hyperparathyroidism taht can't be corrected w/ surgery (eg, unfit pts)

Rheum/Derm/Immuno

topical steroid potency: hydrocortisone < clobetasol butyrate, betamethasone valerate low-dose < betamethasone valerate high-dose, fluticasone propionate < clobetasol propionate

onycholysis: trauma, tinea (infections), thyrotoxicosis, tetracyclines

pseudoxanthoma elasticum is assoc w/ mitral prolapse, renovascular htn, PVD, CAD, GIT bleeds and retinal vessel abnormalities

IgE values are normally distributed, so about 2.5% of the pop has raised IgE and 2.5% has reduced

s/p parathyroidectomy → acute drop in PTH → bones that are used to high levels of PTH experience a relative hypoPTHism → ↑blastic ↓clastic activity → acute bony uptake of calcium, PO4 and importantly magnesium = hungry bone syndrome (replace calcium and magnesium!)

carpal tunnel pain can radiate retrogradely to the forearm and sometimes even the arm

periarticular osteoporosis → RA

punched out erosions in juxtaarticular bone → gout

GIT

Peutz-Jeghers: small bowel hamartomas → intussusception, colorectal cancer, pigmented lesions (classically perioral/mucosal, but also palms/soles)

pernicious anaemia: parietal cell Abs (common) > intrinsic factor Abs (specific)

haemochromatosis: venesection → keep ferritin <50 and transferrin sat <50%

passing stools frequently, elevated inflammatory markers, ↑faecal calprotectin, PPI but not in demographic for IBD → take a colonoscopy and biopsy, this is probably microscopic colitis (and PPIs can trigger at any age)

liver biopsy is not indicated for Gilbert's—it is sufficient to do routine CBCs/LFTs w/ bilirubin analysis

pancreolauryl (fluorescein dilaurate) is quite nonspecific and will not pinpoint the exact pancreatic disease

hep A can be precided by short diarrhoeal illness`

in an IBD (esp UC) pt who comes >10 yrs after initial symptoms with recent change in bowel habits, offer urgent colonoscopy to r/o ca colon BEFORE starting on treatment

Onc/Haem

MTX + antifolate antibiotics: makes sense not to give them together—they can cause fulminant marrow failure

leukaemia can very rarely lead to acute painful scrotal swelling

5q- syndrome = myelodysplasia, but with thrombocytosis; diff from essential thrombocythaemia by anaemia with normal reticulocyte count and leukopaenia in the former

radiotherapy is a primary modality of tx in retinal, CNS, skin, oesophageal, cervical, vaginal and prostatic tumours; it is adjuvant in all other tumours

the commonest presentations of CMV s/p txp are pneumonia or pulmonary infiltrates

Renal/Biochem

SIADH causing drugs - SIADH Causes Poor Voiding: Sedatives (barbiturates), Indomethacin (NSAIDs), Antidepressants (TCAs/SSRIs), thiazide Diuretics, 1st gen antiHistamines, Cyclophosphamide/antiConvulsants, 1st gen antiPsychotics, Vinca alkaloids

malaria: irreversible nephrosis (esp memb or FSGS) > nephritis

2° syphilis: reversible nephritis > nephrosis

even if the patient doesn't qualify for ACEis/ARBs for HTN, give them first-line anyway if concomitant renal disease

kidney size difference >1 cm is significant

for drugs that will be dialysed out on dialysis days, dose them immediately after dialysis on those days

only urge incontinence is not primarily managed with pelvic floor exercises

Pharm/Toxo

valproate ADRs - VALPROATE: Vomiting, Alopecia/Anorexia, Liver tox, Pancreatitis/PCOS, Redistributed fat (weight gain/lipodystrophy), Oedema, hyperAmmonaemia/Ataxia, Tremor/Thrombocytopaenia, Enzyme inhibitor

opioid withdrawal: methadone is the best single tx and avoids needing to give multiple drugs to cover ssx (eg, clonidine + dextromethorphan + loperamide)

aminoglycosides preferentially affect proximal tubular cells

the classic pattern of symptoms in both cotton workers and workers at factories that process nitrates is that of 'Monday disease'

toxicities for which measuring the blood levels is indicated - SLIME TiPP: Salicylates, Lithium, Iron, Methanol, Ethylene glycol, Theophylline, Paraquat, Paracetamol

amphetamine tox → hyponatraemia due to water retention, worsened by the excessive thirst; hyperkalaemia → rhabdo; hypokalaemia not seen because amphetamines tho sympathetomimetic do not have affinity for the β2 receptor like cocaine does

[biomedicool]

Kidney function tests

Creatinine

Creatinine is a waste product produced in muscles from the breakdown of a creatine. 

Creatine is part of the cycle that produces energy needed to contract  muscles. 

Both creatine and creatinine are produced at a relatively constant rate. 

Almost all creatinine is excreted by the kidneys, so blood levels are a good measure of how well your kidneys are working.

If low: 

Low levels are not common and are not usually a cause for concern. 

As creatinine levels are related to the amount of muscle the person has, low levels may be a consequence of decreased muscle mass (such as in the elderly) but may also be occasionally found in advanced liver disease.

If high:  

Kidneys break down creatinine - if levels are high, they’re not working properly -->

Damage to or swelling of blood vessels in the kidneys (glomerulonephritis) caused by, eg, infection or autoimmune diseases bacterial infection of the kidneys (pyelonephritis)

Death of cells in the kidneys’ small tubes (acute tubular necrosis) caused, for example, by drugs or toxins

Prostate disease, kidney stone, or other causes of urinary tract obstruction.

Reduced blood flow to the kidney due to shock, dehydration, congestive heart failure, atherosclerosis, or complications of diabetes

Creatinine blood levels can also increase temporarily as a result of muscle injury and are generally slightly lower during pregnancy.

Urea

Urea is the final breakdown product of the amino acids found in proteins. Nitrogen in the form of ammonia is produced in the liver when protein is broken down. The nitrogen combines with other chemicals in the liver to form the waste product urea.  Healthy kidneys remove more than 90% of the urea the body produces.

If Low: 

Low urea levels are not common and are not usually a cause for concern. They can be seen in severe liver disease or malnutrition but are not used to diagnose or monitor these conditions. Low urea levels are also seen in normal pregnancy.

·   If high: 

High urea levels suggest poor kidney function. 

Acute or chronic kidney disease. 

However, there are many things besides kidney disease that can affect urea levels such as decreased blood flow to the kidneys as in congestive heart failure, shock, stress, recent heart attack or severe burns; bleeding from the gastrointestinal tract; conditions that cause obstruction of urine flow; or dehydration.

Albumin

Albumin is the most abundant protein in the blood. It keeps fluid from leaking out of blood vessels; nourishes tissues; and transports hormones, vitamins, drugs, enzymes, and ions like calcium throughout the body. Albumin is made in the liver and is extremely sensitive to liver damage. 

If low:

Low albumin concentrations in the blood can suggest liver disease. Liver enzyme tests are requested to help determine which type of liver disease.

Diseases in which the kidneys cannot prevent albumin from leaking from the blood into the urine and being lost.

Also seen in severe inflammation or shock.

Conditions in which the body does not properly absorb and digest protein such as Crohn’s disease.

If high: 

High albumin concentrations in the blood usually reflect dehydration.

This is a very long list so click keep reading to read the rest!

Phosphate

In the body, phosphorus is combined with oxygen to form a variety of phosphates (PO4). Phosphates are vital for energy production, muscle and nerve function, and bone growth. They also play an important role as a buffer, helping to maintain the body’s acid-base balance.

If low:  (hypophosphataemia)

Hypercalcaemia (high levels of calcium), especially when due to high levels of parathyroid hormone (PTH)

Overuse of diuretics (drugs that encourage urination)

Severe burns

Diabetic ketoacidosis after treatment

Hypothyroidism

Hypokalaemia (low levels of potassium)

Chronic antacid use

Rickets and osteomalacia (due to Vitamin D deficiencies)

Increased production of insulin

If high:  (hyperphosphataemia) 

 Kidney failure

 Hypoparathyroidism (underactive parathyroid gland)

 Hypocalcaemia (abnormally low levels of calcium)

 Diabetic ketoacidosis when first seen

 Phosphate supplementation

Alkaline phosphatase

Alkaline phosphatase is an enzyme found in high levels in bone and liver. Smaller amounts of ALP are found in the placenta and in the intestines. Each of these makes different forms of ALP (isoenzymes).

If low

Zinc deficiency. Magnesium deficiency. Anaemia. Poor nutrition.

Hypophosphatasia (Metabolism disorder, in born). Hypothyroidism.  Wilsons disease. 

If High: 

Raised levels of ALP are usually due to a disorder of either the bone or liver. 

If other liver function tests are also raised, this usually indicates that the ALP is coming from the liver. 

However, if calcium and phosphate measurements are abnormal, this suggests that the ALP might be coming from bone.

In some forms of liver disease, such as hepatitis, ALP is usually much less elevated than AST or ALT. 

However, when the bile ducts are blocked (for example by gallstones, scars from previous gallstones or surgery, or by a tumour), ALP and bilirubin may be increased much more than either AST or ALT. 

ALP can also be raised in bone diseases such as Paget’s disease (where bones become enlarged and deformed), in certain cancers that spread to bone or in vitamin D deficiency.

Calcium

 99% of calcium is found in the bones, and most of the rest circulates in the blood. Roughly half of calcium is referred to as 'free' (or 'ionized') and is active within the body; the remaining half, referred to as 'bound' calcium, is attached to protein and other compounds and is inactive.

If low: (hypocalcaemia)

The most common cause of low total calcium is low protein levels, especially low albumin. When low protein is the problem, the 'free' calcium level remains normal. 

Underactive parathyroid gland (hypoparathyroidism)

Decreased dietary intake of calcium

Decreased levels of vitamin D

magnesium deficiency

too much phosphate

acute inflammation of the pancreas

chronic kidney disease

calcium ions becoming bound to protein (alkalosis)

bone disease

malnutrition, and alcoholism.

 If high: (hypercalcaemia)

Hyperparathyroidism (increase in parathyroid gland function) usually caused by a benign tumour on the parathyroid gland. 

Cancer when spread to the bones, which releases calcium into the blood, or when it causes a hormone similar to PTH to increase calcium levels.

Hyperthyroidism, Sarcoidosis, Tuberculosis, Too much Vit D, Drugs that increase diuretics.

Potassium: 

Abnormal concentration can alter the function of the nerves and muscles.

If low: (hypokalaemia)

vomiting,

diarrhoea, and insufficient potassium intake (rare).

In diabetes, potassium concentration may fall after insulin injection.

If high:

(hyperkalaemia)

kidney disease

Addison's disease

tissue injury

infection

diabetes

excessive intravenous potassium intake (in patients on a drip)

Glucose: 

If low: (hypoglycaemia)  

Adrenal disease (Addison's disease)

Alcohol/ drugs, such as: paracetamol and anabolic steroids

Extensive liver disease

Hypopituitarism

Hypothyroidism

Insulin overdose

Insulinomas (insulin-producing pancreatic tumours)

If high: 

High levels of glucose most frequently indicate diabetes, in fasting blood glucose test: <7mmol/L is indicative and in oral glucose test ites <11 mmol/L .

Acromegaly

Acute stress (response to trauma, heart attack, and stroke for instance)

Long-term kidney disease

Cushing's syndrome

Drugs, including: corticosteroids, tricyclic antidepressants, oestrogens (birth control pills and hormone replacement therapy [HRT]), lithium..

Hyperthyroidism

Pancreatic cancer. Pancreatitis

Triglyceride: 

Most triglycerides are found in fat (adipose) tissue, but some circulate in the blood to provide fuel for muscles to work. 

If low: 

Hyperthyroidism. Malnutrition. Certain medications and drugs can deplete fat, leading to low triglycerides. 

If high: (e.g. at least 10-15 mmol/L) --> pancreatitis. 

Parathyroid hormone: 

Part of a ‘feedback loop’ that includes calcium, PTH, vitamin D, and to some extent phosphate and magnesium.  PTH is secreted into the bloodstream in response to low blood calcium concentration. 

If both PTH and calcium results are normal, and appropriate relative to each other, then it is likely that the body’s calcium regulation system is functioning properly.

Low --> conditions causing hypercalcaemia, or to an abnormality in PTH production causing hypoparathyroidism. 

High --> hyperparathyroidism, which is most frequently caused by a benign parathyroid tumour.

Calcium - PTH Relationship

Calcium  low and PTH high, then PTH working. Low calcium may be investigated.

Calcium  low and PTH normal or low --> hypoparathyroidism.

Calcium high and PTH  --> hyperparathyroidism.

Calcium  normal and PTH high --> vitamin D deficiency or chronic kidney disease.

Amylase

Released from the pancreas into the digestive tract to help digest starch. It is usually present in the blood in small quantities. When cells in the pancreas are injured or if the pancreatic duct is blocked (by a gallstone or rarely by a tumour) increased amounts of amylase find their way into the bloodstream.

If high:

 Pancreatitis which is a severe inflammation (often 5-10 times normal)

Cancer of the pancreas, gallbladder disease, a perforated ulcer, obstruction of the intestinal tract, mumps or ectopic pregnancy. 

Increased blood amylase with normal or low urine amylase may indicate decreased kidney function or the presence of macroamylase.

[gastroenterologyucgconferences]

TRACK 8: PANCREATIC AND BILIARY DISEASE

 

Introduction:

Pancreatic and biliary diseases encompass a range of conditions that affect the pancreas and the biliary system, including the liver, gallbladder, and bile ducts. These diseases can have significant impacts on health and quality of life, making understanding their symptoms, causes, and treatment options essential.

Pancreatic Diseases:

Pancreatitis:

Let's delve deeper into pancreatitis, covering both acute and chronic pancreatitis, including their causes, symptoms, and treatment options:

Acute Pancreatitis:

Causes:

Gallstones: One of the leading causes of acute pancreatitis, gallstones can obstruct the pancreatic duct, leading to inflammation.

Alcohol Consumption: Excessive alcohol intake can irritate the pancreas, causing acute inflammation.

Trauma: Physical trauma or injury to the abdomen can trigger pancreatitis.

Certain Medications: Certain medications, such as corticosteroids, diuretics, and some antibiotics, can cause pancreatitis.

High Levels of Triglycerides: Elevated triglyceride levels in the blood can increase the risk of pancreatitis.

Symptoms:

Sudden and severe abdominal pain, usually centered in the upper abdomen.

Nausea and vomiting.

Fever and increased heart rate.

Tenderness or swelling of the abdomen.

Jaundice (yellowing of the skin and eyes) in severe cases.

Treatment:

Hospitalization: Patients with acute pancreatitis often require hospitalization for pain management and monitoring.

Fasting: In severe cases, fasting may be necessary to allow the pancreas to rest and heal.

Intravenous (IV) Fluids: Fluid replacement is essential to prevent dehydration and maintain electrolyte balance.

Pain Management: Pain medications, such as opioids or nonsteroidal anti-inflammatory drugs (NSAIDs), may be prescribed to alleviate discomfort.

Treatment of Underlying Causes: If gallstones are the cause, surgery to remove the gallbladder (cholecystectomy) may be necessary.

Chronic Pancreatitis:

Long-Term Management:

Pain Management: Chronic pancreatitis can cause persistent abdominal pain, which may require ongoing pain management with medications and lifestyle modifications.

Enzyme Replacement Therapy: Chronic pancreatitis can lead to pancreatic insufficiency, where the pancreas does not produce enough digestive enzymes. Enzyme replacement therapy helps improve digestion and nutrient absorption.

Nutritional Support: Patients with chronic pancreatitis may require dietary adjustments, including a low-fat diet and small, frequent meals.

Alcohol and Smoking Cessation: Lifestyle changes, such as avoiding alcohol and quitting smoking, are crucial in managing chronic pancreatitis and preventing further damage to the pancreas.

Monitoring for Complications: Chronic pancreatitis increases the risk of complications such as diabetes, pancreatic pseudocysts, and pancreatic cancer. Regular monitoring and screening are essential for early detection and intervention.

Complications:

Diabetes Mellitus: Chronic pancreatitis can lead to the destruction of insulin-producing cells in the pancreas, resulting in diabetes mellitus.

Pancreatic Pseudocysts: Fluid-filled sacs may develop in the pancreas, causing pain and potentially obstructing nearby organs.

Pancreatic Cancer: Long-standing inflammation and damage to the pancreas increase the risk of pancreatic cancer in patients with chronic pancreatitis.

Conclusion:

Pancreatitis, whether acute or chronic, can significantly impact an individual's health and quality of life. Understanding the causes, symptoms, and treatment options for pancreatitis is essential for effective management and prevention of complications. Early diagnosis and prompt medical intervention can improve outcomes and help individuals lead healthier lives.

Pancreatic Cancer:

Let's explore pancreatic cancer, including its risk factors, early detection methods, and treatment options:

Risk Factors:

Age: Pancreatic cancer is more common in older adults, with the majority of cases diagnosed in individuals over the age of 65.

Tobacco Use: Cigarette smoking is one of the most significant risk factors for pancreatic cancer. Smokers are at a higher risk compared to non-smokers.

Family History: Individuals with a family history of pancreatic cancer, especially first-degree relatives (parents, siblings, children) with the disease, have an increased risk.

Chronic Pancreatitis: Long-standing inflammation of the pancreas, such as in chronic pancreatitis, can elevate the risk of developing pancreatic cancer.

Obesity and Diabetes: Being overweight or obese and having diabetes mellitus are associated with an increased risk of pancreatic cancer.

Certain Genetic Syndromes: Inherited genetic mutations, such as in the BRCA2 gene or Lynch syndrome, can predispose individuals to pancreatic cancer.

Exposure to Certain Chemicals: Prolonged exposure to certain chemicals, such as benzene and certain pesticides, may increase the risk of pancreatic cancer.

Early Detection Methods:

Imaging Tests: Imaging techniques such as computed tomography (CT) scans, magnetic resonance imaging (MRI), and endoscopic ultrasound (EUS) can help detect pancreatic tumors and evaluate their size and extent.

Tumor Markers: Blood tests for specific tumor markers, such as CA 19-9, may be elevated in individuals with pancreatic cancer. However, these markers are not always reliable for early detection and are often used to monitor disease progression and response to treatment.

Genetic Testing: Individuals with a strong family history of pancreatic cancer or certain genetic syndromes may benefit from genetic testing to identify inherited mutations associated with the disease.

Treatment Options:

Surgery: Surgical resection is the only potentially curative treatment for pancreatic cancer. Depending on the size and location of the tumor, surgical options may include a Whipple procedure (pancreaticoduodenectomy), distal pancreatectomy, or total pancreatectomy.

Chemotherapy: Chemotherapy may be used before surgery (neoadjuvant chemotherapy) to shrink the tumor, after surgery (adjuvant chemotherapy) to kill any remaining cancer cells, or as a palliative treatment to alleviate symptoms and slow disease progression in advanced cases.

Radiation Therapy: Radiation therapy may be used alone or in combination with chemotherapy to target and destroy cancer cells, relieve pain, and improve quality of life.

Targeted Therapy and Immunotherapy: Targeted therapies and immunotherapies are newer treatment approaches that aim to target specific molecular pathways involved in pancreatic cancer growth and metastasis. These treatments may be used in combination with chemotherapy in certain cases.

Clinical Trials:

Participation in clinical trials offers access to innovative treatments and therapies that may not be available through standard care. Patients with pancreatic cancer are encouraged to discuss clinical trial options with their healthcare providers.

Conclusion:

Pancreatic cancer is a challenging disease with a relatively poor prognosis, largely due to late diagnosis and limited treatment options. However, advancements in early detection methods, treatment modalities, and supportive care have improved outcomes for some patients. Early detection, timely intervention, and a multidisciplinary approach involving surgery, chemotherapy, radiation therapy, and supportive care are crucial in the management of pancreatic cancer.

Biliary Diseases:

Gallstones

Here's a breakdown of gallstones, including their formation, symptoms, complications, and treatment options:

Formation:

Gallstones are solid particles that form in the gallbladder, a small organ located beneath the liver.

The formation of gallstones occurs when substances in bile, such as cholesterol and bilirubin, become too concentrated and crystallize, forming stones.

Gallstones can vary in size from tiny grains to large stones that can obstruct the bile ducts.

Symptoms:

Gallstone Colic: The most common symptom of gallstones is sudden and intense abdominal pain, known as gallstone colic. The pain typically occurs in the upper right abdomen and may radiate to the back or shoulder blades.

Nausea and Vomiting: Gallstone colic may be accompanied by nausea and vomiting.

Indigestion and Gas: Some individuals may experience indigestion, bloating, and gas.

Jaundice: In cases where gallstones obstruct the bile ducts, jaundice (yellowing of the skin and eyes) may occur, along with dark urine and pale stools.

Fever and Chills: In severe cases of gallbladder inflammation (cholecystitis), fever and chills may develop.

Complications:

Cholecystitis: Gallstones can block the cystic duct, leading to inflammation of the gallbladder (cholecystitis), which can cause severe abdominal pain, fever, and infection.

Choledocholithiasis: Gallstones can migrate from the gallbladder into the bile ducts, causing obstruction (choledocholithiasis), which may lead to jaundice, pancreatitis, and infection.

Gallstone Pancreatitis: Gallstones that obstruct the pancreatic duct can trigger inflammation of the pancreas (pancreatitis), characterized by severe abdominal pain, nausea, and vomiting.

Gallstone Ileus: In rare cases, large gallstones can erode through the gallbladder wall and enter the small intestine, causing obstruction (gallstone ileus).

Treatment Options:

Medication:

Ursodeoxycholic acid (ursodiol) may be prescribed to dissolve small cholesterol stones over time, but it is not always effective and can take months to years to work.

Oral medications such as bile salt binders may help dissolve or prevent the formation of cholesterol gallstones.

Lithotripsy:

Extracorporeal shock wave lithotripsy (ESWL) is a non-invasive procedure that uses shock waves to break up gallstones into smaller pieces, which can then be passed naturally or flushed out of the bile ducts.

Surgical Removal:

Cholecystectomy: Surgical removal of the gallbladder is the most common and definitive treatment for gallstones and associated complications. It can be performed laparoscopically or through traditional open surgery.

Endoscopic Retrograde Cholangiopancreatography (ERCP): In cases of choledocholithiasis, ERCP may be performed to remove gallstones from the bile ducts using specialized instruments and techniques.

Prevention:

Maintaining a healthy weight and following a balanced diet low in fat and cholesterol can help reduce the risk of gallstone formation.

Eating a diet high in fiber and staying hydrated may also help prevent gallstones.

Avoiding rapid weight loss and crash diets can help prevent the formation of gallstones.

Conclusion:

Gallstones are a common digestive problem that can cause significant discomfort and complications if left untreated. Recognizing the symptoms and seeking prompt medical attention is essential for proper diagnosis and treatment. With the appropriate interventions, including medication, lithotripsy, or surgical removal, individuals with gallstones can find relief and reduce the risk of complications associated with this condition.

Cholecystitis:

Here's an overview of cholecystitis, including its causes, symptoms, and treatment:

Causes:

Gallstones: The most common cause of cholecystitis is the presence of gallstones that block the cystic duct or the bile ducts, leading to inflammation of the gallbladder.

Biliary Sludge: Thickened bile or biliary sludge can also obstruct the bile ducts and predispose individuals to cholecystitis.

Tumor or Growth: Rarely, a tumor or growth in the bile ducts or gallbladder can cause obstruction and inflammation.

Infection: Infection of the bile ducts or gallbladder can lead to acute cholecystitis, particularly in individuals with compromised immune systems.

Ischemia: Reduced blood flow to the gallbladder, often associated with critical illness or surgery, can cause ischemic cholecystitis.

Symptoms:

Abdominal Pain: The hallmark symptom of cholecystitis is severe, steady pain in the upper right abdomen, which may radiate to the right shoulder or back.

Fever: Fever and chills are common, especially if the cholecystitis is due to an infection.

Nausea and Vomiting: Nausea and vomiting may occur, particularly after meals or when the pain worsens.

Tenderness: The abdomen may be tender to the touch, especially over the area of the gallbladder.

Jaundice: In severe cases, jaundice (yellowing of the skin and eyes) may develop if the bile ducts are obstructed.

Diagnosis:

Physical Examination: A healthcare provider may perform a physical examination to assess for abdominal tenderness and signs of inflammation.

Imaging Tests: Imaging studies such as ultrasound, CT scan, or MRI may be ordered to visualize the gallbladder and assess for signs of inflammation, gallstones, or complications.

Blood Tests: Blood tests may reveal elevated white blood cell count (indicating infection) and abnormal liver function tests (suggesting bile duct obstruction).

Treatment:

Nonsurgical Treatment:

NPO Status: Patients may be advised to avoid eating and drinking (NPO status) to rest the gallbladder and reduce stimulation of bile production.

Pain Management: Pain medications, such as NSAIDs or opioids, may be prescribed to alleviate discomfort.

Antibiotics: Antibiotics are often prescribed if the cholecystitis is due to an infection.

Intravenous Fluids: Intravenous fluids may be administered to maintain hydration and electrolyte balance.

Surgical Treatment:

Cholecystectomy: Surgical removal of the gallbladder (cholecystectomy) is the definitive treatment for acute cholecystitis, especially if it is recurrent or severe.

Laparoscopic cholecystectomy is the preferred approach, offering less postoperative pain and a quicker recovery compared to open surgery.

Percutaneous Cholecystostomy: In cases where surgery is not immediately feasible or safe, a percutaneous cholecystostomy tube may be inserted to drain the gallbladder and relieve pressure.

Complications:

Gangrene: Severe cases of cholecystitis can lead to tissue death (gangrene) in the gallbladder.

Perforation: Inflammation and pressure buildup can cause the gallbladder to rupture or perforate, leading to peritonitis (inflammation of the abdominal cavity).

Abscess Formation: Pus-filled pockets (abscesses) may develop around the gallbladder, requiring drainage and antibiotic therapy.

Prevention:

Preventing gallstones through lifestyle modifications, such as maintaining a healthy weight, eating a balanced diet, and staying hydrated, can reduce the risk of cholecystitis.

Conclusion:

Cholecystitis is a painful condition characterized by inflammation of the gallbladder, often due to gallstones or infection. Prompt diagnosis and appropriate treatment, including pain management, antibiotics, and surgical intervention when necessary, are crucial in managing cholecystitis and preventing complications.

Biliary Tract Obstruction:

Here's an overview of biliary tract obstruction, including its causes, symptoms, and treatment options:

Causes:

Biliary tract obstruction occurs when the flow of bile from the liver to the small intestine is blocked. Common causes include:

Gallstones: Gallstones can obstruct the common bile duct or the cystic duct, leading to bile duct obstruction.

Tumors: Tumors in the bile ducts, liver, pancreas, or nearby organs can cause compression or blockage of the bile ducts.

Inflammation: Inflammatory conditions such as primary sclerosing cholangitis (PSC), autoimmune pancreatitis, or chronic pancreatitis can cause narrowing or strictures in the bile ducts, leading to obstruction.

Biliary Strictures: Narrowing of the bile ducts due to scarring from previous surgeries, trauma, or infections can result in biliary tract obstruction.

Parasitic Infections: Parasitic infections such as liver flukes can cause obstruction of the bile ducts, particularly in regions where these parasites are endemic.

Symptoms:

Jaundice: Yellowing of the skin and eyes (jaundice) is a common symptom of biliary tract obstruction due to the buildup of bilirubin in the bloodstream.

Dark Urine: Bilirubin excreted in the urine may cause it to appear dark or tea-colored.

Pale Stools: Lack of bile in the stool can cause it to become pale or clay-colored.

Abdominal Pain: Pain in the upper right abdomen, particularly after eating fatty foods, may occur.

Nausea and Vomiting: Nausea and vomiting may result from bile duct obstruction and impaired digestion.

Itching (Pruritus): Accumulation of bile salts in the bloodstream can cause itching, particularly on the hands and feet.

Diagnosis:

Blood Tests: Blood tests may reveal elevated levels of bilirubin, liver enzymes, and alkaline phosphatase.

Imaging Studies: Imaging tests such as ultrasound, CT scan, MRI, or endoscopic retrograde cholangiopancreatography (ERCP) can help visualize the bile ducts and identify the site and cause of obstruction.

Liver Biopsy: A liver biopsy may be performed to assess for underlying liver disease or to obtain tissue samples for diagnosis.

Treatment Options:

Endoscopic Retrograde Cholangiopancreatography (ERCP):

ERCP is a minimally invasive procedure used to diagnose and treat biliary tract obstruction.

During ERCP, a flexible endoscope is passed through the mouth, down the esophagus, and into the duodenum to access the bile ducts.

Therapeutic interventions during ERCP may include balloon dilation of strictures, placement of stents to relieve obstruction, or removal of gallstones using specialized instruments.

Surgical Intervention:

Surgical intervention may be necessary in cases of severe or complex biliary tract obstruction, particularly if ERCP is unsuccessful or contraindicated.

Surgical procedures such as bile duct reconstruction, hepaticojejunostomy, or partial liver resection may be performed to bypass or remove the obstructed bile ducts.

Palliative Care:

In cases where the underlying cause of biliary tract obstruction is advanced cancer or inoperable tumors, palliative care measures may focus on symptom management and improving quality of life.

Palliative interventions may include pain management, drainage procedures, and supportive care.

Conclusion:

Biliary tract obstruction can have significant consequences on liver function and overall health. Prompt diagnosis and appropriate treatment, including endoscopic or surgical interventions, are essential in relieving obstruction, alleviating symptoms, and preventing complications associated with biliary tract obstruction.

Symptoms of Pancreatic and Biliary Diseases:

These symptoms can be indicative of both pancreatic and biliary diseases. Here's how they manifest:

Abdominal Pain, particularly in the upper abdomen:

Abdominal pain is a common symptom of pancreatic and biliary diseases. It often manifests as a dull, persistent ache or a sharp, stabbing pain in the upper abdomen. The pain may radiate to the back or shoulder blades.

Nausea and Vomiting:

Nausea and vomiting frequently accompany pancreatic and biliary diseases, especially during episodes of acute inflammation or obstruction. Nausea may be persistent, and vomiting may occur intermittently.

Jaundice (Yellowing of the skin and eyes):

Jaundice is a hallmark symptom of biliary diseases, particularly when the flow of bile from the liver is obstructed. It causes a yellowing of the skin, sclera (whites of the eyes), and mucous membranes due to the buildup of bilirubin.

Changes in Stool Color and Consistency:

Changes in stool color and consistency can occur in pancreatic and biliary diseases, particularly when bile flow is obstructed. Stools may become pale or clay-colored due to reduced bilirubin excretion. In some cases, individuals may experience greasy or fatty stools (steatorrhea) due to impaired fat digestion.

Fever and Chills:

Fever and chills often accompany acute inflammation or infection associated with pancreatic and biliary diseases. Fever is the body's response to infection or inflammation, while chills may occur as the body attempts to regulate its temperature.

Unexplained Weight Loss:

Unexplained weight loss is a common symptom of both pancreatic and biliary diseases, particularly in chronic or advanced cases. Weight loss may occur due to decreased appetite, malabsorption of nutrients, and metabolic changes associated with the underlying disease process.

Causes of Pancreatic and Biliary Diseases:

Here are the causes of pancreatic and biliary diseases:

Gallstones:

Gallstones are solid particles that form in the gallbladder when substances in bile, such as cholesterol and bilirubin, become too concentrated and crystallize. Gallstones can obstruct the bile ducts, leading to inflammation, infection, and other complications.

Alcohol Consumption:

Excessive alcohol consumption can contribute to the development of both pancreatic and biliary diseases. Chronic alcohol abuse can cause inflammation of the pancreas (pancreatitis) and increase the risk of gallstone formation.

Smoking:

Smoking is a significant risk factor for pancreatic cancer. It is believed that tobacco smoke contains carcinogens that can damage pancreatic cells and increase the likelihood of cancer development.

Genetic Factors:

Genetic factors play a role in the development of certain pancreatic and biliary diseases. Inherited genetic mutations, such as those associated with hereditary pancreatitis or familial pancreatic cancer syndromes, can increase the risk of developing pancreatic cancer.

Chronic Inflammation:

Chronic inflammation of the pancreas (chronic pancreatitis) or the biliary tract (primary sclerosing cholangitis, autoimmune pancreatitis) can contribute to the development of pancreatic and biliary diseases. Long-term inflammation can cause tissue damage, scarring, and impaired organ function.

Pancreatic or Biliary Tract Tumors:

Tumors in the pancreas or the biliary tract can lead to the development of pancreatic and biliary diseases. Pancreatic cancer is one of the most serious malignancies affecting the pancreas, while tumors in the bile ducts or gallbladder can cause obstruction, inflammation, and other complications.

Diagnosis:

Here's an overview of the diagnostic methods used for pancreatic and biliary diseases:

Physical Examination and Medical History:

A thorough physical examination and review of medical history are the initial steps in diagnosing pancreatic and biliary diseases. The healthcare provider may inquire about symptoms, risk factors, family history, and past medical conditions to guide further evaluation and testing.

Blood Tests to Assess Liver and Pancreatic Function:

Blood tests can help assess liver and pancreatic function by measuring levels of enzymes, bilirubin, and other substances in the blood. Elevated levels of liver enzymes (e.g., alanine transaminase, aspartate transaminase) and bilirubin may indicate liver or biliary tract disorders, while elevated pancreatic enzymes (e.g., amylase, lipase) may suggest pancreatic inflammation or injury.

Imaging Tests:

Ultrasound: Ultrasound imaging uses sound waves to create images of the pancreas, liver, gallbladder, and bile ducts. It can help identify gallstones, tumors, or other abnormalities in the abdominal organs.

CT Scan (Computed Tomography): CT scan provides detailed cross-sectional images of the pancreas, liver, bile ducts, and surrounding structures. It is useful for detecting tumors, inflammation, and structural abnormalities.

MRI (Magnetic Resonance Imaging): MRI uses magnetic fields and radio waves to produce detailed images of the pancreas, liver, bile ducts, and adjacent organs. It can provide information about the size, location, and characteristics of tumors and other abnormalities.

Endoscopic Ultrasound (EUS): EUS involves inserting an ultrasound probe into the digestive tract via an endoscope to obtain high-resolution images of the pancreas, bile ducts, and surrounding tissues. EUS can help visualize small lesions, assess tumor size and extent, and guide tissue sampling (biopsy) if needed.

ERCP (Endoscopic Retrograde Cholangiopancreatography):

ERCP is a specialized endoscopic procedure used to diagnose and treat disorders of the bile ducts and pancreas. It involves inserting an endoscope through the mouth and into the duodenum to access the bile ducts and pancreatic duct. Contrast dye is injected, and X-ray imaging is used to visualize the bile ducts, pancreatic duct, and any obstructions, strictures, or abnormalities. Therapeutic interventions, such as stent placement or stone removal, can be performed during ERCP.

Biopsy for Suspected Pancreatic Cancer:

In cases where pancreatic cancer is suspected based on imaging studies or clinical findings, a biopsy may be performed to obtain tissue samples for pathological examination. Biopsy techniques may include fine-needle aspiration (FNA), core needle biopsy, or surgical biopsy. Pathological analysis of the biopsy samples can confirm the diagnosis of pancreatic cancer and provide information about tumor type, grade, and stage.

Treatment Options:

Here's an elaboration on the treatment options for pancreatic and biliary diseases based on the provided list:

Pain Management:

Pain management is a critical aspect of treatment for pancreatic and biliary diseases, especially in conditions like pancreatitis and biliary colic.

Pain medications, such as nonsteroidal anti-inflammatory drugs (NSAIDs), opioids, and antispasmodics, may be prescribed to alleviate abdominal pain and discomfort.

In some cases, nerve blocks or celiac plexus neurolysis may be performed to provide pain relief for patients with chronic or severe pain refractory to other treatments.

Medications to Relieve Symptoms and Prevent Complications:

Medications may be prescribed to manage symptoms and prevent complications associated with pancreatic and biliary diseases.

For example, proton pump inhibitors (PPIs) or histamine receptor blockers may be used to reduce gastric acid production and alleviate symptoms of gastroesophageal reflux disease (GERD) associated with pancreatic diseases.

Ursodeoxycholic acid (ursodiol) may be prescribed to dissolve cholesterol gallstones and prevent the recurrence of gallstone-related complications.

Surgery:

Surgery plays a crucial role in the management of pancreatic and biliary diseases, particularly for conditions like gallstones, pancreatic cancer, and biliary tract obstruction.

Cholecystectomy, the surgical removal of the gallbladder, is the standard treatment for symptomatic gallstones and complications such as cholecystitis.

Tumor resection, including pancreaticoduodenectomy (Whipple procedure), distal pancreatectomy, and liver resection, may be performed for localized pancreatic or biliary tract tumors.

Surgical interventions aim to remove the underlying cause of the disease, alleviate symptoms, and prevent complications.

Chemotherapy and Radiation Therapy for Pancreatic Cancer:

Chemotherapy and radiation therapy are essential components of treatment for pancreatic cancer, especially for advanced or unresectable tumors.

Chemotherapy drugs, such as gemcitabine, 5-fluorouracil (5-FU), nab-paclitaxel, and combination regimens, are used to shrink tumors, alleviate symptoms, and improve survival rates.

Radiation therapy may be used alone or in combination with chemotherapy to target and destroy cancer cells, relieve pain, and improve quality of life for patients with pancreatic cancer.

Lifestyle Changes:

Lifestyle modifications, including diet modification and smoking cessation, play a significant role in the prevention and management of pancreatic and biliary diseases.

A low-fat diet rich in fruits, vegetables, whole grains, and lean proteins is recommended to reduce the risk of gallstone formation and manage symptoms of pancreatitis and biliary diseases.

Smoking cessation is crucial, as smoking is a significant risk factor for pancreatic cancer and can worsen outcomes for patients with pancreatic and biliary diseases.

Conclusion:

Treatment for pancreatic and biliary diseases encompasses a multidisciplinary approach, including pain management, medications, surgery, chemotherapy, radiation therapy, and lifestyle modifications. The selection of treatment modalities depends on the underlying condition, disease severity, patient preferences, and response to therapy. By addressing symptoms, removing the underlying cause, and promoting lifestyle changes, healthcare providers aim to improve outcomes and enhance the quality of life for patients with pancreatic and biliary diseases.

Conclusion:

Pancreatic and biliary diseases can have serious consequences if left untreated. Recognizing the symptoms and seeking prompt medical attention are crucial for effective management and improved outcomes. With advances in medical technology and treatment modalities, many patients can achieve symptom relief and better quality of life despite these challenging conditions.

References:

American College of Gastroenterology. (n.d.). Pancreatitis.

National Institute of Diabetes and Digestive and Kidney Diseases. (2021). Gallstones.

Cancer Treatment Centers of America. (n.d.). Pancreatic Cancer.

Important Information:

Conference Name: 14th World Gastroenterology, IBD & Hepatology Conference Short Name: 14GHUCG2024 Dates: December 17-19, 2024 Venue: Dubai, UAE Email:  gastroenterology@ucgcmeconference.com Visit: https://gastroenterology.universeconferences.com/ Call for Papers: https://gastroenterology.universeconferences.com/submit-abstract/ Register here: https://gastroenterology.universeconferences.com/registration/ Exhibitor/Sponsor: https://gastroenterology.universeconferences.com/exhibit-sponsor-opportunities/ Call Us: +12073070027 WhatsApp Us: +442033222718

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gastrointestinal system studies

case study – 43 yo female, dyspepsia and fatigue

» physical examination

abdominal pain

pale skin, looks ill

» laboratory testing and assays

macrocytic anemia (large red blood cells, few in number) | possibly arrest in early stages of differentiation in bone marrow

(microcytic anemia is a small RBC size, having to do with iron deficiency)

low Vitamin B12 levels | B12 is important for RBC differentiation and development

elevated serum gastrin levels (marker of abnormal GI activity)

» endoscopy / colonoscopy

run a probe with attached light down esophagus (can also grab biopsy samples) | colonoscopy is from rectum

healthy stomach has folds with glands in it

patient’s stomach has atrophic folds - it’s smooth, regressed folds

presence of cyst / tumor / polyp

pH = 6, low gastric acid aka hypochlorhydria

» biopsy procedure

cardia → body → antrum of stomach, which all have different linings

general: stomach lumen → lumen lining cells → (area-specific linings)

(body = pink and mitochondria-heavy, mutinous and oxyntic glands with gastric acid secretions, as well as ECL) specifically pink, mitochondria, and presence of oxyntic glands in histology 

(antrum = mutinous glands and G-neuroendocrine hormonal cells, secreting gastrin)

G-cell gastrin from antrum binds ECL → ECL secretes histamine → histamine stimulates acid from oxyntic glands

patient biopsy from antrum has glands spaced far apart, and spatial extension causes stomach folds to pull out and become smooth

patient biopsy from antrum has lymphocytes (increased purple nucleus stains) – chronic gastritis | acute is neutrophils

patient’s body has “antralized” → metaplasia, or a change in tissue to look like another organ’s tissue after injury and bodily adaptations

verdict from biopsy: atrophic metaplasia chronic lymphatic gastritis

» assessing the cyst / tumor mass

carcinoid - neuroendocrine cells form malignant tumor 

cancer cells have bypassed stroma

» summary

pale skin = anemic = bleeding or low RBC count

fold atrophy = chronic inflammation stretches lamina of stomach = high pH because glands ≠ making acid

biopsy = metaplastic, atrophic, lymphocyte proliferations, tumor mass

» AMAG diagnosis: autoimmune metaplastic atrophic gastritis

auto-antibodies are made against oxyntic gland’s parietal cells

antibodies recruit lymphocytes, which begin destroying oxyntic glands

body becomes “antralized” because pink oxyntic glands are destroyed

stomach grows back cells, but they are mucin-secreting cells and pH stays low because gastrin ≠ responded to

gastrin over-secretion to compensate → gastrin becomes a growth factor and  NE cells in antrum begin to proliferate

NE cells acquire some cancerous mutation → and the tumor forms 

case study – 40 yo female, episodic abdominal pain, jaundice, fever

» physical examination

colicky upper right quadrant – pain occurs intermittently

especially after a meal or when contact is made to area

painful jaundice

» laboratory assays

WBC, bilirubin, amylase and lipase build-up | possible pancreatic injury

alkaline phosphatase – made by cells in bile ducts

» imaging – abdominal ultrasound and ERCP

ultrasound: gallbladder is enlarged, contains gallstones

ERCP: analyze tiny bile and pancreatic ducts, as well as gallbladder, via injection of dye through esophageal line to duodenum 

imaging of dye from bile, cystic, and pancreatic ducts and can see all three organs

filling defect - dye cannot get to pancreatic duct or gallbladder

slow transit - dye takes a long time to get to liver from bile ducts

bile duct injury, pancreatic injury, gallbladder blockage

bile stops moving and grows infected → fever and inflammation, WBC up

» verdict from the ERCP: gallstone pancreatitis

gallbladder stones exit the gallbladder alongside bile after a fatty meal, and stone blocks pancreatic duct

another stone blocks the cystic duct and causes pain

stones - commonly cholesterol, or other types and compositions

digestive enzymes spill out into pancreas and auto-digest it causing more pain 

can inject stone-dissolving substances, or elective cholecystectomy (gallbladder removal, voluntary) if needed

any GI surgical procedure → adhesin tissue builds up and pins parts of bowel, blocks it → need to re-operate when things build up and infection occurs

case study – 45 yo male, rectal bleeding

» physical examination:

medical history: HIV+ 

otherwise normal

» laboratory testing and assays

undetectable HIV viral load (i.e., taking anti-retroviral medications well)

normal T-cell counts (visit is not due to HIV flare-up)

RPR+ (IgG) against syphilis | IgM is recent infection, IgG is long-time infection, high sensitivity

rectal bleeding could be due to gonorrhea, HPV

» colonoscopy findings

flat, barely raised polyp on right, sessile → removed for biopsy

glands of the area are crowded, overgrown and hypertrophic

lumens are irregular, branched and serrated instead of round in healthy patients

diagnosis: sessile serrated adenoma, pre-cancerous so removed

large, raised polyp on left, pedunculated → removed

overgrown, hypertrophic lining - cancerous epithelial cells

pre-cancerous polyp, mushroom-like → has not yet invaded stroma

diagnosis: tubular adenoma, where the growth looks like a tube

upper colon is spotted with white plaques (ulcers - fibrin and inflammatory cells), and inflamed, eroded → biopsy

» rectal biopsy to find source of bleeding

abundance of inflammatory cells, lamina expanded as a result of overcrowding

neutrophils from acute inflammation; plasma cells from chronic inflammation

acute inflammation turned chronic, essentially → silver staining reveals syphilis organisms in rectum

» verdict: syphilis in rectum causing rectal bleeding

[mcatmemoranda]

Alkaline phosphatase (Alk. Phos.) comprises a group of related enzymes found in biliary tract epithelium, bone, and placenta. Elevated Alk. Phos. is normal in growing children (because their epiphyseal plates remain open) and pregnant women. If Alk. Phos. is elevated and there is doubt as to its source, concurrent elevations in 5'-nucleotidase (5-NT) and gamma-glutamyl transferase (GGT) establish a hepatic or biliary source since these enzymes are specific for hepatic origin. While serum Alk. Phos. may be elevated in any active liver disease it is most sensitive to biliary tract obstruction and serum levels generally correlate with the severity of obstruction. As discussed below, those processes confined to the gallbladder do not cause biliary obstruction and are thus associated with infrequent and mild Alk. Phos. elevations while those processes caused by stones in the common bile duct are usually associated with Alk. Phos. elevations, which can be severe. In uncomplicated cholelithiasis, any degree of Alk. Phos. elevation is rare, even in patients with severe symptoms. In acute cholecystitis mild elevations of bilirubin and Alk. Phos. with normal aminotransferases can often be documented. Significant Alk. Phos. elevation is not common and suggests choledocholithiasis with possible obstruction of the extrahepatic ducts. Most patients with choledocholithiasis have a significant degree of Alk. Phos. elevation. The amount of elevation depends on the degree of obstruction present, but Alk. Phos. is often the first of the liver function tests to become abnormal. Elevations of greater than 2.5x normal have been shown to be predictive of choledocholithiasis in patients with known cholelithiasis.(1) Approximately 78% of patients with cholangitis present with Alk. Phos. elevations due to obstruction of the common bile duct. (2) In gallstone pancreatitis Alk. Phos. elevation is common since the stone causing pancreatitis may also cause some degree of obstruction. The degree of Alk. Phos. elevation is related to the degree of common bile duct obstruction and not necessarily to the severity of pancreatitis. Alk. Phos. levels can be useful in distinguishing the aforementioned disease entities and, in conjunction with other liver function tests can also help distinguish them from other hepatocellular diseases or nonhepatobiliary processes.

[lustgarten22]

Elevated Liver Enzymes: A Possible Sign of Pancreatic Cancer

Elevated liver enzymes are a common sign of liver damage, irritation, or inflammation. However, they can also be a sign of other serious conditions, including pancreatic cancer.

Pancreatic cancer is a rare but deadly cancer that begins in the pancreas, an organ that produces enzymes that help with digestion and hormones that regulate blood sugar. Pancreatic cancer is often difficult to diagnose in its early stages, but elevated liver enzymes can be an early sign of the disease.

Other possible causes of elevated liver enzymes include:

Hepatitis

Cirrhosis

Fatty liver disease

Alcohol abuse

Medications

Liver infections

Autoimmune diseases

If you have elevated liver enzymes, it is important to see a doctor to determine the cause. If pancreatic cancer is suspected, your doctor may order additional tests, such as a CT scan, MRI, or PET scan.

There is no cure for pancreatic cancer, but there are treatments that can help prolong life. If you are diagnosed with pancreatic cancer, it is important to work with a team of doctors who specialize in this type of cancer.

Blood Tests for Pancreatic Cancer

There are a few blood tests that can be used to screen for pancreatic cancer. These tests include:

CA 19-9: This is a tumor marker that is often elevated in people with pancreatic cancer. However, it can also be elevated in people with other conditions, such as pancreatitis.

CEA: This is another tumor marker that can be elevated in people with pancreatic cancer. However, it is not as specific as CA 19-9.

Lipid profile: This test measures levels of cholesterol and other fats in the blood. High levels of triglycerides and low levels of HDL cholesterol have been linked to an increased risk of pancreatic cancer.

If you have elevated liver enzymes or other symptoms of pancreatic cancer, your doctor may order a pancreatic cancer blood test to help diagnose the condition.

If you are concerned about what cancers cause elevated liver enzymes, please talk to your doctor. They can help you determine the cause of your symptoms and recommend the best course of treatment.

[drforambhuta]

Complications Linked to Bile Duct Stones:

Cholangitis: Bile duct stones can induce an infection within the bile ducts, causing cholangitis. This condition is characterized by the inflammation and swelling of the bile ducts, leading to symptoms such as fever, abdominal pain, jaundice, and a general sense of illness. Untreated cholangitis can be life-threatening, potentially resulting in sepsis and liver abscesses.

Pancreatitis: Bile duct stones can obstruct the pancreatic duct, leading to inflammation of the pancreas, a condition known as pancreatitis. Pancreatitis is marked by severe abdominal pain, nausea, vomiting, and elevated levels of pancreatic enzymes in the bloodstream. Severe cases of pancreatitis can result in organ failure and necessitate intensive medical care.

Biliary Stricture: A bile duct stone can cause scarring and narrowing of the bile ducts, giving rise to biliary stricture. This narrowing can obstruct the flow of bile, resulting in jaundice, recurring infections, and liver damage. Biliary strictures often require additional interventions, such as endoscopic or surgical procedures, to restore proper bile flow.

Gallbladder Inflammation and Infection: Bile duct stones can lead to inflammation of the gallbladder, referred to as cholecystitis, which causes severe abdominal pain, fever, and tenderness in the upper right abdomen. In some instances, the gallbladder may become infected, resulting in a condition called empyema. Gallbladder empyema necessitates urgent medical attention and often requires surgical removal of the gallbladder.

It is important to consult a good gastroenterologist at the earliest if you have any gastric problems. Dr. Amit Maydeo is considered to be one of the best gastroenterologists in Mumbai, who can help in the early diagnosis and treatment of bike duct stones. He currently provides consultation at HN Reliance Hospital, Mumbai, which is considered to be one of the best hospitals in the country.

[medtalksblog]

Liver Function and Enzyme Levels

The liver, a vital organ in the human body, plays a key role in the metabolic process. Its primary task is to purify the blood by processing and filtering harmful waste products. This is accomplished through the production and release of various enzymes, ensuring a smooth and efficient detoxification process.

SGPT and SGOT represent common liver enzymes. In cases of liver damage or inflammation, the levels of both SGOT and SGPT enzymes in the blood rise, disrupting the normal balance. These markers aid in diagnosing various liver diseases, including hepatitis, cirrhosis, liver cancer, and other conditions affecting the liver's function. They are also utilized to assess the effectiveness of specific medications or treatments for liver diseases.

Elevated Enzyme Levels: Range and Causes

Normally, SGPT and SGOT levels in a patient's serum should range between 7-56 units/liter and 8-45 units/liter, respectively. However, levels exceeding 56 units/liter for SGPT and 50 units/liter for men or 45 units/liter for women for SGOT should raise serious concerns, indicating a potential chronic underlying condition.

Elevated SGPT and SGOT levels often signal liver damage caused by conditions like:

Acute viral hepatitis

Alcoholic liver disease

Non-alcoholic fatty liver disease

Cirrhosis

Liver cancer

Various clinical conditions, such as kidney disease, celiac disease, myocardial infarction, diabetes, obesity, infectious mononucleosis, cholecystitis, dermatomyositis, pancreatitis, and more, can also contribute to SGOT/SGPT imbalance. Additionally, factors like alcohol abuse, certain medications, strenuous exercise, or muscle damage may lead to high enzyme levels.

Seeking Medical Attention

Consulting a healthcare provider is crucial to identify the underlying cause and receive appropriate treatment. Regular monitoring of liver enzymes aids in early detection of liver disease, preventing long-term damage.

Symptoms of Elevated SGOT & SGPT Levels

While elevated SGOT and SGPT levels often present without noticeable symptoms, some individuals may experience mild indications such as:

Constant fatigue and tiredness

Nausea and vomiting

Abdominal discomfort

Quick bruising

[drmannimal]

Pancreatitis in Dogs and Cats

Pancreatitis is the most common disease of the exocrine pancreas in both cats and dogs. The exocrine pancreas is the part of the pancreas that is involved in digestion, secreting digestive enzymes and bicarbonate. Pancreatitis can be either acute or chronic.

The majority of this post will focus on canine pancreatitis. The ways in which cats differ will be discussed at the end of the post.

Most cases of pancreatitis are idiopathic (unknown cause). Other possible causes include hypercalcemia, diet (dietary indiscretion, high fat), hyperlipidemia, pancreatic duct obstruction, trauma, and certain drugs. Concurrent disease such as DM, Cushings, and hypothyroidism are risk factors.

Clinical signs of Acute Pancreatitis - vomiting - abdominal pain - anorexia with severity: - dehydration - shock - renal failure - DIC - arrhythmias

Acute pancreatitis can develop into a number of diseases including chronic relapsing pancreatitis, EPI, and diabetes mellitus.

How do we diagnose? Bloodwork: May reveal any of the following; inflammatory leukogram, azotemia, mild elevation in liver enzymes, decreased calcium, hypoalbuminemia. Elevated amylase and lipase, though these are not specific to the pancreas (gastroenteritis, liver disease, kidney disease). SNAP cPL: used for screening, follow with Spec cPL. Spec cPL: specific for pancreatic tissue, best test to ID acute pancreatitis. Radiology. US.

Treatment Will vary based on severity and clinical signs. IV fluid therapy. Anti-emetics. Analgesia. Nutrition. Antibiotics only if sepsis is present.

What about chronic pancreatitis? This may arise chronically, or as previously mentioned, as a result of acute pancreatitis. Possible sequelae of chronic pancreatitis include EPI and DM.

Clinical signs of Chronic Pancreatitis (may present as any of the following) - low grade intermittent GI signs - anorexia and post-prandial abdominal pain - present with acute signs - present with EPI in an unusual breed - EPI and DM

Diagnosis isn’t as straightforward as acute... Histopathology is the gold standard diagnostic - though false negatives occur due to patchiness of pathology. US and Spec cPL not as sensitive as with acute.

Treatment  Analgesia. Nutrition. Treatment of any concurrent disease.

So what about cats? Cats can also get acute or chronic pancreatitis. Dietary indiscretion/ high-fat diets are not considered important risk factors as they are in dogs. Concurrent disorders that are often seen: DM, hepatic lipidosis, and lymphocytic cholangitis. Chronic pancreatitis is often associated with ‘triaditis’. This is chronic inflammation of the pancreas, small bowel, and biliary tract.

Clinical signs are often nonspecific - anorexia and lethargy - infrequent vomiting - may present acutely critically ill and in shock - inappetence and gradual weight loss may be seen in chronic cases

Diagnosis Bloodwork: highly variable. Spec fPL. US.

Treatment Acute - similar to dogs. Chronic - appetitie stimulants, anti-emetic, analgesia, corticosteroids especially if concurrent inflammatory disease.

[profoundlyscreechingcowboy]

cal warfare operations being conducted by an unelected, unaccountable Elite against the American people and our allies.Our mental and physical health have suffered immensely over the course of the past year and a half. We have felt the sting of isolation, lockdown, masking, quarantines, and other completely nonsensical acts of healthcare theater that have done absolutely nothing to protect the health or wellbeing of the public from the ongoing COVID-19 pandemic.Now, we are watching the medical establishment inject literal poison into millions of our fellow Americans without so much as a fight.We have been told that we will be fired and denied our livelihoods if we refuse to vaccinate. This was the last straw.We have spent thousands of hours analyzing leaked footage from Wuhan, scientific papers from primary sources, as well as the paper trails left by the medical establishment.What we have discovered would shock anyone to their core.First, we will summarize our findings, and then, we will explain them in detail. References will be placed at the end.Summary:COVID-19 is a blood and blood vessel disease. SARS-CoV-2 infects the lining of human blood vessels, causing them to leak into the lungs. Current treatment protocols (e.g. invasive ventilation) are actively harmful to patients, accelerating oxidative stress and causing severe VILI (ventilator-induced lung injuries). The continued use of ventilators in the absence of any proven medical benefit constitutes mass murder. Existing countermeasures are inadequate to slow the spread of what is an aerosolized and potentially wastewater-borne virus, and constitute a form of medical theater. Various non-vaccine interventions have been suppressed by both the media and the medical establishment in favor of vaccines and expensive patented drugs. The authorities have denied the usefulness of natural immunity against COVID-19, despite the fact that natural immunity confers protection against all of the virus’s proteins, and not just one. Vaccines will do more harm than good. The antigen that these vaccines are based on, SARS-CoV- 2 Spike, is a toxic protein. SARS-CoV-2 may have ADE, or antibody-dependent enhancement; current antibodies may not neutralize future strains, but instead help them infect immune cells. Also, vaccinating during a pandemic with a leaky vaccine removes the evolutionary pressure for a virus to become less lethal. There is a vast and appalling criminal conspiracy that directly links both Anthony Fauci and Moderna to the Wuhan Institute of Virology. COVID-19 vaccine researchers are directly linked to scientists involved in brain-computer interface (“neural lace”) tech, one of whom was indicted for taking grant money from China. Independent researchers have discovered mysterious nanoparticles inside the vaccines that are not supposed to be present. The entire pandemic is being used as an excuse for a vast political and economic transformation of Western society that will enrich the already rich and turn the rest of us into serfs and untouchables.

COVID-19 Pathophysiology and Treatments:COVID-19 is not a viral pneumonia. It is a viral vascular endotheliitis and attacks the lining of blood vessels, particularly the small pulmonary alveolar capillaries, leading to endothelial cell activation and sloughing, coagulopathy, sepsis, pulmonary edema, and ARDS-like symptoms. This is a disease of the blood and blood vessels. The circulatory system. Any pneumonia that it causes is secondary to that.In severe cases, this leads to sepsis, blood clots, and multiple organ failure, including hypoxic and inflammatory damage to various vital organs, such as the brain, heart, liver, pancreas, kidneys, and intestines.Some of the most common laboratory findings in COVID-19 are elevated D-dimer, elevated prothrombin time, elevated C-reactive protein, neutrophilia, lymphopenia, hypocalcemia, and hyperferritinemia, essentially matching a profile of coagulopathy and immune system hyperactivation/immune cell exhaustion.COVID-19 can present as almost anything, due to the wide tropism of SARS-CoV-2 for various tissues in the body’s vital organs. While its most common initial presentation is respiratory illness and flu-like symptoms, it can present as brain inflammation, gastrointestinal disease, or even heart attack or pulmonary embolism.COVID-19 is more severe in those with specific comorbidities, such as obesity, diabetes, and hypertension. This is because these conditions involve endothelial dysfunction, which renders the circulatory system more susceptible to infection and injury by this particular virus.The vast majority of COVID-19 cases are mild and do not cause significant disease. In known cases, there is something known as the 80/20 rule, where 80% of cases are mild and 20% are severe or critical. However, this ratio is only correct for known cases, not all infections. The number of actual infections is much, much higher. Consequently, the mortality and morbidity rate is lower. However, COVID-19 spreads very quickly, meaning that there are a significant number of severely-ill and critically-ill patients appearing in a short time frame.In those who have critical COVID-19-induced sepsis, hypoxia, coagulopathy, and ARDS, the most common treatments are intubation, injected corticosteroids, and blood thinners. This is not the correct treatment for COVID-19. In severe hypoxia, cellular metabolic shifts cause ATP to break down into hypoxanthine, which, upon the reintroduction of oxygen, causes xanthine oxidase to produce tons of highly damaging radicals that attack tissue. This is called ischemia-reperfusion injury, and it’s why the majority of people who go on a ventilator are dying. In the mitochondria, succinate buildup due to sepsis does the same exact thing; when oxygen is reintroduced, it makes superoxide radicals. Make no mistake, intubation will kill people who have COVID-19.The end-stage of COVID-19 is severe lipid peroxidation, where fats in the body start to “rust” due to damage by oxidative stress. This drives autoimmunity. Oxidized lipids appear as foreign objects to the immune system, which recognizes and forms antibodies against OSEs, or oxidation-specific epitopes. Also, oxidized lipids feed directly into pattern recognition receptors, triggering even more inflammation and summoning even more cells of the innate immune system that release even more destructive enzymes. This is similar to the pathophysiology of Lupus.COVID-19’s pathology is dominated by extreme oxidative stress and neutrophil respiratory burst, to the point where hemoglobin becomes incapable of carrying oxygen due to heme iron being stripped out of heme by hypochlorous acid. No amount of supplemental oxygen can oxygenate blood that chemically refuses to bind O2.The breakdown of the pathology is as follows:SARS-CoV-2 Spike binds to ACE2. Angiotensin Converting Enzyme 2 is an enzyme that is part of the renin-angiotensin-aldosterone system, or RAAS. The RAAS is a hormone control system that moderates fluid volume in the body and in the bloodstream (i.e. osmolarity) by controlling salt retention and excretion.

This protein, ACE2, is ubiquitous in every part of the body that interfaces with the circulatory system, particularly in vascular endothelial cells and pericytes, brain astrocytes, renal tubules and podocytes, pancreatic islet cells, bile duct and intestinal epithelial cells, and the seminiferous ducts of the testis, all of which SARS-CoV-2 can infect, not just the lungs.SARS-CoV-2 infects a cell as follows: SARS-CoV-2 Spike undergoes a conformational change where the S1 trimers flip up and extend, locking onto ACE2 bound to the surface of a cell. TMPRSS2, or transmembrane protease serine 2, comes along and cuts off the heads of the Spike, exposing the S2 stalk-shaped subunit inside. The remainder of the Spike undergoes a conformational change that causes it to unfold like an extension ladder, embedding itself in the cell membrane. Then, it folds back upon itself, pulling the viral membrane and the cell membrane together. The two membranes fuse, with the virus’s proteins migrating out onto the surface of the cell. The SARS-CoV-2 nucleocapsid enters the cell, disgorging its genetic material and beginning the viral replication process, hijacking the cell’s own structures to produce more virus.SARS-CoV-2 Spike proteins embedded in a cell can actually cause human cells to fuse together, forming syncytia/MGCs (multinuclear giant cells). They also have other pathogenic, harmful effects. SARS-CoV- 2’s viroporins, such as its Envelope protein, act as calcium ion channels, introducing calcium into infected cells. The virus suppresses the natural interferon response, resulting in delayed inflammation. SARS-CoV-2 N protein can also directly activate the NLRP3 inflammasome. Also, it suppresses the Nrf2 antioxidant pathway. The suppression of ACE2 by binding with Spike causes a buildup of bradykinin that would otherwise be broken down by ACE2.This constant calcium influx into the cells results in (or is accompanied by) noticeable hypocalcemia, or low blood calcium, especially in people with Vitamin D deficiencies and pre-existing endothelial dysfunction. Bradykinin upregulates cAMP, cGMP, COX, and Phospholipase C activity. This results in prostaglandin release and vastly increased intracellular calcium signaling, which promotes highly aggressive ROS release and ATP depletion. NADPH oxidase releases superoxide into the extracellular space. Superoxide radicals react with nitric oxide to form peroxynitrite. Peroxynitrite reacts with the tetrahydrobiopterin cofactor needed by endothelial nitric oxide synthase, destroying it and “uncoupling” the enzymes, causing nitric oxide synthase to synthesize more superoxide instead. This proceeds in a positive feedback loop until nitric oxide bioavailability in the circulatory system is depleted.Dissolved nitric oxide gas produced constantly by eNOS serves many important functions, but it is also antiviral against SARS-like coronaviruses, preventing the palmitoylation of the viral Spike protein and making it harder for it to bind to host receptors. The loss of NO allows the virus to begin replicating with impunity in the body. Those with endothelial dysfunction (i.e. hypertension, diabetes, obesity, old age, African-American race) have redox equilibrium issues to begin with, giving the virus an advantage.Due to the extreme cytokine release triggered by these processes, the body summons a great deal of neutrophils and monocyte-derived alveolar macrophages to the lungs. Cells of the innate immune system are the first-line defenders against pathogens. They work by engulfing invaders and trying to attack them with enzymes that produce powerful oxidants, like SOD and MPO. Superoxide dismutase takes superoxide and makes hydrogen peroxide, and myeloperoxidase takes hydrogen peroxide and chlorine ions and makes hypochlorous acid, which is many, many times more reactive than sodium hypochlorite bleach.Neutrophils have a nasty trick. They can also eject these enzymes into the extracellular space, where they will continuously spit out peroxide and bleach into the bloodstream. This is called neutrophil

extracellular trap formation, or, when it becomes pathogenic and counterproductive, NETosis. In severe and critical COVID-19, there is actually rather severe NETosis.Hypochlorous acid building up in the bloodstream begins to bleach the iron out of heme and compete for O2 binding sites. Red blood cells lose the ability to transport oxygen, causing the sufferer to turn blue in the face. Unliganded iron, hydrogen peroxide, and superoxide in the bloodstream undergo the Haber- Weiss and Fenton reactions, producing extremely reactive hydroxyl radicals that violently strip electrons from surrounding fats and DNA, oxidizing them severely.This condition is not unknown to medical science. The actual name for all of this is acute sepsis.We know this is happening in COVID-19 because people who have died of the disease have noticeable ferroptosis signatures in their tissues, as well as various other oxidative stress markers such as nitrotyrosine, 4-HNE, and malondialdehyde.When you intubate someone with this condition, you are setting off a free radical bomb by supplying the cells with O2. It’s a catch-22, because we need oxygen to make Adenosine Triphosphate (that is, to live), but O2 is also the precursor of all these damaging radicals that lead to lipid peroxidation.The correct treatment for severe COVID-19 related sepsis is non-invasive ventilation, steroids, and antioxidant infusions. Most of the drugs repurposed for COVID-19 that show any benefit whatsoever in rescuing critically-ill COVID-19 patients are antioxidants. N-acetylcysteine, melatonin, fluvoxamine, budesonide, famotidine, cimetidine, and ranitidine are all antioxidants. Indomethacin prevents iron- driven oxidation of arachidonic acid to isoprostanes. There are powerful antioxidants such as apocynin that have not even been tested on COVID-19 patients yet which could defang neutrophils, prevent lipid peroxidation, restore endothelial health, and restore oxygenation to the tissues.Scientists who know anything about pulmonary neutrophilia, ARDS, and redox biology have known or surmised much of this since March 2020. In April 2020, Swiss scientists confirmed that COVID-19 was a vascular endotheliitis. By late 2020, experts had already concluded that COVID-19 causes a form of viral sepsis. They also know that sepsis can be effectively treated with antioxidants. None of this information is particularly new, and yet, for the most part, it has not been acted upon. Doctors continue to use damaging intubation techniques with high PEEP settings despite high lung compliance and poor oxygenation, killing an untold number of critically ill patients with medical malpractice.Because of the way they are constructed, Randomized Control Trials will never show any benefit for any antiviral against COVID-19. Not Remdesivir, not Kaletra, not HCQ, and not Ivermectin. The reason for this is simple; for the patients that they have recruited for these studies, such as Oxford’s ludicrous RECOVERY study, the intervention is too late to have any positive effect.The clinical course of COVID-19 is such that by the time most people seek medical attention for hypoxia, their viral load has already tapered off to almost nothing. If someone is about 10 days post-exposure and has already been symptomatic for five days, there is hardly any virus left in their bodies, only cellular damage and derangement that has initiated a hyperinflammatory response. It is from this group that the clinical trials for antivirals have recruited, pretty much exclusively.In these trials, they give antivirals to severely ill patients who have no virus in their bodies, only a delayed hyperinflammatory response, and then absurdly claim that antivirals have no utility in treating or preventing COVID-19. These clinical trials do not recruit people who are pre-symptomatic. They do not test pre-exposure or post-exposure prophylaxis.This is like using a defibrillator to shock only flatline, and then absurdly claiming that defibrillators have no medical utility whatsoever when the patients refuse to rise from the dead. The

intervention is too late. These trials for antivirals show systematic, egregious selection bias. They are providing a treatment that is futile to the specific cohort they are enrolling.India went against the instructions of the WHO and mandated the prophylactic usage of Ivermectin. They have almost completely eradicated COVID-19. The Indian Bar Association of Mumbai has brought criminal charges against WHO Chief Scientist Dr. Soumya Swaminathan for recommending against the use of Ivermectin.Ivermectin is not “horse dewormer”. Yes, it is sold in veterinary paste form as a dewormer for animals. It has also been available in pill form for humans for decades, as an antiparasitic drug.The media have disingenuously claimed that because Ivermectin is an antiparasitic drug, it has no utility as an antivirus. This is incorrect. Ivermectin has utility as an antiviral. It blocks importin, preventing nuclear import, effectively inhibiting viral access to cell nuclei. Many drugs currently on the market have multiple modes of action. Ivermectin is one such drug. It is both antiparasitic and antiviral.In Bangladesh, Ivermectin costs $1.80 for an entire 5-day course. Remdesivir, which is toxic to the liver, costs $3,120 for a 5-day course of the drug. Billions of dollars of utterly useless Remdesivir were sold to our governments on the taxpayer’s dime, and it ended up being totally useless for treating hyperinflammatory COVID-19. The media has hardly even covered this at all.The opposition to the use of generic Ivermectin is not based in science. It is purely financially and politically-motivated. An effective non-vaccine intervention would jeopardize the rushed FDA approval of patented vaccines and medicines for which the pharmaceutical industry stands to rake in billions upon billions of dollars in sales on an ongoing basis.The majority of the public are scientifically illiterate and cannot grasp what any of this even means, thanks to a pathetic educational system that has miseducated them. You would be lucky to find 1 in 100 people who have even the faintest clue what any of this actually means.COVID-19 Transmission:COVID-19 is airborne. The WHO carried water for China by claiming that the virus was only droplet- borne. Our own CDC absurdly claimed that it was mostly transmitted by fomite-to-face contact, which, given its rapid spread from Wuhan to the rest of the world, would have been physically impossible.The ridiculous belief in fomite-to-face being a primary mode of transmission led to the use of surface disinfection protocols that wasted time, energy, productivity, and disinfectant.The 6-foot guidelines are absolutely useless. The minimum safe distance to protect oneself from an aerosolized virus is to be 15+ feet away from an infected person, no closer. Realistically, no public transit is safe.Surgical masks do not protect you from aerosols. The virus is too small and the filter media has too large of gaps to filter it out. They may catch respiratory droplets and keep the virus from being expelled by someone who is sick, but they do not filter a cloud of infectious aerosols if someone were to walk into said cloud.The minimum level of protection against this virus is quite literally a P100 respirator, a PAPR/CAPR, or a 40mm NATO CBRN respirator, ideally paired with a full-body tyvek or tychem suit, gloves, and booties, with all the holes and gaps taped.Live SARS-CoV-2 may potentially be detected in sewage outflows, and there may be oral-fecal transmission. During the SARS outbreak in 2003, in the Amoy Gardens incident, hundreds of people were infected by aerosolized fecal matter rising from floor drains in their apartments.COVID-19 Vaccine Dangers:The vaccines for COVID-19 are not sterilizing and do not prevent infection or transmission. They are “leaky” vaccines. This means they remove the evolutionary pressure on the virus to become less lethal. It also means that the vaccinated are perfect carriers. In other words, those who are vaccinated are a threat to the unvaccinated, not the other way around.All of the COVID-19

vaccines currently in use have undergone minimal testing, with highly accelerated clinical trials. Though they appear to limit severe illness, the long-term safety profile of these vaccines remains unknown.Some of these so-called “vaccines” utilize an untested new technology that has never been used in vaccines before. Traditional vaccines use weakened or killed virus to stimulate an immune response. The Moderna and Pfizer-BioNTech vaccines do not. They are purported to consist of an intramuscular shot containing a suspension of lipid nanoparticles filled with messenger RNA. The way they generate an immune response is by fusing with cells in a vaccine recipient’s shoulder, undergoing endocytosis, releasing their mRNA cargo into those cells, and then utilizing the ribosomes in those cells to synthesize modified SARS-CoV-2 Spike proteins in-situ.These modified Spike proteins then migrate to the surface of the cell, where they are anchored in place by a transmembrane domain. The adaptive immune system detects the non-human viral protein being expressed by these cells, and then forms antibodies against that protein. This is purported to confer protection against the virus, by training the adaptive immune system to recognize and produce antibodies against the Spike on the actual virus. The J&J and AstraZeneca vaccines do something similar, but use an adenovirus vector for genetic material delivery instead of a lipid nanoparticle. These vaccines were produced or validated with the aid of fetal cell lines HEK-293 and PER.C6, which people with certain religious convictions may object strongly to.SARS-CoV-2 Spike is a highly pathogenic protein on its own. It is impossible to overstate the danger presented by introducing this protein into the human body.It is claimed by vaccine manufacturers that the vaccine remains in cells in the shoulder, and that SARS- CoV-2 Spike produced and expressed by these cells from the vaccine’s genetic material is harmless and inert, thanks to the insertion of prolines in the Spike sequence to stabilize it in the prefusion conformation, preventing the Spike from becoming active and fusing with other cells. However, a pharmacokinetic study from Japan showed that the lipid nanoparticles and mRNA from the Pfizer vaccine did not stay in the shoulder, and in fact bioaccumulated in many different organs, including the reproductive organs and adrenal glands, meaning that modified Spike is being expressed quite literally all over the place. These lipid nanoparticles may trigger anaphylaxis in an unlucky few, but far more concerning is the unregulated expression of Spike in various somatic cell lines far from the injection site and the unknown consequences of that.Messenger RNA is normally consumed right after it is produced in the body, being translated into a protein by a ribosome. COVID-19 vaccine mRNA is produced outside the body, long before a ribosome translates it. In the meantime, it could accumulate damage if inadequately preserved. When a ribosome attempts to translate a damaged strand of mRNA, it can become stalled. When this happens, the ribosome becomes useless for translating proteins because it now has a piece of mRNA stuck in it, like a lace card in an old punch card reader. The whole thing has to be cleaned up and new ribosomes synthesized to replace it. In cells with low ribosome turnover, like nerve cells, this can lead to reduced protein synthesis, cytopathic effects, and neuropathies.Certain proteins, including SARS-CoV-2 Spike, have proteolytic cleavage sites that are basically like little dotted lines that say “cut here”, which attract a living organism’s own proteases (essentially, molecular scissors) to cut them. There is a possibility that S1 may be proteolytically cleaved from S2, causing active S1 to float away into the bloodstream while leaving the S2 “stalk” embedded in the membrane of the cell that expressed the protein.SARS-CoV-2 Spike has a Superantigenic region (SAg), which may promote extreme inflammation.Anti-Spike antibodies were found in one study to function as

autoantibodies and attack the body’s own cells. Those who have been immunized with COVID-19 vaccines have developed blood clots, myocarditis, Guillain-Barre Syndrome, Bell’s Palsy, and multiple sclerosis flares, indicating that the vaccine promotes autoimmune reactions against healthy tissue.SARS-CoV-2 Spike does not only bind to ACE2. It was suspected to have regions that bind to basigin, integrins, neuropilin-1, and bacterial lipopolysaccharides as well. SARS-CoV-2 Spike, on its own, can potentially bind any of these things and act as a ligand for them, triggering unspecified and likely highly inflammatory cellular activity.SARS-CoV-2 Spike contains an unusual PRRA insert that forms a furin cleavage site. Furin is a ubiquitous human protease, making this an ideal property for the Spike to have, giving it a high degree of cell tropism. No wild-type SARS-like coronaviruses related to SARS-CoV-2 possess this feature, making it highly suspicious, and perhaps a sign of human tampering.SARS-CoV-2 Spike has a prion-like domain that enhances its infectiousness.The Spike S1 RBD may bind to heparin-binding proteins and promote amyloid aggregation. In humans, this could lead to Parkinson’s, Lewy Body Dementia, premature Alzheimer’s, or various other neurodegenerative diseases. This is very concerning because SARS-CoV-2 S1 is capable of injuring and penetrating the blood-brain barrier and entering the brain. It is also capable of increasing the permeability of the blood-brain barrier to other molecules.SARS-CoV-2, like other betacoronaviruses, may have Dengue-like ADE, or antibody-dependent enhancement of disease. For those who aren’t aware, some viruses, including betacoronaviruses, have a feature called ADE. There is also something called Original Antigenic Sin, which is the observation that the body prefers to produce antibodies based on previously-encountered strains of a virus over newly- encountered ones.In ADE, antibodies from a previous infection become non-neutralizing due to mutations in the virus’s proteins. These non-neutralizing antibodies then act as trojan horses, allowing live, active virus to be pulled into macrophages through their Fc receptor pathways, allowing the virus to infect immune cells that it would not have been able to infect before. This has been known to happen with Dengue Fever; when someone gets sick with Dengue, recovers, and then contracts a different strain, they can get very, very ill.If someone is vaccinated with mRNA based on the Spike from the initial Wuhan strain of SARS-CoV-2, and then they become infected with a future, mutated strain of the virus, they may become severely ill. In other words, it is possible for vaccines to sensitize someone to disease.There is a precedent for this in recent history. Sanofi’s Dengvaxia vaccine for Dengue failed because it caused immune sensitization in people whose immune systems were Dengue-naive.In mice immunized against SARS-CoV and challenged with the virus, a close relative of SARS-CoV-2, they developed immune sensitization, Th2 immunopathology, and eosinophil infiltration in their lungs.We have been told that SARS-CoV-2 mRNA vaccines cannot be integrated into the human genome, because messenger RNA cannot be turned back into DNA. This is false. There are elements in human cells called LINE-1 retrotransposons, which can indeed integrate mRNA into a human genome by endogenous reverse transcription. Because the mRNA used in the vaccines is stabilized, it hangs around in cells longer, increasing the chances for this to happen. If the gene for SARS-CoV-2 Spike is integrated into a portion of the genome that is not silent and actually expresses a protein, it is possible that people who take this vaccine may continuously express SARS-CoV-2 Spike from their somatic cells for the rest of their lives.By inoculating people with a vaccine that causes their bodies to produce Spike in-situ, they are being inoculated with a pathogenic protein. A toxin that may cause long-term inflammation, heart problems, and a raised risk of cancers. In the long-term, it may

also potentially lead to premature neurodegenerative disease.Absolutely nobody should be compelled to take this vaccine under any circumstances, and in actual fact, the vaccination campaign must be stopped immediately.COVID-19 Criminal Conspiracy:The vaccine and the virus were made by the same people.In 2014, there was a moratorium on SARS gain-of-function research that lasted until 2017. This research was not halted. Instead, it was outsourced, with the federal grants being laundered through NGOs.Ralph Baric is a virologist and SARS expert at UNC Chapel Hill in North Carolina. This is who Anthony Fauci was referring to when he insisted, before Congress, that if any gain-of-function research was being conducted, it was being conducted in North Carolina.This was a lie. Anthony Fauci lied before Congress. A felony.Ralph Baric and Shi Zhengli are colleagues and have co-written papers together. Ralph Baric mentored Shi Zhengli in his gain-of-function manipulation techniques, particularly serial passage, which results in a virus that appears as if it originated naturally. In other words, deniable bioweapons. Serial passage in humanized hACE2 mice may have produced something like SARS-CoV-2.The funding for the gain-of-function research being conducted at the Wuhan Institute of Virology came from Peter Daszak. Peter Daszak runs an NGO called EcoHealth Alliance. EcoHealth Alliance received millions of dollars in grant money from the National Institutes of Health/National Institute of Allergy and Infectious Diseases (that is, Anthony Fauci), the Defense Threat Reduction Agency (part of the US Department of Defense), and the United States Agency for International Development. NIH/NIAID contributed a few million dollars, and DTRA and USAID each contributed tens of millions of dollars towards this research. Altogether, it was over a hundred million dollars.EcoHealth Alliance subcontracted these grants to the Wuhan Institute of Virology, a lab in China with a very questionable safety record and poorly trained staff, so that they could conduct gain-of-function research, not in their fancy P4 lab, but in a level-2 lab where technicians wore nothing more sophisticated than perhaps a hairnet, latex gloves, and a surgical mask, instead of the bubble suits used when working with dangerous viruses. Chinese scientists in Wuhan reported being routinely bitten and urinated on by laboratory animals. Why anyone would outsource this dangerous and delicate work to the People’s Republic of China, a country infamous for industrial accidents and massive explosions that have claimed hundreds of lives, is completely beyond me, unless the aim was to start a pandemic on purpose.In November of 2019, three technicians at the Wuhan Institute of Virology developed symptoms consistent with a flu-like illness. Anthony Fauci, Peter Daszak, and Ralph Baric knew at once what had happened, because back channels exist between this laboratory and our scientists and officials.December 12th, 2019, Ralph Baric signed a Material Transfer Agreement (essentially, an NDA) to receive Coronavirus mRNA vaccine-related materials co-owned by Moderna and NIH. It wasn’t until a whole month later, on January 11th, 2020, that China allegedly sent us the sequence to what would become known as SARS-CoV-2. Moderna claims, rather absurdly, that they developed a working vaccine from this sequence in under 48 hours.Stephane Bancel, the current CEO of Moderna, was formerly the CEO of bioMerieux, a French multinational corporation specializing in medical diagnostic tech, founded by one Alain Merieux. Alain Merieux was one of the individuals who was instrumental in the construction of the Wuhan Institute of Virology’s P4 lab.The sequence given as the closest relative to SARS-CoV-2, RaTG13, is not a real virus. It is a forgery. It was made by entering a gene sequence by hand into a database, to create a cover story for the existence of SARS-CoV-2, which is very likely a gain-of-function chimera produced at the Wuhan Institute of Virology and was either leaked by accident or intentionally

released.The animal reservoir of SARS-CoV-2 has never been found.This is not a conspiracy “theory”. It is an actual criminal conspiracy, in which people connected to the development of Moderna’s mRNA-1273 are directly connected to the Wuhan Institute of Virology and their gain-of-function research by very few degrees of separation, if any. The paper trail is well- established.The lab-leak theory has been suppressed because pulling that thread leads one to inevitably conclude that there is enough circumstantial evidence to link Moderna, the NIH, the WIV, and both the vaccine and the virus’s creation together. In a sane country, this would have immediately led to the world’s biggest RICO and mass murder case. Anthony Fauci, Peter Daszak, Ralph Baric, Shi Zhengli, and Stephane Bancel, and their accomplices, would have been indicted and prosecuted to the fullest extent of the law. Instead, billions of our tax dollars were awarded to the perpetrators.The FBI raided Allure Medical in Shelby Township north of Detroit for billing insurance for “fraudulent COVID-19 cures”. The treatment they were using? Intravenous Vitamin C. An antioxidant. Which, as described above, is an entirely valid treatment for COVID-19-induced sepsis, and indeed, is now part of the MATH+ protocol advanced by Dr. Paul E. Marik.The FDA banned ranitidine (Zantac) due to supposed NDMA (N-nitrosodimethylamine) contamination. Ranitidine is not only an H2 blocker used as antacid, but also has a powerful antioxidant effect, scavenging hydroxyl radicals. This gives it utility in treating COVID-19.The FDA also attempted to take N-acetylcysteine, a harmless amino acid supplement and antioxidant, off the shelves, compelling Amazon to remove it from their online storefront.This leaves us with a chilling question: did the FDA knowingly suppress antioxidants useful for treating COVID-19 sepsis as part of a criminal conspiracy against the American public?The establishment is cooperating with, and facilitating, the worst criminals in human history, and are actively suppressing non-vaccine treatments and therapies in order to compel us to inject these criminals’ products into our bodies. This is absolutely unacceptable.COVID-19 Vaccine Development and Links to Transhumanism:This section deals with some more speculative aspects of the pandemic and the medical and scientific establishment’s reaction to it, as well as the disturbing links between scientists involved in vaccine research and scientists whose work involved merging nanotechnology with living cells.On June 9th, 2020, Charles Lieber, a Harvard nanotechnology researcher with decades of experience, was indicted by the DOJ for fraud. Charles Lieber received millions of dollars in grant money from the US Department of Defense, specifically the military think tanks DARPA, AFOSR, and ONR, as well as NIH and MITRE. His specialty is the use of silicon nanowires in lieu of patch clamp electrodes to monitor and modulate intracellular activity, something he has been working on at Harvard for the past twenty years. He was claimed to have been working on silicon nanowire batteries in China, but none of his colleagues can recall him ever having worked on battery technology in his life; all of his research deals with bionanotechnology, or the blending of nanotech with living cells.The indictment was over his collaboration with the Wuhan University of Technology. He had double- dipped, against the terms of his DOD grants, and taken money from the PRC’s Thousand Talents plan, a program which the Chinese government uses to bribe Western scientists into sharing proprietary R&D information that can be exploited by the PLA for strategic advantage.Charles Lieber’s own papers describe the use of silicon nanowires for brain-computer interfaces, or “neural lace” technology. His papers describe how neurons can endocytose whole silicon nanowires or parts of them, monitoring and even modulating neuronal activity.Charles Lieber was a colleague of Robert Langer. Together, along with Daniel S. Kohane, they worked on a paper describing

artificial tissue scaffolds that could be implanted in a human heart to monitor its activity remotely.Robert Langer, an MIT alumnus and expert in nanotech drug delivery, is one of the co-founders of Moderna. His net worth is now $5.1 billion USD thanks to Moderna’s mRNA-1273 vaccine sales.Both Charles Lieber and Robert Langer’s bibliographies describe, essentially, techniques for human enhancement, i.e. transhumanism. Klaus Schwab, the founder of the World Economic Forum and the architect behind the so-called “Great Reset”, has long spoken of the “blending of biology and machinery” in his books.Since these revelations, it has come to the attention of independent researchers that the COVID-19 vaccines may contain reduced graphene oxide nanoparticles. Japanese researchers have also found unexplained contaminants in COVID-19 vaccines.Graphene oxide is an anxiolytic. It has been shown to reduce the anxiety of laboratory mice when injected into their brains. Indeed, given SARS-CoV-2 Spike’s propensity to compromise the blood-brain barrier and increase its permeability, it is the perfect protein for preparing brain tissue for extravasation of nanoparticles from the bloodstream and into the brain. Graphene is also highly conductive and, in some circumstances, paramagnetic.In 2013, under the Obama administration, DARPA launched the BRAIN Initiative; BRAIN is an acronym for Brain Research Through Advancing Innovative Neurotechnologies®. This program involves the development of brain-computer interface technologies for the military, particularly non-invasive, injectable systems that cause minimal damage to brain tissue when removed. Supposedly, this technology would be used for healing wounded soldiers with traumatic brain injuries, the direct brain control of prosthetic limbs, and even new abilities such as controlling drones with one’s mind.Various methods have been proposed for achieving this, including optogenetics, magnetogenetics, ultrasound, implanted electrodes, and transcranial electromagnetic stimulation. In all instances, the goal is to obtain read or read-write capability over neurons, either by stimulating and probing them, or by rendering them especially sensitive to stimulation and probing.However, the notion of the widespread use of BCI technology, such as Elon Musk’s Neuralink device, raises many concerns over privacy and personal autonomy. Reading from neurons is problematic enough on its own. Wireless brain-computer interfaces may interact with current or future wireless GSM infrastructure, creating neurological data security concerns. A hacker or other malicious actor may compromise such networks to obtain people’s brain data, and then exploit it for nefarious purposes.However, a device capable of writing to human neurons, not just reading from them, presents another, even more serious set of ethical concerns. A BCI that is capable of altering the contents of one’s mind for innocuous purposes, such as projecting a heads-up display onto their brain’s visual center or sending audio into one’s auditory cortex, would also theoretically be capable of altering mood and personality, or perhaps even subjugating someone’s very will, rendering them utterly obedient to authority. This technology would be a tyrant’s wet dream. Imagine soldiers who would shoot their own countrymen without hesitation, or helpless serfs who are satisfied to live in literal dog kennels.BCIs could be used to unscrupulously alter perceptions of basic things such as emotions and values, changing people’s thresholds of satiety, happiness, anger, disgust, and so forth. This is not inconsequential. Someone’s entire regime of behaviors could be altered by a BCI, including such things as suppressing their appetite or desire for virtually anything on Maslow’s Hierarchy of Needs.Anything is possible when you have direct access to someone’s brain and its contents. Someone who is obese could be made to feel disgust at the sight of food. Someone who is involuntarily celibate could have their libido disabled so they don’t even desire sex to begin with.

Someone who is racist could be forced to feel delight over cohabiting with people of other races. Someone who is violent could be forced to be meek and submissive. These things might sound good to you if you are a tyrant, but to normal people, the idea of personal autonomy being overridden to such a degree is appalling.For the wealthy, neural laces would be an unequaled boon, giving them the opportunity to enhance their intelligence with neuroprosthetics (i.e. an “exocortex”), and to deliver irresistible commands directly into the minds of their BCI-augmented servants, even physically or sexually abusive commands that they would normally refuse.If the vaccine is a method to surreptitiously introduce an injectable BCI into millions of people without their knowledge or consent, then what we are witnessing is the rise of a tyrannical regime unlike anything ever seen before on the face of this planet, one that fully intends to strip every man, woman, and child of our free will.Our flaws are what make us human. A utopia arrived at by removing people’s free will is not a utopia at all. It is a monomaniacal nightmare. Furthermore, the people who rule over us are Dark Triad types who cannot be trusted with such power. Imagine being beaten and sexually assaulted by a wealthy and powerful psychopath and being forced to smile and laugh over it because your neural lace gives you no choice but to obey your master.The Elites are forging ahead with this technology without giving people any room to question the social or ethical ramifications, or to establish regulatory frameworks that ensure that our personal agency and autonomy will not be overridden by these devices. They do this because they secretly dream of a future where they can treat you worse than an animal and you cannot even fight back. If this evil plan is allowed to continue, it will spell the end of humanity as we know it.Conclusions:The current pandemic was produced and perpetuated by the establishment, through the use of a virus engineered in a PLA-connected Chinese biowarfare laboratory, with the aid of American taxpayer dollars and French expertise.This research was conducted under the absolutely ridiculous euphemism of “gain-of-function” research, which is supposedly carried out in order to determine which viruses have the highest potential for zoonotic spillover and preemptively vaccinate or guard against them.Gain-of-function/gain-of-threat research, a.k.a. “Dual-Use Research of Concern”, or DURC, is bioweapon research by another, friendlier-sounding name, simply to avoid the taboo of calling it what it actually is. It has always been bioweapon research. The people who are conducting this research fully understand that they are taking wild pathogens that are not infectious in humans and making them more infectious, often taking grants from military think tanks encouraging them to do so.These virologists conducting this type of research are enemies of their fellow man, like pyromaniac firefighters. GOF research has never protected anyone from any pandemic. In fact, it has now started one, meaning its utility for preventing pandemics is actually negative. It should have been banned globally, and the lunatics performing it should have been put in straitjackets long ago.Either through a leak or an intentional release from the Wuhan Institute of Virology, a deadly SARS strain is now endemic across the globe, after the WHO and CDC and public officials first downplayed the risks, and then intentionally incited a panic and lockdowns that jeopardized people’s health and their livelihoods.This was then used by the utterly depraved and psychopathic aristocratic class who rule over us as an excuse to coerce people into accepting an injected poison which may be a depopulation agent, a mind control/pacification agent in the form of injectable “smart dust”, or both in one. They believe they can get away with this by weaponizing the social stigma of vaccine refusal. They are incorrect.Their motives are clear and obvious to anyone who has been paying attention. These

megalomaniacs have raided the pension funds of the free world. Wall Street is insolvent and has had an ongoing liquidity crisis since the end of 2019. The aim now is to exert total, full-spectrum physical, mental, and financial control over humanity before we realize just how badly we’ve been extorted by these maniacs.The pandemic and its response served multiple purposes for the Elite:

Concealing a depression brought on by the usurious plunder of our economies conducted by rentier-capitalists and absentee owners who produce absolutely nothing of any value to society whatsoever. Instead of us having a very predictable Occupy Wall Street Part II, the Elites and their stooges got to stand up on television and paint themselves as wise and all-powerful saviors instead of the marauding cabal of despicable land pirates that they are.

Destroying small businesses and eroding the middle class.

Transferring trillions of dollars of wealth from the American public and into the pockets of billionaires and special interests.

Engaging in insider trading, buying stock in biotech companies and shorting brick-and-mortar businesses and travel companies, with the aim of collapsing face-to-face commerce and tourism and replacing it with e-commerce and servitization.

Creating a casus belli for war with China, encouraging us to attack them, wasting American lives and treasure and driving us to the brink of nuclear armageddon.

Establishing technological and biosecurity frameworks for population control and technocratic- socialist “smart cities” where everyone’s movements are despotically tracked, all in anticipation of widespread automation, joblessness, and food shortages, by using the false guise of a vaccine to compel cooperation.

Any one of these things would constitute a vicious rape of Western society. Taken together, they beggar belief; they are a complete inversion of our most treasured values.What is the purpose of all of this? One can only speculate as to the perpetrators’ motives, however, we have some theories.The Elites are trying to pull up the ladder, erase upward mobility for large segments of the population, cull political opponents and other “undesirables”, and put the remainder of humanity on a tight leash, rationing our access to certain goods and services that they have deemed “high-impact”, such as automobile use, tourism, meat consumption, and so on. Naturally, they will continue to have their own luxuries, as part of a strict caste system akin to feudalism.Why are they doing this? Simple. The Elites are Neo-Malthusians and believe that we are overpopulated and that resource depletion will collapse civilization in a matter of a few short decades. They are not necessarily incorrect in this belief. We are overpopulated, and we are consuming too many resources. However, orchestrating such a gruesome and murderous power grab in response to a looming crisis demonstrates that they have nothing but the utmost contempt for their fellow man.To those who are participating in this disgusting farce without any understanding of what they are doing, we have one word for you. Stop. You are causing irreparable harm to your country and to your fellow citizens.To those who may be reading this warning and have full knowledge and understanding of what they are doing and how it will unjustly harm millions of innocent people, we have a few more words.Damn you to hell. You will not destroy America and the Free World, and you will not have your New World Order. We will make certain of that.