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This is an overview of the different electrolytes in the human body, the pathologies associated with imbalances of them, and how to manage them clinically.
Videos in this module - view all
Cardiology
Ahmed Zaafran MD presents clinical aspects of the chest pain including: How to approach the chief complaint of chest pain? History and physical examination of a patient with the chest pain. Differential diagnosis of the chest pain. EKG considerations. Lab tests, Troponin levels and CK-MB levels. Characteristics of the cardiac and non-cardiac chest pains.
Presenter: Ahmed Zaafran M.D. In this video we discuss following topics about myocardial ischemia: Coronary blood supply vs. cardiac demand for the blood. Pathophysiology and types of myocardial ischemia are discussed. Risk factors. Clinical Symptoms. Stable vs unstable angine.
Presenter: Ahmed Zaafran M.D. In this video we discuss ST elevated myocardial infarction (STEMI) Diagnosis Treatment Key Labs ECG Analysis with corresponding anatomy Percutaneous coronary intervention Thrombolysis
This video presents the introductory concepts to understand heart failure. Following concepts are discussed:
- Chambers of a human heart.
- Structures of a human heart.
- Valves between various chambers.
- Why is our heart divided two pumps?
- What are the two circulatory circuits?
- What is Ejection Fraction?
- How to calculate ejection fraction?
- How to visualize ejection fraction?
- Clinical considerations for heart failure.
- Signs and Symptoms of left heart failure vs right heart failure.
- Major pathologies leading to heart failure.
Following terms are discussed:
- Atria
- Ventricles
- Mitral valve
- Tricuspid valve
- Ejection fraction
- Calculating the ejection fraction
- End systolic volume
- End diastolic volume
- Left heart failure
- Right heart failure
- Systemic circulation
- Pulmonary circulation
- Etiology of the heart failure
- Signs and symptoms of the left heart failure
- Signs and symptoms of the right heart failure
- Right heart failure vs left heart failure
- Primary reasons for the heart failure
- Heart failure as a disease of old age
By Ahmed Zaafran Etiology Classes Symptomology Work-up Labs Diagnosis Treatment
Presented by: Ahmed Zaafran, M.D. Dr. Zaafran presents the definition, management, and treatment of clinical hypertension.
Are you tucked in the bed? Listen to the medical bedtime stories with Dr. Syed. This story presents the first session on the management of hypertension and JNC8. (Disclaimer: every patient's situation needs to be assessed by you and your colleagues and managed as is appropriate. This information is to help you understand the management approaches and by itself does not consist of a prescription for any patient.)
Are you tucked in the bed? Listen to the medical bedtime stories with Dr. Syed. This story presents the second session on the management of hypertension and JNC8. Fables about: Drugs: ACE Inhibitors, ARBs Topics: Renin-Angiotensin System Aldosterone ADH (Disclaimer: every patient's situation needs to be assessed by you and your colleagues and managed as is appropriate. This information is to help you understand the management approaches and by itself does not consist of a prescription for any patient.)
Dr. Syed continues the fable about the management of the hypertension. Topics discussed are: High renin vs. low renin hypertension. Causes of the hypertension including: Cushing disease and cushing syndrome Parathyroid abnormalities Hypothyroidism and hyperthyroidism Cardiac conditions Coarctation of Aorta Vascular conditions Supra-renal conditions including, 11 betahydroxylase deficiency, primary aldosteronism and pheochromocytoma Chronic kidney disease Fibromuscular dysplasia Atherosclerosis and the ostia of the renal arteries
List of anti-hypertensive drugs. Principles of therapy JNC-8 lifestyle guidelines JNC-8 high-level summary JNC-8 algorithm Important notes about various anti-hypertensive drugs Traditional therapeutic approaches. Disclaimer: these are generalized and high-level points to inform the healthcare professionals. These messages do not consist of a prescription for an individual patient. Each patient needs to have a complete assessment with physical examination, labs, other tests, etc. before a therapeutic approach.
Dr. Zaafran presents following topics: DefinitionClassificationDiagnosisTreatment
This is an overview of the different electrolytes in the human body, the pathologies associated with imbalances of them, and how to manage them clinically.
Dr. Zaafran provides overview of the most common medications used to affect the sympathetic nervous system and their clinical applications.
Dr. Tatayana Travkina, MD/Anesthesiologist presents following topics for shock and its management: 1. Normal Cardiac Functions 2. Hypovolemic Shock 3. Distributive Shock 4. Pharmacology of the Shock Management 5. Cardiogenic Shock 6. Obstructive Shock
Dr. Zaafran explores the various types of medications used to treat arrythmia. While basic pharmacology and pathophysiology are discussed, he also goes into clinical signs and symptoms and the standard of care in treatment.
Dr. Zaafran covers the key factors of anti hypertensive medications, their mechanisms, and how they are utilized in the clinical setting. Pharmacological principles are discussed for different types of agents, including:
- Adrenergic agents
- Angiotensin-converting enzyme (ACEI) inhibitors
- Angiotensin II receptor blockers
- Calcium channel blockers
- Diuretics
- Vasodilators
EKG
Why do we measure cardiac electrical activity (ECG)? Conduction medium of the heart ECG measurement from the body surfaces Properties of the ECG voltmeter ECG Paper Normal ECG
A healthy individual's standard wave form ECG waves ECG intervals ECG segments Interpretation of the ECG waveform
This video presents the 12 ECG leads and Einthoven's triangle. Leads presented are: 3 Bipolar Limb Leads 3 Unipolar Augmented Leads 6 Chest Leads Earth lead
Dr. Syed presents the first chapter in the series of the EKG Interpretation lectures. This chapter contains:
1. EKG waves.
2. EKG segments.
3. EKG intervals.
4. Various shapes of the QRS complex and how to articulate them.
5. EKG paper properties.
Session 2 of the EKG interpretation.
Dr. Syed presents:
1. EKG leads setup.
2. Surfaces that the EKG leads look at.
3. Properties of QT interval.
4. QRS progression.
This video presents the isoelectric lead method to determine the cardiac axis. (Digital media video)
This video presents the quadrant method to determine the cardiac axis. (Digital media video)
Dr. Syed discusses the EKG leads and normal waveform. {article:https://articles.drbeen.com/2016/05/22/electrocardiogram-clinical-review/}
Dr. Syed presents:
The terminology used for the cardiac chamber enlargement.
Principles of the EKG changes when chamber enlargement is present.
Right atrial enlargement, EKG changes, diagnostic criteria, and the pathologies.
Left atrial enlargement, EKG changes, diagnostic criteria, and the pathologies.
Right ventricular enlargement, EKG changes, diagnostic criteria, and the pathologies.
Left ventricular enlargement, EKG changes, diagnostic criteria, and the pathologies.
Both ventricular enlargement, EKG changes, diagnostic criteria, and the pathologies.
Lecture 2 Part 1.
Dr. Syed starts the set of talks on arrhythmias as part of the interpretation of the EKG series. Following topics are covered:
*How to detect arrhythmias?
*Types of arrhythmias.
*Sinus arrhythmias (first type) are presented as well.
Errata: Note the QRS complex duration is from 80ms to 120ms and not 1.2ms as I have incorrectly written.
Lecture 2 part 2
Dr. Syed continues the discussion of arrhythmias. In this talk he discusses:
Ectopic Rhythms
Identifying Atrial Ectopic Rhythms on the EKG
Identifying Junctional Ectopic Rhythms on the EKG
Identifying Ventricular Ectopic Rhythms on the EKG
Dr. Syed presents the first session in the series of supraventricular extrasystole. Topics covered are: Atrial Premature Beat/Premature Atrial Contraction (PAC) Junctional Premature Beat Difference between the Junctional Premature Beat and the Junctional Escape Beat Blocked Atrial Premature Beat
Dr. Syed presents following topics about Atrial Flutter
1. Definition and difference from atrial tachycardia.
2. Types of Atrial Flutter (Typical and atypical.)
3. EKG changes.
4. Interpreting atrial flutter on an EKG.
5. Pathogenesis.
6. Clinical presentation.
7. Management:
a) Pharmacological
b) Cardioversion
c) Pacing
d) Radiofrequency ablation
Let us continue with the EKG interpretation series.
This lecture discusses the premature ventricular contractions (PVCs.) PVCs can be benign or malignant.
History and lifestyle are essential considerations while working up PVCs. The patient usually contacts their provider because of the palpitations. They also may have issues sleeping correctly or sleeping on one side of their body etc.
In this lecture, we will go over the signs, symptoms, pathophysiology, EKG changes, diagnostic criteria, and clinical and surgical management of the PVCs.
In this lecture we will discuss Ventricular Tachycardia, also known as V-Tach.
V-Tach is defined as rapid and repetitive firing of 3 or more PVCs in a row, with a rate of 100-250 beats per minute, originating in the ventricles of the heart.
Pathophysiology
This video presents following topics about Atherosclerosis: Definition Epidemiology Risk factors Clinical aspects.
This video presents following topics about Atherosclerosis: Cellular and chemical mechaisms of the atherosclerotic plaque development. Mechanism of damage that starts/accelerates atherosclerosis Initiation of the atherosclerosis Progression of the atherosclerosis Complications of the atherosclerosis
This video presents following topics about Atherosclerosis: Pathological progression and clinical outcomes. Including a discussion of the clinical horizon.
Dr. Syed continues the discussion of the atherosclerosis pathogenesis.
Continuing the discussion of cellular events involved in atherosclerosis.
Mechaisms of the atherosclerotic plaque development. Initiation, progression, and complications of the atherosclerosis.
This video presents following topics about the right heart failure: Definition Causes Morphology Clinical points Compensatory mechanisms
This video presents following topics about the left heart failure: Statastics of this leading cause of death. Definition Why is it called congestive heart failure? Pathogenesis: reduced compliance reduced contractility. Findings Clinical signs and symptoms
This video presents the physiological arrythmias namely: Sinus tachycardia Sinus bradycardia Sinsu arrythmia associated with respiration We will discuss the reflexes that result in the cardiac rhytm change
This video discusses AV nodal blocks with following topics: First and second degree heart blocks Mobitz type I and type II heart blocks. Hay block.
This video discusses: Third degree heart block Stoke adam syndrome Pathogenesis and ECG for these pathologies.
This video discusses following: Difference between fibrillatoin and flutter. Causes of fibrillation and flutter Mechanism of the circus movements. Causes of the circus movements. Causes of the torsades de pointes
This video presents the premature beats or extrasystoles generated due to pathologies in the atria. We will also review the ECG changes associated with atrial premature beats.
This video presents the premature beats or extrasystoles generated due to pathologies in the AV nodes. These extrasystoles are also called junctional extrasystoles. We will also explain the junctional rhytm vs junctional beat. We will also review the ECG changes associated with junctional premature beats.
This video presents the premature beats or extrasystoles generated due to pathologies in the ventricular tissue. We will also review the ECG changes and explain the pathogenesis of the: Tall and wide QRS complexes. Inverted T waves Torsades De Pointes Long QT Syndrome
This video discusses following: Primary diseases of the heart muscle. Diseases discussed are: Dilated cariac myopathies Hypertrophic cardiac myopathies Restrictive cardiac myopathies
This video presents: Ischemic heart disease (causes about half of the yearly deaths in western world.) Epidemiology Clinical progress Pathophysiology of the ischemic heart disease Types of angina and their properties
This video discusses following topics: Definition of MI Types of MI Clinical presentation and variations Pathophysiology
This video discusses following topics: Cellular and morphological events during the MI Diagnosis of an MI by the cardiac enzymes and EKG changes Management approach Complications including dressler's syndrome
This video presents the physiology of the cardiac cycle.
We will discuss:
- Definition
- Duration
- Electrical activity of the heart during a cardiac cycle
- Mechanical changes
- Pressure changes in the atria ventricles and aorta
- Volume changes in heart chambers
- Heart sounds
- Venous pulse graph
This video presents the measurement of the cardiac output using Fick's method. We will also touch upon the doppler and thermodilution.
This video presents normal and abnormal heart sounds. Heart sound posts for auscultation Mechanism of the sound generation Abnormalities that can generate additional heart sounds or change the sounds
This video presents the mechanics of the murmur generation and the types of murmurs. Pathologies that give rise to murmurs are handled in the Pathology module.
This video presents: Pathology phase shape type munuver location and radiation of various murmurs. Murmurs covered are: Aortic Stenosis Aortic Regurge Mitral/Tricuspid Regurge Mitral Stenosis Mitral Prolapse Ventral Septal Defect Patent Ductus Arteriosis
This video presents following topics:
Re-entry
Types of Supraventricular Tachycardia.
Mnemonic to remember supraventricular tachycardia.
Characteristics of Supraventricular Tachycardia.
AV Nodal Reentrant Tachycardia.
EKG changes
Pseudo R waves
This video looks how we can identify systolic an diastolic left heart failure through mathematical representation.
This video presents following topics about the left heart failure: Statistics of this leading cause of death. Definition of backward vs forward and systolic vs diastolic failures
Here is an overview of multiple myeloma.
We will discuss the following:
1. Type of immune cells.
2. Type of cells involved in multiple myeloma.
3. High level pathology of multiple myeloma.
4. Immune system dysregulation due to multiple myeloma.
5. Why are there so many monoclonal antibodies in multiple myeloma?
References:
Robin's pathology (9th Edition) Page 437.
Current Medical Diagnosis and Treatment 2016. Location 21702 (Kindle Edition.)
https://www.yahoo.com/news/colin-powells-death-doesnt-challenge-efficacy-of-coronavirus-vaccines-173102331.html
https://en.wikipedia.org/wiki/Multiple_myeloma#Pathophysiology
Disclaimer:
This video is not intended to provide assessment, diagnosis, treatment, or medical advice; it also does not constitute provision of healthcare services. The content provided in this video is for informational and educational purposes only.
Please consult with a physician or healthcare professional regarding any medical or mental health related diagnosis or treatment. No information in this video should ever be considered as a substitute for advice from a healthcare professional.
Diabetes
This video presents the following about diabetes mellitus:
Definition of Diabetes Mellitus. Molecular structure of Insulin Clinical importance of the C-Peptides.
Classification of diabetes mellitus. Defects of Insulin secretion. Defects of Insulin actions.
Classes presented are:
- Type 1 diabetes mellitus.
- Type 2 diabetes mellitus.
- Maturity onset diabetes mellitus.
- Genetic causes resulting in molecular polymorphism.
- Exocrine pancreatitis.
- Infections.
- Endocrine pathologies.
- Drugs.
- Gestational diabetes mellitus.
Dr. Syed presents pathological events leading up to the type 1 diabetes mellitus (T1DM). Topics covered are:
+T1DM is an autoimmune disease.
+Role of genetic mutations and allele inheritance for DQ, DR3 and DR4 in the HLA region on chromosome 6p21.
+Role of polymorphism in insulin, CTLA4, and other molecules.
+Role of incorrect T cell training in Thymus.
+Role of cytotoxic T cells in beta cell damage. Leading to insulitis.
+Role of humoral/antibody response causing beta cell damage. Leading to insulitis.
+Incorrect formation of MHC molecules increasing affinity for the self-antigens.
+Other autoimmune diseases that may be present with T1DM.
This video discusses the following:
Classes of type 1 diabetes mellitus based on the signs and symptoms.
Early onset type 1 diabetes mellitus.
Diabetic ketoacidosis.
Silent type 1 diabetes mellitus.
Explanation of:
Polyuria/Glycosuria
Polydipsia
Catabolic state/weight loss/polyphagia
Lens blurring and visual problems
Reasons for the recurrent candidial infections.
Diabetic Ketoacidosis (DKA) is the second most common presentation of type 1 diabetes mellitus. (First most common being early onset diabetes Mellitus.)
In this first part of the lecture we discuss:
The reason for the higher propensity of type 1 diabetes mellitus patients to develop DKA.
Polyuria/Glycosuria/Polydipsia
Hypovolemia/Hypotension
Tachycardia/Skin Turgor
Kussmaul Breathing
Fruity Odor
The role of Insulin, Glucagon, Epinephrine, and Hormone Sensitive Lipase is discussed.
Potassium level disturbance in patients presenting with DKA.
Mechanism of acidosis in DKA.
Diabetic Ketoacidosis (DKA) is the second most common presentation of type 1 diabetes mellitus. (First most common being early onset diabetes mellitus.)
In this second part of the lecture we discuss:
Mechanism of the gastrointestinal (GIT) symptoms.
Bicarb levels in DKA.
A quick comparison of the metabolic disturbances in DKA and HHS.
The impact of acidosis and membrane potential predisposing cell to arrhythmias.
Metabolic picture of DKA.
Working up the labs' data for DKA patient.
Calculating osmolality.
Calculating expected PaCO2 levels using Winter's equation.
This lecture presents the management approach for the patients presenting with diabetic Ketoacidosis.
Following management methods and the principles behind the management are explained:
Volume replenishment, volume types, the reason for choosing various types, benefits of the volume replenishment, and the complications of aggressive volume replenishment.
Insulin administration. Caution for insulin administration when potassium levels are low. The amount of insulin to administer and the rate of fall of glucose levels.
Why do insulin and glucose need to continue even after a good glucose level has been established?
What to expect in terms of potassium levels? How to manage potassium? How to correlated potassium levels to insulin and volume?
What labs and signs and symptoms to monitor and how to adjust when ref-flags show up?
How to approach bicarb deficiency?
This short video identifies the patients that must receive insulin.
All type 1 diabetes mellitus patients.
Type 2 diabetes mellitus patients that fit the criteria shared in the video.
Notes
For the type 2 diabetes mellitus patients, here is the criteria.
a) If the first line therapy fails, then consider the second line of oral drugs. However, in case HbA1c is greater than 8.5% then consider insulin instead of another oral agent.
b) type 2 diabetes mellitus patients that fit the following criteria:
- HbA1c levels equal or greater than 9.5%.
- Fasting blood glucose levels equal or greater than 250 mg/dL.
- Random blood glucose levels greater than 300 mg/dL.
- Ketosis.
- Unexplained weight loss associated with hyperglycemia.
- A hyperglycemic patient whose status (type 1 diabetes mellitus vs. type 2 diabetes mellitus) is not known.
Further considerations:
- first line therapy is metformin.
- Assure the patient that it is not a personal failure to start on insulin. Instead, it is important to manage hyperglycemia reliably.
In this part of the insulin therapy webinar, Dr. Mobeen presents:
- Insulin types
- Differences among various types of insulin.
- Mnemonic to remember insulin types.
- Objectives of the insulin therapy.
- Considerations for the dose adjustment.
- Insulin dose adjustment considerations for various physiological or pathological conditions. For example:
- Pregnancy
- Exercise
- Obeseity
- Various eating habits.
- Hospitialized patient.
- Patients with infections.
- Elderly.
- Patients with chronic kidney disease.
- Patients with liver disease.
- The dawn phenomenon.
- The somogyi effect.
- Dose calculation:
- Total daily insulin (TDI)
- Calculating basal insulin dose/units.
- Calculating bolus insulin dose/units.
- Insulin therapy types:
- Intensive insulin therapy.
- Conventional insulin therapy.
- Sliding scale insulin therapy.
- Insulin injection sites and their properties:
- Abdomen
- Thighs and buttocks
- Arms
- Insulin syringes.
- Insulin mixing.
- Insulin filling in the syringe.
In this session Dr. Mobeen presesents following topics:
*Sources of glucose and contribution from carbs, fats, and proteins.
*Is it useful to go to protein high or fat high diets? Or is it useful to cut carbs?
*What is the effect of combining carbs with proteins and carbs with fats to the glucose peak that occurs after a meal? Does it matter from a therapeutic point of view?
*What is the final common pathway of energy production from the three macro classes of the food - namely, proteins, fats, and carbs.
In this talk Dr. Mobeen discusses:
1. Why do fats contribute to the insulin insensitivity?
2. Why does eating carb cause hunger again?
Dr. Mobeen presents:
*The role of FAT cells in modifying FFA levels, Liponectin levels, and Resistin levels.
*Insulin resistance due to the substances mentioned above.
*Burnout of the beta cells after the consistent elevation of glucose due to insulin resistance.
In this session Dr. Mobeen discusses how chronically elevated blood glucose levels cause tissue damage.
Following pathological mechanisms are discussed:
- Non-enzymatic glycosylation or glycation.
- Advanced glycation end products (AGE) are discussed.
- Extracellular matrix thickening and fibrosis is discussed.
- Tunica intima damage and the acceleration of atheroma formations is discussed.
- Micro and macro vascular damage.
- Neuropathies due to microvascular pathologies.
- Activation of the inflammatory processes due to glycation is reviewed.
- Renal tissue damage is discussed.
- Formation of the HbA1c is discussed.
- Albumin glycation is discussed.
- Activation of the protein kinase C (PKC) and tissue damage due to the raised levels of the PKC.
- Diacylglyceroal (DAG) pathway is presented.
- Elevated glucose levels leading to increased formation of the DAG.
- Angiogenesis/Neovascularization due to the eleveated DAG. This leads to retinal pathologies.
- Tumor growth factor beta (TGF-beta) levels increased leading to increased formation of the extracellular matrix. This in turn leads to the thickening of the skin and other tissues.
- Polyol pathway acceleration and osmotic damage due to sorbitol accumulation in various tissues.
- Sorbitol accumulation.
- Increased working of the polyol pathway allows reactive oxygen species to accumulate and cause damage.
- Myeline sheath pathologies due to the osmotic damage.
Dr. Mobeen presents the clinical presentation of the type II diabetes mellitus. Following presentations and their reasons are discussed:
- Polyuria (increased volume of urine and and increased frequency of urination)
- Reduced blood volume due to polyuria leading to:
- Polydypsia (increased water drinking due to increased thirst)
- Postural hypotension (not always)
- Low blood pressure
- Retinopathies
- Lens blurring and cataract
- Centripital fat distribution. Increased fat on trunk and almost none on the limbs
- Difficulty developing and maintaining erection
- Autonomic system damage leading to:
- Heart rate abnormalities
- Abnormal sweating
- Bladder control issues
- Incontinence
- Feeling of incomplete urine voiding
- No urge to urinate. Pressing bladder causes urination
- Bowel control issues.
- Diahrrhea
- Constipation
- Neuropathies.
- Tingling in the foot
- Paraesthesias in the distal lower limb
- Foot drop.
- Pregnancy issues:
- Multiple abortions
- Hydatiform mole
- Preeclempsia
- Previous deliveries of large babies
- Acanthosis nigricans
- Eruptive xanthomas
- Blanoposthesis
Dr. Mobeen presents diagnostic criteria for diabetes mellitus. Fasting, random, and post prandial blood glucose levels for normal, pre-diabetes, and diabetes are presented. Glucose tolerance test is presented. Hemoglobin A1 C levels are discussed.
Following topics are discussed:
- Elevated irine glucose levels. Why these are less reliable for the diagnosis of diabetes mellitus?
- SGLT2 gene abnormalities leading to increased urine glucose without diabetes mellitus.
- Fanconi syndrome leading to increase urine glucose without diabetes mellitus.
- Increased glomerular filtration rate (GFR) during pregnancy leading to glucose in urine without diabetes mellitus.
- Urine and blood ketone levels.
- Serum glucose levels vs., blood glucose levels.
- Capillary blood glucose measurement method.
- Devices to measure blood glucose levels including:
- External sensors.
- Artificial pancrease.
- Others.
Dr. Mobeen presents the approach to managing a type II diabetic patient. Following classes of drugs are presented:
- Drugs that increase the levels of inuslin (insulin secretogogues).
- Drugs that work on the beta cells.
- Sulfonylureases.
- Potassium channel blockade causing deploraization of a beta cell leading to the secretion of insulin.
- Incretins.
- GLP1
- GIP
- Exanatide
- Drugs that increase peripheral sensitivity to insulin.
- Metformin
- First line drug for managing type II diabetes mellitus.
- Mechanism of action of metformin.
- Actions of metformin on hepatocyte:
- AMPK levels increased leading to the reduced cAMP levels. This reduces PKA levels. This leads to increased glycolysis and reduced gluconeogenesis.
- FFA are reduced leading to increased insulin sensitivity.
- Improves function of the insulin receptors.
- Improves glucose transport inside the cell.
- TZDs
- Work on the lipid cells.
- Open the genes in lipid and muscle cells leading to increased sensitivity to insulin.
- LPL receptors are increased in density. Imprving triglyceride levels. Cholestrol levels are not improved.
- Number of lipid cells increase. Lipogenesis increases. (Not a good effect. However, lipid storage will increase reducing glucose levels temporarily.)
- Metformin
- Drugs that increase ejection of the glucose from the gut. That is, reduce its absorption from the gut.
- Alpha glucosidase enzyme's role.
- Function of Acarbose.
- Acarbose binding to alpha glucosidase. Preventing glucose polymer breakdown.
- Diahrrhea, gas, discomfort, abdominal pain dur to increased glucose levels in the large intestine.
- Drugs that eject glucose in urine.
- Sodium glucose co transporter type 2 (SGLT2) inhibitors.
- Increased risk of UTIs especially in women.
- Polyuria. Low blood volume leading to thirst and postural hypotension.
- Role of diet to reduce intake of glucose.
- Role of exercise to increase glucose uptake in the peripheral tissues.
Dr. Mobeen presents a clinician's approach to manage a type II diabetic patient. Following topics are discussed:
- Lifestyle management:
- Couseling
- Diet
- Exercise (150 mins per week.)
- American diabetic academy (ADA) 2016 guidelines.
- Metformin as the first line drug.
- Discussion of mono, dual, tripple, and combination therapy with insulin.
- Why combine metrormin with meals?
- Metformin's half life.
- Metformin's dose.
- Metformin's function:
- Hepatocyte effects.
- Reduced gluconeogenesis.
- Reduced lipogenesis.
- Block lactic acid uptake.
- A visual mnemonic to remember metformin and glitazones.
- Considerations for patients that may have heart failure, renal failure, or perform rigorous exercises while taking metformin.
- Why metformin is not indicated in type I diabetes mellitus?
- B12 absorption reduction due to Ca++ channel blockade by metformin.
Dr. Syed discusses properties, mechanism of action, metabolism, clinical use, dosage, side effects, and contraindications for biguanides/Sulfonylureases.
Dr. Syed presents glucose absorption inhibitors. Drugs discussed are: Acarbose Miglitol Type II Diabetes Mellitus management algorithm is also reviewed.
Dyslipidemias
First fable in the series of dyslipidemias bedtime stories. Dr. Syed presents: Difference between the detergent and emulsification action of various enzymes. Review of lipid structures. Classification of lipids. What we mean by the lipid saturation? Formation of a chylomicron. Difference between a chylomicron and micelle.
Dr. Syed presents the second bedtime story. Topics covered are: Lipid particles. The structure of various lipid particles. How statins and other cholesterol-lowering drugs work. Micelle vs. Lipid Particle. Should a patient fast for lipid profile?
Dr. Syed presents the story of an intense coal with a lip gem that lounges around in an EZ chair and hates it when you try to view him! This fable covers the site and mechanism of action of dyslipidemia drugs. Drugs covered are: Statins Niacin Colestipol Ezetimibe gemfibrozil (fibrates)
Dr. Syed presents: Understanding the positive and negative risk factors for the CAD. Mnemonic for the desired LDL levels. Lipid panel review. When to treat LDL-C in routine cases. Treatment approach. Drugs Step 1 and Step 2 diets. Lipid Fractionation
Dr. Syed presents Patient groups in light of the ACC/AHA guidelines. Statin prescription intensities. Prescription approach for various groups. Criticism of the ACC/AHA guidelines. Mobeen's summary of managing a patient with dyslipidemias. Disclaimer: these lectures are to inform healthcare workers and patients for the possible management approaches. Each patient needs to be individually assessed, tested, diagnosed and treated in light of their unique presentation. These lectures do not have a prescription for any specific patient.
Clinical ENT
Dr. Zaafran explores the most common ENT conditions and introduces the pathology, history and physical examinations, and treatments necessary for primary care. He also incorporates the times advanced specialists need to be consulted. This lecture series is comprised of 3 parts and is meant to serve as a primer for subsequent lectures that delve deeper into each pathological condition.
Dr. Zaafran continues to explore the most common ENT conditions and introduces the pathology, history and physical examinations, and treatments necessary for primary care. He also incorporates the times advanced specialists need to be consulted. This lecture series is comprised of 3 parts and is meant to serve as a primer for subsequent lectures that delve deeper into each pathological condition. This is the second part.
Dr. Zaafran continues to explore the most common ENT conditions and introduces the pathology, history and physical examinations, and treatments necessary for primary care. He also incorporates the times advanced specialists need to be consulted. This lecture series is comprised of 3 parts and is meant to serve as a primer for subsequent lectures that delve deeper into each pathological condition. This is the third and final part.
Gastroenterology
Dr. Islam presents following topics about oropharyngeal dysphagia. Symptoms History D/D from esophageal dysphagia.
Dr. Sameer will discuss the following in gastrointestinal bleeding.
- Upper gastrointestinal bleeding (UGIB)
- Definition
- Lesions proximal to ligament of treitz
- Hematemesis
- Hematochezia
- Melena
- Peptic Ulcer Disease
- Esophagitis
- Gastritis
- Initial Management
- Management of Varices
- Resuscitation
- Endoscopic Management
- Definition
- Lower gastrointestinal bleeding (LGIB)
- Definition
- History and physical examination
- Diagnosis
- Diverticular Bleeding
- Colon Cancer
- Inflammatory Bowel Disease
- Infectious Diarrhea
- Treatment
Dr. Islam discusses following topics about gastroesophageal reflux and heartburn. Introduction Definition Risk Factors Diagnosis Treatment
Dr. Sameer Islam MD presents following topics: Definition of gastritis and gastropathy. Types of gastritis. Pathophysiology.
Dr. Islam presents: Peptic ulcer disease and NSAIDs. Peptic ulcer disease and the role of H. Pylori. Complications including ulcers and cancer (lymphoma).
Dr. Islam presents What is peptic ulcer disease? What causes peptic ulcer disease? What is the role of proton pump Inhibitors? What are the complications of PPIs?
Epidemiology
95% of the gallbladder diseases are cholelithiasis (gallstones.)
About 2% of the US health budget goes towards the management of cholelithiasis and its complications.
10%-20% of the population in the western hemisphere has gallstones.
25-50 tons of the gallstones are carried by more than 20 million Americans.
In the US about 1 million new cases are diagnosed annually, out of these, 2/3 will undergo surgery for the gallstones.
Gallstones are of two main types. 80% are cholesterol stones. Consisting of crystalline cholesterol monohydrate. The remainder are mainly bilirubin calcium salts and are called pigment stones.
High-Level Pathophysiology
The basic reason for the formation of the cholesterol stones is the following:
They only path for the cholesterol removal from the body is via the bile system. Cholesterol is not water soluble. We need to make it water soluble to traverse this path. To solve this, our body forms bile salts and lecithins. These bind with cholesterol and allow the passage through the bile system. These salts and lecithins are like boats on the water to which cholesterol is bound. If the quantity of the cholesterol is more than the binding capacity of these salts, then the unbound cholesterol forms cholesterol monohydrate crystals. These crystals precipitate in solid form. These precipitations irritate the gallbladder layers that in turn release mucus which traps these solid structures in the gallbladder resulting in the stone formation.
In summary, the following four events occur simultaneously for the formation of a gallstone:
1. Amount of cholesterol more than the binding capacity of the bile salts (supersaturation.)
2. Formation of the cholesterol monohydrate crystals.
3. Precipitation and aggregation of these crystals forming solid stone particles.
4. Mucus secretion by the gallbladder's inner surface resulting in the entrapment of these solid particles in the gallbladder.
Pigment Stones
These stones are predominantly composed of bilirubin calcium salts. Their formation is a complex phenomenon. However, it is clear that the presence of unconjugated bilirubin in the bile tree predisposes to the formation of the pigment stones. An example is hemolytic anemia, where the premature RBC breakdown overwhelms the hepatocyte's bilirubin conjugation capacity and the unconjugated bilirubin appears in blood plasma and bile. Infections of the biliary tree can also result in unconjugated bilirubin in the bile.
Also, note that the prevalence of the gallstones is age and gender-related.
Age
Population < 40 has 5% to 6% prevalence of the gallstones.
Population > 80 y has 25% to 30% prevalence of the gallstones.
Gender
Prevalence in white women is twice as high as in men.
Ethnic and geographic
The native American population has a 75% prevalence of cholesterol gallstones. Pigment stones are rare in this group.
Gallstones are more prevalent in western industrialized societies compared to the developing countries.
Robins 8th Edition Page 667
https://www.aafp.org/afp/2004/0115/p299.html
http://eclinpath.com/hematology/anemia/mechanisms-of-anemia/extravascular-hemolysis-new/
Cholelithiasis (Gallstones). Clinical Features.
Frequently cholelithiasis is asymptomatic. It is usually discovered during a radiographic study or during a surgery, or an autopsy.
Clinical features of gallstones occur due to the obstruction and inflammation of the gallbladder by a large stone, or the small stones that move down in the biliary tree and get stuck in it, or due to the irritation and inflammation of the biliary tree.
Pain is usually excruciating (severe). It may be constant or colicky. The pain of acute cholecystitis is in the upper right quadrant can be associated with fever, nausea, and a positive Murphy's sign. Biliary or episodic gallbladder pain occurs in 10-25% of the patients. Acute cholecystitis occurs in 20% of these symptomatic patients.
Occasionally gallstone ileus or Bouveret or Mirizzi syndrome occurs as a clinical complication of a gallstone. Bouveret syndrome occurs when the stone obstructs pylorus or duodenum.
Murphy's sign is positive when you palpate the upper right quadrant during inspiration, and the patient's breathing is interrupted or stopped due to the pain.
You can also perform an indirect fist percussion to compare any difference in pain in the right upper quadrant and the left upper quadrant.
Robbins 8th Edition: Page 668
Current Medical Diagnosis and Treatment 2016 - Cholelithiasis chapter.
https://www.youtube.com/watch?v=9L7N89sOSuc
Continuing with our discussion of cholecystitis and cholelithiasis, in this lecture, we will discuss the risk factors for the cholelithiasis and acute cholecystitis, and the management of the cholecystitis.
​
Keep the following questions in mind while studying the notes or the video:
- What drugs can help against gallstone diseases?
- What drugs increase the risk of gallstone diseases?
- How to assess a patient's risk of cholelithiasis?
- What advice to offer about dietary and lifestyle habits to a person at risk of gallbladder diseases?
- Important risk factors for gallbladder diseases, including gallstones/cholelithiasis and eventual cholecystectomy.
​We will discuss
- The risk factors for cholecystitis and cholelithiasis.
- The usual causes for the flare-ups
- The management approaches including:
- NSAIDs
- Cholecystectomy
- Laproscopic
- Open
- Ursodeoxycholic Acid
- Management consideration in the pregnant women.
Dr. Sameer Islam, MD., Gastroenterologist presents: General introduction to the Liver Function Tests Categories of Liver abnormalities. • Acute hepatitis • Chronic hepatitis • Cholestatic hepatitis • Hyperbillirubinemia • PT/INR and albumin Liver biopsy and non-invasive testing
Dr. Sameer Islam provides an overview of Liver Function Tests, the multiple causes of abnormailites in LFT's, and their applicability as a tool for multiple pathology settings, and their clinical value in medical management.
Dr. Syed presents liver function tests data and their interpretation for hepatitis B. Hepatitis B virus labs are discussed. The window period is discussed. Hepatitis B Virus. Immune response. ALT and AST enzyme. Differentiating between the labs of a chronic alcoholic vs viral hepatitis. {article:https://articles.drbeen.com/2016/05/25/hepatitis-b-and-its-labs/}
Sameer Islam MD discusses the Ulcerative colitis and Crohn's disease. He presents epidemiology, symptoms, diagnosis, treatment and extraintestinal manifestations.
In this talk Dr. Hameed presents: Natural history of cirrhosis and varices. Primary and secondary prophylaxis. Managing bleeds
Dr. Sameer Islam presents the following topics about obesity Background Surgical Treatment Endoscopic Treatment
Psychiatry
In this lecture, Dr. Zaafran discusses depression, psychosis, mania, cyclothymia,dysthymia, severe depression, mild depression, going into depth on how they are diagnosed and what managment of these mood disorders entail.
Dr. Zaafran presents substance abuse, especially alcoholism. He discusses biological, psychological, and social models leading to the positive rewards. Role of impulsive personality and alcohol abuse. Physiological aspects leading to habit forming behaviors and alcoholism. Family history. Children of alcoholics (COA.) Genetic evidence of alcoholism tendency. Gender susceptibility. Type 1 Alcoholism. Psychological characteristics of alcoholism. Social factors. And, finally the media and its role in alcoholism.
In this lecture, we will talk about the presentation to a range of personality disorders.
A person with a personality disorder will
think differently,
Feel differently
behave differently
or relates to others very differently from the average person.
The DSM-V states there are several different types of personality disorder, split into 3 clusters:
Cluster A: Peculiar thought processes, inappropriate affect – remember them as WEIRD
Cluster B: Mood lability, dissociative symptoms, preoccupation with rejection remember them as WILD
Cluster C: Anxiety, preoccupation with criticism or rigidity remember them as WORRIED
Causes
It's not clear exactly what causes personality disorders, but they're thought to result from a combination of the genes a person inherits and early environmental influences – for example, a distressing childhood experience (such as abuse or neglect).
Prevalence:
All are relatively common.
More males have antisocial and narcissistic PDs
More females have borderline and histrionic PDs.
Onset:
Usually not diagnosed until late adolescence or early adulthood
Course.
Usually very chronic over decades without treatment.
Symptoms of paranoid, schizoid, and narcissistic PD often worsen with age;
symptoms of antisocial and borderline PD often ameliorate.
Key Symptoms.
A long pattern of difficult interpersonal relationships, problems adapting to stress, failure to achieve goals, chronic unhappiness, low self-esteem
Personality disorders are usually associated with mood disorders.
Treatment:
Psychotherapy is the mainstay of treatment. Intensive and long-term psychodynamic and cognitive therapy are treatments of choice for most PDs.
Use of mood stabilizers and antidepressants is sometimes useful for Cluster B PDs.
Differential Diagnosis:
Major rule-outs are mood disorders, personality change due to a general medical condition, and adjustment disorders.
Urology
Dr. Amr Madkour presents atypical cases of the urinary tract infections, diagnosis, treatment approach, and cases.
Pulmonology
Chest X-Ray is a routine clinical investigation. It is important for healthcare professionals to be comfortable approaching and interpreting it. In this webinar, Dr. Alikhan shares his excellent method to identify key elements that are frequently encountered on the chest x-ray.
Dr. Ahmed Zaafran presents Clinical Hypoxemia and its causes Differential diagnosis Management approach
Dr. Zaafran presents asthma, signs, symptoms, and treatment.
Mir Alikhan MD, Pulmonologist discusses upper respiratory tract infections.
Dr. Alikhan discusses the diagnosis and management of: 1. Bronchitis 2. Pneumonia
Mir Alikhan, MD presents pulmonary function tests. Topics discussed are: Spirogram - volumes and capacities. Flow-volume loops Components of PFTs Pattern recognition Accessory PFTs
This is a comprehensive insight into the conditions that affect and interact with the pulmonary vasculature. The lecture will focus on the areas of pulmonary edema, pulmonary embolism, and pulmonary hypertension.
Cholinergic type medications are a mainstay in clinical practice today. Dr. Zaafran goes over the
-
Basic physiology
-
Pharmacology
-
Usage of these medications in clinical practice.
Dr. Zaafran goes into clinical depth regarding respiratory drugs and their application in practice.
Topics include:
- Usage of bronchodilators
- Leukotriene inhibitors
- Mast cell stabilizers
- Alpha and beta agonists
- Cortoicosteroids
- Anti-cholinergic agents
Dr. Zaafran goes into clinical depth regarding respiratory drugs and their application in practice.
Topics include:
Usage of bronchodilators
Leukotriene inhibitors
Mast cell stabilizers
Alpha and beta agonists
Corticosteroids
Anti-cholinergic agents.
All healthcare professionals must master the understanding and management of asthma. This lectures series helps us master asthma, its pathophysiology, diagnosis, and management. In this lecture Dr. Mobeen presents:
Asthma definition.
Asthma and COPD.
Asthma's pathophysiological triad.
Types of asthma including:
- Phasic (Immediate and late).
- Clinical types: Intermittent and status asthmaticus.
- Aetiology: atopic, non-atopic.
- Hygine theory.
Immune system abnormality to give rise to atopy.
Immune system behaviour for cytotoxic and humoral responses.
Airway structures that are affected by asthma:
- Respiratory epithelial cells.
- Mucoa and its glands.
- Smooth muscles of the airways.
- Submcosa, its glands, and nerves.
- Fibroblasts.
- T cells.
- B cells.
Why are eosinophils the dominant players in asthma pathology?
Cytokines and chemokines active in asthma development.
- IL2, IL3, IL4, IL5, IL13
A normal Acid-Base status is essential for the proper functioning of all physiologic processes, and our bodies work hard to maintain pH homeostasis. This lecture gives a basic review of acids, bases, pH, and how our bodies compensate for acid-base disorders
Acid-Base disorders are complicated, but some clinical presentation are common. This lecture discusses three common clinical presentations of Acid-Base disorders and evaluates the arterial blood gases for appropriate compensation.
Dr. Mobeen discusses the following classifications of Asthma.
National Asthma Education and Prevention Program (NAEPP), Veteran’s Administration/Department of Defense (DoD). This classification is based on the severity assessment and guides the management approach.
2016 Global Initiative for Asthma (GINA). This classification is retrospective and establishes a category based on the management regime that worked for the patient
In this lecture Dr. Mobeen discusses the severeity assessment of asthma, management approach according to the severeity, and drugs with their dose adjustment in a 6 step approach.
Initial visit workup:
- Diagnosis (separate lecture)
- Severity assessment
- Medication.
- Inhaled Corticosteroids (ICS)
- Short acting beta agonists (SABA)
- Long acting beta agonists (LABA)
- Leukotrine Receptor Antagonists (LTRA)
- Cromolyn
- Theophyline
- Oral Corticosteroids
- Plan of treatment.
- Follow up
Follow up visit:
- Assess control
- Review medication compliance
- Review side-effects
- Decide medication modification if needed.
- Update the plan if necessary.
- Plan follow up.
In this part of the clinical approach to asthma we will discuss the background to asthma. That includes:
- Background
- Asthma vs COPD
- Reversibility in asthma
- Difficulty to manage when asthma is chronic
- Varying airflow obstruction
- Need to prevent remodeling of the lung tissue while managing asthma.
- Higher prevalence of asthma in affluent countries.
- Peak age for asthma (3 years of age)
- Gender in childhood is predominantly boys, however, the gender difference goes away in adults.
- Asthma by itself is not a fatal disease, however, asthma related deaths can occur due to the underlying inflammation and tissue damage.
- The basic principle of the management is to control the inflammation - not just the symptoms.
- Why did the mere use of beta agonists actually increased deaths in the asthma patients? (happened in 1960)
- Atopy (Antigen vs. allergen)
- Infections
- Diet
- Air Pollution
- Occupational exposure
- Why does laughing and coughing trigger asthma?
- Role of the mast cells in triggering asthma.
- Nerve irritation leading to the asthma.
- Beta blockers (can be fatal.)
- Exercise. Why does exercise trigger asthma?
- Cold air, hyperventilation
- Food
- Air pollution
- Occupational factors
- Hormones (some women before periods can have attacks of asthma.)
- Gastroeosphageal reflux
- Stress. Why will stress cause asthma?
- Airway inflammation
- Airway hyper-responsiveness
- Epithelial shedding due to irritation and inflammation.
- Loss of epithelium derived nitric oxide.
- Protection mechanism disappears leading to nerve exposure and nerve irritation.
- Thickening of the basement membrane leading to irreversibility/difficulty in management.
- Beta receptor decoupling
- Hyperplasia and hypertrophy of the airway smooth muscles
- Increased blood vessels.
- More blood flow.
- Edema
- Inflammation
- Swelling
- Increased mucus secretion
- Result of chronic irritation and inflammation
- Pulmonary function tests and the changes
- Inhaled SABA based testing to confirm asthma.
- Blood IgE tests
- Imaging
- Skin tests
- Exhaled nitric oxide (NO)
- Asthma vs COPD
In this continuation of the asthma webinar, Dr. Mobeen presents the stepwise approach to managing asthma in patients presenting in the outpatient.
For your reference, the first part of the webinar is here.
Note: Stepwise management starts at minute 13.
Following topics are covered:
- Diagnosis
- Pulmonary function tests and the changes
- Inhaled SABA based testing to confirm asthma.
- Blood IgE tests
- Imaging
- Skin tests
- Exhaled nitric oxide (NO)
- Difference between relievers/rescue drugs, and controllers
- Relievers/Rescue drugs/bronchodilators
- B2 agonists
- Short-acting (SABA)
- Long-acting (LABA)
- Anticholinergics
- Theophylline
- Inhaled corticosteroids
- Systemic corticosteroids
- Antileukotrines
- Cromones
- Anti IgE
- B2 agonists
- Thermoplasty
- Mild
- Mild Persistent
- Moderate persistent
- Severe persistent
- Very severe persistent
ARDS results from lung injury resulting in significant hypoxemia and respiratory distress. This translates into significant morbidity and mortality for patients and is managed primarily in the Intensive Care Unit. This lecture is divided into two modules covering the epidemiology, pathophysiology, and timeline, as well as the clinical presentation and definition of ARDS.
This lecture uses a real case of Pulmonary Embolus to review the clinical presentation of PE and discuss appropriate treatments.
In this lecture, Dr. Zaafran explores the clinical applications of anti-histamine medications.
What does the common cold look like?
What are the most common etiologies that lead to the common cold?
What the treatment regimens for the common cold?
What are anti-histamines and what are the types of receptors involved?
What body systems are affected by histamines and where are the receptors involved?
What is the Mechanism of Action of anti-histamines?
What are the side effects of anti-histamines?
In this lecture, Dr. Zaafran continues to explore the world of anti-histamines. In this presentation, he discusses:
-What are decongestants?
-What are the two main types used?
-Are there different administration modalities?
-What are the types of symptoms most often seen in patients requiring -
nasal decongestants?
-Discussion of cough physiology
-Different types of cough
- Mechanisms of anti-tussive (cough) medications
-What are the different types of anti-tussives?
-Review of the anti-tussive side effects
In this lecture, Dr. Zaafran continues to explore the world of anti-histamines. In this presentation, he discusses:
-What are decongestants?
-What are the two main types used?
-Are there different administration modalities?
-What are the types of symptoms most often seen in patients requiring -
nasal decongestants?
-Discussion of cough physiology
-Different types of cough
- Mechanisms of anti-tussive (cough) medications
-What are the different types of anti-tussives?
-Review of the anti-tussive side effects
Pathology
This video presents following topic Meaning of Atelectasis Definition Types Pathogenesis and Etiology Clinical Diagnosis Treatment Overview
In this video we present the following topics:
- Definition of Asthma
- Triad of Events
- Types Pathogenesis
- Role of allergens
- Role of Mast cells, T Cells, and B cells.
- Role of eosinophils, and neutrophils.
- Role of IL4, IL5, and other cytokines.
- Role of various chemokines.
- Airway Remodeling
- Clinical Aspects
This video presents following topics: Definition of a thrombus DVT and Pulmonary Embolism Veins affected by the DVT Pathogenesis Tests Homan Sign Troussau Sign Treatment
This video presents following topic Epidemiology Risk Factors Size and Consequences Clinical (Saddle vs Small) Labs Diagnosis A-a Gradient Change Hypocapnia
This video presents following topic Definition of Emphysema COPD vs Asthma Ch. Bronchitis vs Emphysema Emphysema: Types Pathogenesis Clinica/Dx Pure Emphysema COPD
This video presents following topic COPD Definition CB Definition CB vs Bronchiolitis CB vs Emphysema Pathogenesis of Ch. Bronchitis Clinical Findings of Ch. Bronchitis Treatment of Ch. Bronchitis
This video presents following topics about tuberculosis: Epidemiology Etiology Pathogenesis Primary Tuberculosis Morphology Clinical
This video presents following topics about tuberculosis: Epidemiology Etiology Pathogenesis Secondary Tuberculosis Morphology Clinical
This video presents following topics: Causes Complications Clinical approach
We will present pneumonia classification based on: Clinical types i.e. acute, fulminent, and chronic Histological patterns and tissue involved Anatomical types based on the lugn lobes invovled And clinical settings for example community acquired or nosocomial pneumonia
This video presents following topics about the Atypical pneumonia: Definition Onset and Risk Factors Presentation Clinical Findings Pathogenesis X-Ray findings Following pathogens are disucssed: Mycoplasma Coxiella Burnetti Chlamoydophila Pneumoniae Influence A,B,C Rhinovirus Coronavirus Rubella Adenovirus Vericella
This video presents following topics about the typical pneumonia: Definition Onset and Risk Factors Presentation Clinical Findings Pathogenesis Stages X-Ray findings Histopathology Complications
This video presents following topics: Nosocomial Pneumniae Aspiration Pneumonia Chronic Pneumonae
Sarcoidosis is discussed as part of restrictive lung diseases We will cover: Connection of Sarcoidosis with respiratory system Definition Pathogenesis Organs involved Clinical
This video presents a group of restrictive lung diseases called pneumoconiosis We will discuss: What diseases are part of this group Definition of the pneumoconiosis Non-neoplastic characteristics of these diseases Coal workers lungs Silicosis Asbestosis A brief mention of brylliosis
This video is part of the series of videos discussing restrictive lung diseases.
We will discuss hypersensitivity pneumonitis in this talk.
- Definition
- Alveolitis due to inhaled external allergens.
- Involves smaller airways and the respiratory zones instead of the large airways.
- The difference of this disease from asthma.
- This is a mixture of type III and type IV allergies.
- Pathophysiology of the hypersensitivity pneumonitis
- Macrophages
- Allergen presentation to T and B cells in the lymph nodes.
- Interleukins released.
- Phases
- Acute and Chronic.
- Role of neutrophils and T cells in the acute phase.
- Granuloma formation in the chronic phase.
- Why hypersensitivity pneumonitis is also classified as a granulomatous disease.
- IL4, IL5, IL12, C5a
- Scarring of the respiratory zones.
- Clinical Presentation
- Fever, dyspnea, cough, lethargy, malaise, restrictive lung disease.
- FEV1 reduced
- FEV1/FVC increased due to increased elasticity and rapid expulsion.
- Monday morning blues experienced by the patients.
- Industries/tasks that can cause this disease
- Fungi and bacteria from farming work - farmers lungs.
- Micropolyspora fanny and bagassosis.
- Thermophilic actinomycetes.Cheese workers - moldy cheese.
- Penicillium casey.
- Miller's lungs.
- Dusty grain.Animal products, pigeon breeder's lungs.
- Pigeon droppings have pigeon serum proteins.
- Other chemical industry workers.
This video presents the introduction to the restrictive lung diseases We will discuss:
Definition
- Types
- Extrapulmonary restrictive lung diseases
- Obesity
- Scoliosis
- Pulmonary parenchymal restrictive lung diseases
- Idiopathic
- Autoimmune
- Granulomatous (Wagner's granulomatosis, Sarcoidosis)
- Occupational (pneumoconiosis, silicosis, asbestosis, coal, etc.)
- Other irritants
- Chronic infections (Tuberculosis)
- Neuromuscular restrictive lung diseases
- Myasthenia gravis
- Diaphragm issues
- Polio
- Extrapulmonary restrictive lung diseases
Cellular events/pathogenesis
- Damaged Type I Pneumocytes
- Hypertrophy of Type II Pneumocytes
- Irritated epithelium
- Irritated macrophages
- Apoptosis of epithelium
- Tissue damage leading to local inflammation and lung destruction/scaring.
- Neutrophils releasing cytokines, proteases, tumor growth factors (TGF)
- Macrophages releasing transforming growth factor beta, tumor necrosis factor (TNF), platelet activation factor.
- Fibroblasts overactivity resulting in more extracellular matrix and hardening.
- Epithelial-mesenchymal transformation.
- Smooth muscle proliferation.
- Respiratory interface thickening. Disrupted gaseous exchange.
Clinical Presentation
- Dry hacking cough
- Dyspnea
- Hypoxia
- Respiratory alkalosis
- Late inspiratory crackles
Abnormal chest X-Ray
- Reduced volume in chest X-Ray
- Lower lobes show more involvement and the reason why.
- Right heart failure/cor pulmonale
Lung Function Changes
- FEV1/FVC ratio increases > 80% (normal or above normal)
Treatment
- Anti-inflammatory (may not be very effective)
- TGF Beta-blockers
- Oxygen
- Lung transplant
This video presents Cystic Fibrosis a type of obstructive lung disease. Following topics are discussed: Definition Causes CFTR gene mutation and the sweat glands CFTR gene mutation and the pulmonary issues
This video presents Bronchiectasis a type of obstructive lung disease. Bronchiectasis is irreversible, chronic, dilatation of the bronchi and bronchioles due to or associated with the chronic infectious disease process.
We will discuss the foundational concepts that lead to the obstructive pulmonary diseases. Following topics are discussed:
- Diseases that are classified as obstructive pulmonary diseases.
- Anatomical and physiological functions.
- Airway structure.
- Parts of the airway that are involved in chronic obstructive pulmonary diseases (COPD)
- Pathology of chronic bronchitis.
- Pathology of emphysema.
- Pathology of bronchiolitis.
- Definition of chronic bronchitis and emphysema.
- COPD vs. Asthma
- How smoke and pollutants cause damage to large and small airways.
- Immune system and obstructive diseases.
- Protease and anti-protease imbalance. We will discuss acquired and genetic deficiencies of protease inhibitors, for example, alpha-1 antitrypsin.
- Oxidant and anti-oxidant imbalance.
This video presents following topics about lung tumors: Epidemiology Classification Pathogenesis Metastasis sites Histopathology Paraneoplastic Syndrome Clinical points
Physiology
This video presents: Anatomical and Physiological Dead Spaces Composition of gases in the respiratory zones Composition of gases at the end of inspiration and expiration Minute ventilation rate Alveolar ventilation rate
This video presents: Tidal Volum (TD) Insipratory Reserve Volume (IRV) Expiratory Reserve Volume (ERV) Residual Volume (RV) Inspiratory Capacity (IC) Functional Residual Capacity (FRC) Vital Capacity (VC) Total Lung Capacity (TLC)
This brief video presents: Apneustic breathing pattern Biot/Ataxic breathing pattern Cheyne Stoke breathing pattern Kussmal breathing pattern
This video presents: Pressure dynamics in the alveoli and pleura during the restful breathing cycle. Pleural pressures are discussed at: a) Restful state (breath held) b) Inspiration c) Expiration
This brief video presents: Quite breathing Chest wall mechanics including: Pump handle movement Bucket handle movement Muscles of quite and forced inspiration Muscles of quite and forced expiration
This video presents: Lung Mechanics. Following topics are discussed: Lung environment Inward or recoil forces Outward or expansile forces Terminology to express various pressures Laplaces law Atelactasis Special case of premature babies
This video presents: Lung Mechanics. Following topics are discussed: Lung environment Inward or recoil forces Outward or expansile forces Terminology to express various pressures Laplaces law Atelactasis Special case of premature babies
This video presents pneumothorax
The following topics are discussed:
- Pleural cavity formation
- Simple Pneumothorax
- Tension Pneumothorax
This video presents: Postivie Pressure Ventilation (PPV) Positive End Expiratory Pressure Ventilation (PEEPV) Advantages and disadvantages of these methods
This video presents: Chest wall compliance Lung tissue compliance Combined compliance of the chest wall and lung tissue Pathological conditions that change compliance.
This video presents the relationship of the flow, pressure, and resistance in the lung airways.
This video discusses: Atmospheric gas pressures Water vapor pressure and its effect on the atmospheric pressure Pressure changes during inspiration Composition of the exhaled gases Factors affecting partial pressure of the oxygen Factors affecting partial pressure of the carbon dioxide
This video presents: Ficks law of diffusion of gases Ficks equation Calcuating oxygen diffusion rate Assessing respiratory interface health
This video discusses: Gas pressure gradient across respiratory membrane Causes of the pressure gradient Capillary diffusion dynamics Adaptation during the exercise
This video discusses: Structure of the Hemoglobin Hb dissociation curve Factors affecting the dissociation curve Oxygen buffering by Hb
This video discusses: Total volume of the carbon dioxide transport to the lungs Three forms of the carbon dioxide transport Chloride shift Carbonic anhydrase Carbon dioxide pressure gradients in the tissue and lungs
This video discusses Bohr Effect Increased carbon dioxide pressure in the tissue helps unload oxygen in the tissues. This is opposite to the Haldene effect where increased oxygen pressure helps unload carbon dioxide in the lungs.
Dr. Mobeen discusses oxygen pressure changes to help load or unload carbon dioxide from the hemoglobin.
Oxygen pressure changes are critical for CO2 movement in and out of the body.
In lungs, we have more oxygen pressure which favors unloading of the carbon dioxide. This will help carbon dioxide eject from the body.
On the other hands in the peripheral tissues oxygen pressure is less. This allows carbon dioxide to be loaded on to the hemoglobin and move away from the tissue.
This video discusses: Alveolar ventilation Blood flow through lungs Calculating the ratio Evaluating the V/Q ratio Generalizations
This video presents the lung function tests.
This video introduced the normal protective mechanisms of the respiratoty system. Mechanism introduced are: Protections in the nose, mouth, pharynx, and upper airways Mucocilliary elevator Antibodies Macrophages Moisture on the airway surfaces Etc.
Ophthalmology
Dr. Zaina Al-Mohtaseb presents following topics:
- Important points while taking the history of a patient with eye injury/pathology.
- Vision testing.
- Important points to keep in mind when checking the patient's pupils.
- The importance of measuring pressure, and when not to measure.
- External examination.
- Examining the motility of the eye.
- CVF
In this exclusive webinar, Dr. Zaina Al-Mohtaseb joins Dr. Ahmed Zaafran to present the most important aspects of the basic eye examination with an emphasis on the following topics:
1)History and Physial Examination of Opthalmic Emergencies
2) Vision testing
3) Retinopathy due to Diabetes Mellitus
4) Hypertensive Retinopathy
5) Intraocular Pressures
6) External Examinations
Clinical Hematology
By: Dr. Tabraiz Mohammed On June 15th 2016 Presented to the Advanced Practitioners Group
Dr. Tabraiz Mohammed discusses functional and quantitative disorders of the immune system. Immune reactions are also discussed.
Tabraiz Mohammed, MD, Hematologist/Oncologist presents an excellent talk on the hemolytic anemia. Following topics are covered: Hemolysis Defective Hemoglobin Abnormal RBC Membrane Abnormal Enzymes Other pathologies
Dr. Syed discusses the liver function tests. {article:https://articles.drbeen.com/2016/05/25/hepatitis-b-and-its-labs/}
Clinical Gynecology
Dr. Sayed continues his lecture series on evaluation and management of common conditions presenting with an acute abdomen.
Clinical Microbiology
In this lecture, Dr. Zaafran discusses the etiology of syphilis as an infectious disease, the diagnosis of treponema pallidum, the clinical manifestations at different stages of the disease, and the clinical management used to treat the disease.
In this lecture, Dr. Mobeen discusses the following topics about Staphylococci:
- Definition
- Description
- Morphology
- Shape
- Color
- Cell wall
- Cell membrane
- Penicillin-binding protein
- Species
- S. Aureus
- S. Epidermidis
- S. Saprophyticus
- Diagnostic Tests
- Gram staining
- Catalase test
- Coagulase test
- Novobiocin test
- NaCl test
- Mannitol fermentation
- Diseases
- Skin infections
- Infective endocarditis
- Bacteremia
- Wound, catheters, and splinter infections
- Prosthesis infections
- Splenic abscesses
- The Management Approach to Staphylococci
- IV vs Oral medications
- MRSA vs. Penicillin sensitive pathogen management
How do staphylococci cause toxic shock syndrome?
Superantigens are the answer.
In this important video session, Dr. Syed discusses superantigens in the context of staphylococci.
Following topics are discussed:
- What are superantigens?
- What important pathogens release superantigens?
- What superantigens are released?
- Normal controlled immune response to an antigen.
- How does a superantigen cause massive abnormal activation of the immune system?
- Symptoms of the toxic shock syndrome as a result of superantigen activity.
- Labs
Toxic shock syndrome is a rare but deadly disease most common in young women using super-absorbent tampons. Staphylococcal toxin TSST-1 is responsible for this syndrome. Majority of the patient that fall ill with toxic shock syndrome also lack an adequate humoral response to the toxic shock syndrome toxin. In this brief video Dr. Mobeen discusses the syndrome, its presentation, diagnosis, pathophysiology, and the management.
Dr. Mobeen discusses the modified duke's criteria and the clinical presentation of acute infective endocarditis.
Dr. Mobeen starts the discussion of the staphylococcal infections caused by organ invasion. This lecture is the introduction to infective endocarditis in the context of staphylococcus.
Topics discussed are:
- What is infective endocarditis?
- Terms to know when studying or managing infective endocarditis.
- Infective endocarditis (IE)
- Native valve endocarditis (NVE)
- Prosthetic valve endocarditis (PVE)
- Nosocomial infective endocarditis (NIE)
- Community acquired infective endocarditis (CIE)
- What tissues are susceptible to infective endocarditis?
- What is the composition of an infective endocarditis vegetation?
- What is the mechanism of tissue damage that leads to IE?
- Which population group is at a higher risk of right sided IE?
- Why are ventricular septal defects at a higher risk of developing IE in contrast to atrial septal defects?
Dr. Mobeen discusses the pathophysiology, presentation, and management of staphylococcal scalded skin syndrome.
Course: Microbiology
Series: Staphylococcus
Staphylococcal gastroenteritis is an exotoxin mediated pathology with sudden onset of nausea, vomiting, diarrhea, and abdominal pain.
​​Dr. Mobeen discusses the transmission, growth, toxin production, pathology, clinical presentation, and management of staphylococcal gastroenteritis.
We are sure that strep/sore throat is a routine presentation in your clinic. In the US only streptococci pyogenes cause millions of yearly visits to healthcare facilities. Streptococci cause disease by direct organ invasion, by their enzymes, and by releasing exotoxins. Understanding streptococci thoroughly and then wielding a great command over the management approach will help you continue to be amazing for your patients. In this two-part series, we will talk about the streptococcal foundations necessary to understand and manage the disease, and then various diseases and their management. Let's start with the first part here. Make sure that you have understood this before the second part about the diseases and their management.
In this lecture we will discuss the following topics:
- Virulence potential
- Habitat
- Throat
- Skin
- Tests
- Erythrogenic/Pyogenic exotoxin
- Gram +
- PYR +
- RAD
- Catalase -
- Bacitracin sensitive
- Antigenic components of the cell wall
- Hyaluronic acid
- C carbs
- M Proteins
- Exotoxins
- Enzymes
- Streptolysin O
- Streptolysin S
- Streptokinase
- Hyaluronidase
- DNAse
- C5a Peptidase
These foundations will be used to look at the disease process, disease types, and the disease management in the next lecture.
What 3 categories of diseases are caused by streptococcus pyogenes?
What are the CDC's recommendations for managing strep throat?
How does the flesh eating disease pathogen (streptococcus pyogenes) cause the tissue to die?
Why most of the post-streptococcal glomerulonephritis patients may not need hospitalization?
What is the role of clindamycin while managing streptococcal diseases?
Dr. Mobeen dicusses the following diseases in this lecture:
- Pyogenic (tissue invasion)
- Sore Throat
- Skin Infections
- Folliculitis
- Pyoderma/Pustules
- Cellulitis
- Erysipelas
- Impetigo
- Toxigenic (exotoxin mediated)
- Scarlet Fever
- Toxic Shock Like Syndrome
- Necrotizing Fasciitis
- Immunogenic (immune response mediated)
- Rheumatic Fever
- Post-streptococcal glomerulonephritis
Notes to be posted soon.
Dr. Syed starts the series about the antibiotics' usage. The first lecture in the series presents the following topics about penicillins: 1. Discovery. 2. Types. 3. Mechanism of action. 4. Coverage of gram positive and negative pathogens by various types. 5. Pathogen resistance to penicillins. 6. Penicillin combinations with lavulanic acid etc. to overcome the resistance. 7. Usage in various infections.
Dr. Mobeen presents the classification, diagnostic testing, metabolic properties, antigenicity, treatment, and vaccination for streptococcus pneumoniae. This pathogen is also called S. Pneumoniae, Pneumococcus, and Diplococcus.
Following identifying characteristics are presented:
- Gram positive staining
- Catalase negative
- Bile sensitive
- Optochin sensitive
- Latex agglutination test positive for pneumococcal antigens
- Teichoic acid
- Diseases caused:
- Conjunctivitis
- Meningitis
- Otitis Media
- Pneumonia
- Sinusitis
- Quellung positive testing
- Alpha hemolysis
- Antigenecity
- IgA protease
- Pneumolysin
- Vaccination
- 23 valent polysacchride vaccine
- 13 valent conjugated polysacchride vaccine
- Penicillin G and V
- 3rd Generation cephalosporins
- Ceftriaxone
- Cefotaxime
- Vancomycin
This lecture presents visual memory aid for Pneumococcus identification virulance factors diseases and treatment.
Dr. Mobeen will discuss the following properties and traits of S. Viridans:
- S. Viridans is not a single species of bacteria, instead it is a big group of pathogens.
- S. Viridians are catalase negative.
- S. Viridans are gram positive.
- S. Viridans are bile insoluble.
- S. Viridans are optochin resistant.
- S. Viridans do not have a capsule.
- S. Viridans cause the following infections:
- Dental carries.
- Subacute bacterial endocarditis (SBE.)
- Brain and liver abscesses.
- Pathologies of the above mentioned infections.
- Signs and symptoms of SBE
- Treatment of SBE
ICU
In this video, we review clinically pertinent respiratory anatomy and physiology as it relates to obstructive lung disease. Functional residual capacity, hypoxic pulmonary vasoconstriction and flow loops are reviewed. Obstructive pulmonary disease is discussed with an emphasis on emphysema and its pathophysiology, diagnosis and acute treatment during exacerbations.
Musculoskeletal System
This talk presents the anatomy of the spine with following topics: The function of the spinal column. Parts of the spinal column. Number of the cervical, thoracic, lumbar, sacral, and coccygeal vertebrae. Anatomy of a vertebra. Parts of the vertebra including the processes and articular surfaces. Clinically important joints of the spinal column. A discussion of the facet joint, its pathologies, and management. Presentation of the intervertebral disc structure. A high level overview of the cervical spinal ligaments.
Brown Sequard Syndrome This video presents the hemisection of the spinal cord. This lesion is also called Brown Seqard Syndrome.
Dr. Tim Wang presents: Evaluation of the cervical and lumbar pathologies. Sources of the pain. History taking Strains and Sprains Examination Disc Herniation Disc Degeneration Neck pain Spurling's test Straight leg raise test Hoffman Shoulder exam Clinical Presentation Radiculopathy vs myelopathy Imaging
•Anatomy of the cervical, thoracic, lumbar and sacral spine including bones/joints, muscles, ligaments, spinal nerves and vasculature •Discuss the normal curvature of the spine, and identify scoliosis, kyphosis and lordosis •Identify the risk factors for a vertebral compression fracture •Differentiate spondylosis, spondylolysis and spondylolisthesis •Cite strong indicators for immediate imaging of the lumbar spine. •Acute lumbar/cervical sprain •Disc herniation •Facet arthritis/posterior element disease •Degenerative disc disease •Spinal stenosis •Cauda equina syndrome Ankylosing spondylitis
•Anatomy of the cervical, thoracic, lumbar and sacral spine including bones/joints, muscles, ligaments, spinal nerves and vasculature •Discuss the normal curvature of the spine, and identify scoliosis, kyphosis and lordosis •Identify the risk factors for a vertebral compression fracture •Differentiate spondylosis, spondylolysis and spondylolisthesis •Cite strong indicators for immediate imaging of the lumbar spine. •Acute lumbar/cervical sprain •Disc herniation •Facet arthritis/posterior element disease •Degenerative disc disease •Spinal stenosis •Cauda equina syndrome Ankylosing spondylitis
Dr. Tim Wang presents the following topics on distal radial fracture:
Anatomy and Mechanism of Injury
Clinical Evaluation
Diagnostic Workup
Acute Management
Prognosis and Return to Sport
Arthritis can take many forms in clinical medicine, with Osteoarthritis being one of the most common forms. This lecture by Dr. Zaafran explores the causes of Osteoarthritis and how it is diagnosed versus other medical conditions.
Neurology
Nervous system examination is crucial to identifying the type of lesion, its location, and its extent. Lower limb reflexes are an important part of this examination especially in a patient in coma. Dr. Mobeen discusses the foundations of lower limb examination in this webinar. Next part will present the clinical utility and lesion assessment based on the abnormal reflexes e.g. positive Babinski's sign (plantar reflex), or hyperreflexia vs. hyporeflexia etc.
This second part of the webinar discusses the following topics:
- Cause of hyperreflexia in a patient of upper motor neuron lesion.
- Cause of hypertonia in a patient of upper motor neuron lesion.
- Dysinhibition of the lower centers.
- Clonus
- When does atonia and flacidity occur?
- When will we see fasciculation and twitching in the muscle?
- When will we see muscle wasting?
- Denervation degeneration.
- Difference between the lower motor and upper motor neuron lesion.
- What is plantar reflex or babinski's sign?
- Role of the S1 spinal segment in plantar reflex.
- What does involvement of the L4 and L5 spinal segments do to plantar reflex?
- When is Babinski's sign is positive?
- What is tripe reflex in the lower limb?
- What does involvement of the L2 and L3 spinal segments do to the plantar reflex?
Following topics are discussed in the previous part:
- Neurology examination. How to differentiate between upper and lower motor neuron lesions?
- What is the difference between an upper motor neuron and a lower motor neuron?
- Overview of the corticospinal tract or pyramidal tract.
- What are spinal reflexes?
- What is a reflex arc?
- Components of a reflex arc.
- What is the role of the upper motor neurons in the spinal reflexes?
Nervous system examination is crucial to identifying a type of lesion, its location, and its extent. Lower limb reflexes are an important part of this examination especially in a patient in coma. Dr. Mobeen discusses the foundations of lower limb examination in this webinar. Next part will present the clinical utility and lesion assessment based on the abnormal reflexes e.g. positive Babinski's sign (plantar reflex), or hyperreflexia vs. hyporeflexia etc.
Following topics are discussed:
- Neurology examination. How to differentiate between upper and lower motor neuron lesions?
- What is the difference between an upper motor neuron and a lower motor neuron?
- Overview of the corticospinal tract or pyramidal tract.
- What are spinal reflexes?
- What is a reflex arc?
- Components of a reflex arc.
- What is the role of the upper motor neurons in the spinal reflexes?
Next part will discuss the clinical correlation of the spinal reflex abnormalities.
Dr. Syed presents following topics about the trigeminal neuralgia (tic douloureux) 1. Clinical presentation. 2. Pathophysiology. 3. Differential Diagnosis. 4. Medical Treatment. 5. Surgical Treatment.
Dr. Syed presents Restless Legs Syndrome (RLS/WED) Following topics are discussed: *Restless Legs Syndrome (RLS)/Willis Ekbom Disease (WED) *Periodic Limb Movement of Sleep (PLMS) *Periodic Limb Movement Disorder (PLMD) *DSM-5 Criteria *Etiology *Pathophysiology *Treatment
Dr. Syed discusses the clinical aspects of the amyotrophic lateral sclerosis (ALS) Topics covered are: 1. Definition. 2. Demography and Prevalence 3. Pathophysiology, the role of SOD1 gene mutation and Glutamate accumulation. 4. Clinical presentation. 5. Progression and prognosis 6. Treatment and support
Dr. Syed presents Myyasthenia Gravis. Clinical vignette Presentation Pathophysiology Diagnosis Treatment Differential Contraindicated medications for myasthenia patients
Dr. Syed discusses clinical aspects of the Bell's Palsy. Facial nerve circuit. Upper motor vs. lower motor neuron lesions in the context of the Bell's palsy. Differential diagnosis. Differentiating between the stroke and Bell's Palsy Clinical Presentation Prognosis Treatment options
Presenter: Dr. Syed
Dr. Syed starts the series about the peripheral nerve disorders with this foundational lecture. In this lecture Dr. Syed presents: Structure of a neuron Structure and composition of a peripheral nerve 6 principle categories of the nerve pathology 6 medical terms to depict nerve disorders 6 causative agents of the nerve disorders
Dr. Ahmed Zaafran gives an overview of epilepsy, its diagnosis, treatment, and understanding of basic clinical pathologies related to seizures.
In this lecture Dr. Abdullah presents the following topics:
1. Definition of Febrile seizure
2. Causes and Risk factors
3. Types
4. Simple vs Complex Febrile seizure
5. Clinical presentation
6. Treatment
This discussion covers:
- The classification of strokes
- The common etiologies of ischemic stroke
- Pathophysiology of ischemic stroke
- The clinical management of the ischemic strokes
In this lecture Dr. Crawford presents the definition of coma, the most common etiologies, and uses a case to highlight clinical management strategies.
Case
A 73 year-old female is transferred to the hospital from her nursing home after being found unresponsive.
Topics
- Definition of coma
- Anatomy of awareness
- Three broad categories of coma etiologies
- Brief review of the pathophysiology of comatose states
- Initital evaluation
- Diagnosis
- Management
Cerebrospinal fluid is a colorless fluid that fills the nervous system cavities. It acts as a protective cushion, and also is the vehicle for nutrient's exchange.
Understanding the production, flow, drainage, and composition of the CSF is critical for a medical professional.
In this talk Dr. Mobeen presents the following topics:
- 1. The structures taking part in the formation of the blood-brain barrier
- 2. Production of the cerebrospinal fluid (CSF)
- 3. Circulation of CSF
- 5. The composition of CSF in the following events:
- Bacterial meningitis
- Viral meningitis
- Fungal meningitis
- Tuberculosis
- Trauma
Cerebrospinal fluid is a colorless fluid that fills the nervous system cavities. It acts as a protective cushion, and also is the vehicle for nutrient's exchange.
Understanding the production, flow, drainage, and composition of the CSF is critical for a medical professional.
In this talk Dr. Mobeen presents the following topics:
- 1. The structures taking part in the formation of the blood-brain barrier
- 2. Production of the cerebrospinal fluid (CSF)
- 3. Circulation of CSF
- 5. The composition of CSF in the following events:
- Bacterial meningitis
- Viral meningitis
- Fungal meningitis
- Tuberculosis
- Trauma
Neuroanatomy
This video presents important cells of the nervous system with their function.
This video presents the congenital abonormalities of the CNS.
This video presents the high yield concepts for the development of the spinal cord.
Following topics are discussed:
Neuropores, their closure, pathologies when the neuropores do not close.
How to find out if the neuropores are not closed?
Structures arising from the neural tube and neural crest cells.
Roof plate.
Floor plate.
Basal plates.
Alar plates.
Intermediate plate.
Sulcus limitans.
Gray matter formation.
Dorsal, intermediolateral, and ventral horn formation.
Formation of the spinal tracts.
Formation of the spinal nerves.
Autonomic Nervous System formation.
White ramus and gray ramus formation.
Parasympathetic system formation.
Origin of the chromaffin cells, supra-renal formation, etc.
Origin of the lining of the central canal.
Dr. Syed discusses the following topics: internal Carotid and its branches: Ophthalmic Anterior Choroidal Middle Cerebral and Lenticulstriate Anterior Cerebral and Anterior Communicating posterior Communicating Verebrobasilar System Vertebral Arteries Anterior Spinal Posterior Inferior Cerebellar Basilar Anterior Inferior Cerebellar Pontine Superior Cerebellar Posterior Cerebellar High yield clinical presentations of the strokes involving these arteries.
This video presents clinical concepts explaining the blood supply of the brain. These are important for practice and exams.
Guys, this video abruptly stops at the posterior communicating artery rupture and the oculomotor nerve palsy ... To find the remaining part of this talk, watch the next video from the same point. Next video contains all the clinical aspects. Here is the link:
https://members.drbeen.com/view/vasculature-and-perfusion-of-the-brain/HJxfiMRO3gW
This video presents the types of motor, sensory, and interneurons.
This video presents one of the most important sensory tracts. The dorsal column or fasciculus gracilis and fasciculus cuneatus.
This video presents the most important motor tract - the Pyramidal Tract or Corticospinal Tract.
This video presents the corticonuclear tract. This is an extrapyramidal tract that helps with motor activity.
This video presents the most important motor tract - the Pyramidal Tract or Corticospinal Tract.
This video presents the lesions of the spinal cord.
Ventricles of the Brain are critical to understand well from clinical and USMLE point of views. One must know ventricles before a good grasp of the CSF, Meningitis, and some of the Degenerative diseases of the brain can be understood.
This video presents the structure, function, and neuronal loops of the Cerebellum.
Review This video presents the structure, function, and neuronal loops of the Cerebellum.
This video presents the neuroanatomy and neuropathology of the Basal Ganglia.
Cranial nerve clinical cases.
Neuropathology
Brown Sequard Syndrome This video presents the hemisection of the spinal cord. This lesion is also called Brown Seqard Syndrome.
This video presents Huntington's disease. A progressive, debilitating, neurodegenrative disease.
This video presents the one of the degenerative disease of the brain - Parkinsonism.
Review This video presents the one of the degenerative disease of the brain - Parkinsonism.
Watch all drbeen lectures at https://www.drbeen.com
[Errata: In the early part of the video, I wrote recurrent function instead of recurrent infections. Please keep this in mind while studying.]
*It is an insidious, progressive, degenerative disease of the neurons.
*Alzheimer's incidence is increasing in the developed nations.
*Alzheimer's disease is one of the most costly disease to manage. Continuous care is needed, recurrent infections, and dehydration are common.
Dr. Mobeen presents the pathophysiology of Alzheimer's disease. Following topics are discussed:
Anterolateral amnesia. (Loss of forming new memories.)
Speech disorders.
Mood imbalance.
Disruption of the executive functions of the brain. (Difficulty with decision making.)
Initiates at the Hippocampus.
Genes involved:
1-14 - Senilin
11 - SDLR1
21 - APP
19 - ApoE4
Alzheimer's can be early onset or late onset. Genes 19 and 21 are involved in the early onset Alzheimer's.
*Tau protein's role.
*Beta amyloid's pathologies. (A-Beta lipoprotein.)
*Role of alpha, beta, and gamma secretase.
*Formation of senile plaques due to the beta and gamma secretase action instead of alpha and beta secretase.
*Immune system activation due to the senile plaque formation.
*Destruction of the brain tissue due to the inflammatory reaction due to the senile plaques.
*Clogging of the neural synapses by the senile plaque proteins.
*Loss of cytoskeletal integrity due to the disruption of the Tau proteins.
*Disruption of the nutrients flow from the neuronal cell body to the axonal terminal.
*Formation of the Tau aggregates.
*ApoE-4 gene's role is discussed.
*Widening of the sulci and gyri as a result of the degeneration is presented.
*Role of increased load of the APP protein or the gene up regulation forming APP.
Watch all drbeen lectures at https://www.drbeen.com
[Errata: In the early part of the video, I wrote recurrent function instead of recurrent infections. Please keep this in mind while studying.]
*It is an insidious, progressive, degenerative disease of the neurons.
*Alzheimer's incidence is increasing in the developed nations.
*Alzheimer's disease is one of the most costly disease to manage. Continuous care is needed, recurrent infections, and dehydration are common.
Dr. Mobeen presents the pathophysiology of Alzheimer's disease. Following topics are discussed:
Anterolateral amnesia. (Loss of forming new memories.)
Speech disorders.
Mood imbalance.
Disruption of the executive functions of the brain. (Difficulty with decision making.)
Initiates at the Hippocampus.
Genes involved:
1-14 - Senilin
11 - SDLR1
21 - APP
19 - ApoE4
Alzheimer's can be early onset or late onset. Genes 19 and 21 are involved in the early onset Alzheimer's.
*Tau protein's role.
*Beta amyloid's pathologies. (A-Beta lipoprotein.)
*Role of alpha, beta, and gamma secretase.
*Formation of senile plaques due to the beta and gamma secretase action instead of alpha and beta secretase.
*Immune system activation due to the senile plaque formation.
*Destruction of the brain tissue due to the inflammatory reaction due to the senile plaques.
*Clogging of the neural synapses by the senile plaque proteins.
*Loss of cytoskeletal integrity due to the disruption of the Tau proteins.
*Disruption of the nutrients flow from the neuronal cell body to the axonal terminal.
*Formation of the Tau aggregates.
*ApoE-4 gene's role is discussed.
*Widening of the sulci and gyri as a result of the degeneration is presented.
*Role of increased load of the APP protein or the gene up regulation forming APP.
Hydrocephalus literally means water in head. It is the excessive accumulation of the fluids in the brain cavities. It can either be due to increased production (rare), reduced flow (common), or impaired reabsorption (less common).
Dr. Mobeen Syed presents the spinal cord lesions to MSAI students.
History Taking and Prescription Writing
Dr. Ahmed Zaafran presents a talk on the history of presenting illness. Type: Webinar Recording
Presented for the NP and PA students.
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Title |
Understanding the relationship between leadership, culture, and data to drive change |
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Objectives: |
1. Learn to define organizational culture 2. Learn the relationship between data and driving changes 3. Learn the impact of leadership on culture and change 4. Learn the predictors of organizational agility and success |
Wound Care
By Hatem Abou-Sayed MD, MBA, FACS Plastic Surgeon
Vaccination
Objectives:
Objectives of this lecture are:
-
Pediatric vaccines and the diseases they help prevent.
-
The typical primary pediatric vaccine schedule.
-
Some myths about vaccination.
Mindfulness
Micah Anderson presents the importance of mindfulness. An exercise to practice daily.
Dr. Merry Ceppie provides an introduction to integrative medicine.
Defining principles of integrative medicine:
- The patient and practitioner are partners in the healing process.
- All factors that influence health, wellness, and disease are taken into consideration, including mind, spirit, and community, as well as the body.
- Appropriate use of both conventional and alternative method facilitates the body's innate healing response.
- Effective interventions that are natural and less invasive should be used whenever possible.
- Integrative medicine neither rejects conventional medicine, nor accepts alternative therapies uncritically.
- Good medicine is based in good science. It is inquiry-driven and open to new paradigms.
- Alongside the concept of treatment, the broader concepts of health promotion and the prevention of illness are paramount.
- Practitioners of integrative medicine should exemplify its principles and commit themselves to self-exploration and self-development
Instructor
Ahmed Zaafran, MD
Ahmed Zaafran, M.D, is a practicing anesthesiologist at Santa Clara Valley Medical Center. He is also an adjunct clinical assistant professor of anesthesiology at Stanford University School of Medicine.