PODCAST · health
K Lectures
by K Med
This podcast is about topics in medicine including human anatomy and physiology among many others.
Episodes
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J receptors
J receptors
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RBC Biochemistry II
RBC Biochemistry
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RBC Biochemistry I
RBC Biochemistry I
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Anemia
Anemia
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HbA1c
HbA1c
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CN III - Internal and External Opthalmoplegia
CN III - Internal and External Opthalmoplegia
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CN3-2
CN3-2
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Oculomotor Nerve 1
Oculomotor Nerve 1
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Medulla Oblongata
Medulla Oblongata
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BrainStem Nuclei
BrainStem Nuclei
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Diaphragmatic excursion
Diaphragmatic excursion
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Therapeutic index
Therapeutic index
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Ionization of drugs
Ionization of drugs
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Volume Distribution of drugs
Volume Distribution of drugs
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Incidence vs Prevalence
Incidence vs Prevalence
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Incidence vs Prevalence
Incidence vs Prevalence
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Alcohol Metabolism
Alcohol Metabolism
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Energy metabolism in hearty
Energy metabolism in hearty
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RTA types
RTA types
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Strategy for solving Acid-Base Problems
Strategy for solving Acid-Base Problems
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HMG-COA reductase regulation via phosphorylation and Dephosphorylation
HMG-COA reductase regulation via phosphorylation and Dephosphorylation
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Cholesterol Synthesis Regulation
Cholesterol Synthesis Regulation| SREBP| SCAP | S1P | S2P| SRE
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Pathophysiology of Atherosclerosis
Pathophysiology of Atherosclerosis
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CETP on HDL
CETP on HDL
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How LDL is formed
How LDL is formed
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Apoproteins
Apoproteins
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Hormone sensitive Lipoprotein Lipase
Hormone sensitive Lipoprotein Lipase
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Lipoprotein Metabolism | Lipoprotein | Apo-protein| B48| B100| HDL| ApoE| ApoCII | VLDL| IDL| LDL
Lipoprotein Metabolism | Lipoprotein | Apo-protein| B48| B100| HDL| ApoE| ApoCII | VLDL| IDL| LDL | LCAT vs ACAT | Pancreatic lipase, hepatic triglyceride lipase, Chylomicron | SRB1 | ABC1| ABCG1| HDL3, HDL2, CETP| Apo-AI |
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How metabolic Acidosis causes Hyperkalemia
How metabolic Acidosis causes Hyperkalemia. H+ enters all cells including Principal cells. K+ leaves principal cells and enters blood. Leading to Hyperkalemia. High K+ level is maintained by decreasing Na+—K+ ATPase and K+ channel activities.
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How Metabolic Alkalosis results in Hypokalemia
How Metabolic Alkalosis results in Hypokalemia | Principal Cells | Basolateral Na+- K+ ATpase | Luminal K+ channel. H+ move from principal cells into blood and K+ move from blood into principal cells and from principal cells into the urinary lumen. Eventual excretion!
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Principal cells | ADH| V2 receptors | Gs Pathway | Aquaporin-2
Principal cells | ADH| V2 receptors | Gs Pathway | Aquaporin-2
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ENAC| K-wasting vs K-Sparing diuretics | Spironolactone | Aldosterone | Lumen Electropositivity
ENAC| K-wasting vs K-Sparing diuretics | Spironolactone | Aldosterone | Lumen Electropositivity
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Thiazides | NCC | PTH | Ca++ Reabsorption
Thiazides | NCC | PTH | Ca++ Reabsorption
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How Furosemide causes Alkalosis and urinary acidification
How Furosemide causes Alkalosis and urinary acidification
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NKCC2| Furosemide induced urinary acidification | Diuretics
NKCC2| Furosemide induced urinary acidification | Diuretics
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CA inhibitors in PCT- Acetazolamide
CA inhibitors in PCT- Acetazolamide
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Urea Cycle
Urea Cycle
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5 Causes of HYPOXEMIA
5 Causes of HYPOXEMIA
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Hyperventilation 2
Hyperventilation 2
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Hyperventilation
Hyperventilation
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Atrial receptors
Atrial receptors
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Baroreceptors
Baroreceptors
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Afterload and Leplace’s Law
Afterload and Leplace’s Law
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P-V loops ESPVR vs EDPVR curves in cardiomyopathies
P-V loops ESPVR vs EDPVR curves in cardiomyopathies
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Digoxin Mechanism of Action
Digoxin Mechanism of Action
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Adrenal Gland aka Suprarenal Gland
Suprarenal Gland
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Cardiac Cycle
Cardiac Cycle
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Cardiac output | PV loops | Frank-Starling Curve or principle
How do PV loops change with increased preload, contractility and afterload? Cardiac output | PV loops | Frank-Starling Curve or principle
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Venous Return and Cardiac Output Curves
Venous Return and Cardiac Output Curves
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