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Myocardial Infarction: Findings on History

L).(Onset: often at rest; crescendo)Activation of reflexive vagal responses (listed below)Weakness, dizziness, nausea, vomitingInflammatory mediators irritates nerves innervating the heart (the cardiac plexus)Cytokines act on hypothalamic T0 regulatorMild fever? Sweating (diaphoresis)Inflammatory cytokines can spread systemicallyBrain perceives nerve irritation as pain coming from T1-T4 dermatomesBlood backs up from the LV, into the left atrium and eventually accumulates in the pulmonary vasculatureHigh pulmonary venous blood pressure forces fluid out of capillaries, into pulmonary interstitium & alveoliRespiratory muscles work harder to ventilate lungsSoggier lung interstitium ? lung complianceDyspnea(Shortness of breath)Fluid compresses airways, ? resistance to airflow 102 kB / 204 words" title="Yu Yan - MI Findings on History - FINAL.pptx - Myocardial Infarction: Findings on HistoryLegend:Published January 30, 2013 on www.thecalgaryguide.comMechanismPathophysiologySign/Symptom/Lab FindingComplicationsAuthor: Yan YuReviewers:Sean SpenceTristan JonesNanette Alvarez** MD at time of publication Systolic function(necrotic myocardium cannot contract as well)Reflexive ? in sympathetic activity (to try to maintain CO)Clammy skin? stroke volume (SV), ? cardiac output (CO)Myocardial infarction (tissue necrosis)Note: Myocardial ischemic pain may differ between patients, but recurrences usually feel the same in any given patient.Generalized vasoconstrictionVasoconstriction of skin arteriolesCool skinLocal myocardial inflammationIrritation of T1-T4 sympathetic afferentsIrritation of cardiac branches of vagus nerveSignals enter spinal cord, mixes with T1-T4 dermatomesCrushing, Diffuse "Pain" or "tightness": Often retrosternal, with radiation to shoulder, neck, and inner aspect of both arms (R > L).(Onset: often at rest; crescendo)Activation of reflexive vagal responses (listed below)Weakness, dizziness, nausea, vomitingInflammatory mediators irritates nerves innervating the heart (the cardiac plexus)Cytokines act on hypothalamic T0 regulatorMild fever? Sweating (diaphoresis)Inflammatory cytokines can spread systemicallyBrain perceives nerve irritation as pain coming from T1-T4 dermatomesBlood backs up from the LV, into the left atrium and eventually accumulates in the pulmonary vasculatureHigh pulmonary venous blood pressure forces fluid out of capillaries, into pulmonary interstitium & alveoliRespiratory muscles work harder to ventilate lungsSoggier lung interstitium ? lung complianceDyspnea(Shortness of breath)Fluid compresses airways, ? resistance to airflow 102 kB / 204 words" />

process

lower-urinary-tract-infections-complications

lower-urinary-tract-infection-pathogenesis-and-clinical-findings

Osteoarthritis (OA): Clinical findings

Osteoarthritis (OA): X-ray features

Diffuse Systemic Sclerosis (Scleroderma)

Takayasu's Arteritis: Pathogenesis and clinical findings

Giant Cell (Temporal) Arteritis: Pathogenesis and investigations

Giant Cell (Temporal) Arteritis: Clinical findings and Complications

Hyperuricemia Pathogenesis and Complications

Gout Pathogenesis and Clinical Findings

Reactive Arthritis

Psoriatic Arthritis: Complications

Psoriatic Arthritis - Pathogenesis and Clinical findings

Ankylosing Spondylitis: Extra-articular Manifestations

Ankylosing Spondylitis: Pathogenesis and Clinical findings

Lupus: Muco-cutaneous manifestations

Pathogenesis of Lupus

Rheumatoid arthritis (RA): X-ray features

Rheumatoid arthritis (RA): Extra-articular manifestations

Rheumatoid arthritis (RA): Pathogenesis and Joint diseases features

Charcot Joint: Pathogenesis and Clinical findings

Osteoarthritis (OA): X-ray features

Degenerative Vs Inflammatory Joint Disease

Hypersensitivity: Definitions

Type I Hypersensitivity: Pathogenesis and clinical findings

Type II Hypersensitivity: Pathogenesis and clinical findings

Type III Hypersensitivity: Pathogenesis and clinical findings

Type IV Hypersensitivity: Pathogenesis and clinical findings

Hypersensitivity Summary

Agammaglobulinemia: Pathogenesis and clinical findings

Acute Otitis Media: Pathogenesis and Clinical Findings (in Children)

Acute Otitis Media: Complications

Endometriosis: Pathogenesis and Complications

Physiology of the Renin-Angiotensin-Aldosterone System (RAAS)

Hypokalemia: Clinical Findings

0.5 of R-R interval)?Flatter T-Waves ?Inverted T-waves (with more severe hypokalemia)Purkinje fibers repolarize after the rest of the myocardium has done soU-waves (upward ECG deviations after the T-wave)Cells become hyperpolarized: Inside of cells are more negative relative to outside, ? Resting Membrane Potential (RMP)In the Kidney:Generalized Muscle weaknessK+ diffuse out of Proximal Convoluted Tubule & Collecting Duct cells ? cells retain acidic H+ inside (maintains electrical neutrality)? pH within PCT cells ? glutaminase activity, ? glutamine breakdown, producing HCO3-, which enters the blood? blood pH, [HCO3-], & pCO2 (respiratory compensation)Low Plasma [K+]Abnormally long diastole means that ventricles are overfilled. Contraction takes greater force; sensed by patientsDyspnea, fatigue, dizziness, syncope? cardiac output ? perfusion of tissues, i.e. lungs & brainCardiac arrhythmias: PACs, PVCs, Sinus Bradycardia, paroxysmal atrial/junctional tachycardia, VT (i.e. Torsades de pointes), V-Fib? smooth muscle contractile abilityBowel ileus (bloating, anorexia, nausea/vomiting, absent bowel sounds)? pH in collecting duct intercalated cells ? H+ secretion into the tubuleMetabolic alkalosisParalysis, muscle cramps (in severe hypokalemia)Respiratory muscle failure (? tidal volume, ? pCO2, ? pO2), may even cause death!? depolarizations ? adenyl cyclase activity ? ? sensitivity of collecting duct cells to ADH? ability of nephron to concentrate urineNephrogenic Diabetes Insipidus? urine osmolality, Hypernatremia, Polyuria, Polydipsia? # of aquaporins in the collecting duct membrane"Insulin Resistance": ? ability to import K+ from the blood in response to insulinIn skeletal muscle: 117 kB / 307 word" title="Yu, Yan - Hypokalemia clinical findings - FINAL.pptx Production of Na+/ K+ transporters in cell membranes ? over timeHypokalemia: Clinical FindingsAuthor: Yan YuReviewers:David WaldnerSean SpenceAndrew Wade** MD at time of publicationLegend:Published May 21, 2013 on www.thecalgaryguide.comMechanismPathophysiologySign/Symptom/Lab FindingComplicationsPalpitationsExcitable cells (muscle cells, neurons) depolarize less readilyK+ efflux out of all cells in the body, down its concentration gradientCardiac myocytes experience electrical conduction defects? muscle impulse conductionECG shows characteristic changes:? skeletal muscle contractile abilityRMP now more negative; myocytes take longer to repolarize to RMP("stretches out" the T-wave)! Long QT interval (>0.5 of R-R interval)?Flatter T-Waves ?Inverted T-waves (with more severe hypokalemia)Purkinje fibers repolarize after the rest of the myocardium has done soU-waves (upward ECG deviations after the T-wave)Cells become hyperpolarized: Inside of cells are more negative relative to outside, ? Resting Membrane Potential (RMP)In the Kidney:Generalized Muscle weaknessK+ diffuse out of Proximal Convoluted Tubule & Collecting Duct cells ? cells retain acidic H+ inside (maintains electrical neutrality)? pH within PCT cells ? glutaminase activity, ? glutamine breakdown, producing HCO3-, which enters the blood? blood pH, [HCO3-], & pCO2 (respiratory compensation)Low Plasma [K+]Abnormally long diastole means that ventricles are overfilled. Contraction takes greater force; sensed by patientsDyspnea, fatigue, dizziness, syncope? cardiac output ? perfusion of tissues, i.e. lungs & brainCardiac arrhythmias: PACs, PVCs, Sinus Bradycardia, paroxysmal atrial/junctional tachycardia, VT (i.e. Torsades de pointes), V-Fib? smooth muscle contractile abilityBowel ileus (bloating, anorexia, nausea/vomiting, absent bowel sounds)? pH in collecting duct intercalated cells ? H+ secretion into the tubuleMetabolic alkalosisParalysis, muscle cramps (in severe hypokalemia)Respiratory muscle failure (? tidal volume, ? pCO2, ? pO2), may even cause death!? depolarizations ? adenyl cyclase activity ? ? sensitivity of collecting duct cells to ADH? ability of nephron to concentrate urineNephrogenic Diabetes Insipidus? urine osmolality, Hypernatremia, Polyuria, Polydipsia? # of aquaporins in the collecting duct membrane"Insulin Resistance": ? ability to import K+ from the blood in response to insulinIn skeletal muscle: 117 kB / 307 word" />

Hyperkalemia: Clinical Findings

6.5 mmol/L:? atrial conduction; slow signal transmission from SA to AV nodeCells become slightly depolarized: Resting Membrane Potential (RMP) is brought closer to thresholdIn the Kidney:Muscle weakness and even paralysis (respiratory muscle weakness is rare)? reabsorption of Na+ from Cortical Collecting Duct (CCD)CCD lumen remains more positively chargedMetabolic Acidosis(normal anion gap)Over time (when patients become symptomatic): Chronic membrane depolarization desensitizes voltage-gated Na+ channels (slows their opening) ? ? membrane excitability ? ? action potential generation[K+] > 7.0 mmol/L:? ventricular conductionBradycardiaProlonged, abnormal QRSAV blocks[K+] > 9.0 mmol/L:more conduction abnormalitiesPEA with bizarre wide-QRS rhythmV-fibAsystole? urinary H+ secretion by alpha-intercalated cellsHIGH Plasma [K+] (potassium ion concentration)Dyspnea, fatigue, dizziness, syncope? cardiac output ? ? perfusion of tissues, i.e. lungs & brainCardiac arrhythmias: Conduction blocks (AV block, Bundle branch blocks), VT , V-Fib, Bradycardia, Asystole.?? PR interval ?P-wave flattens, eventually disappearsIf severe, QRS & T-waves fuse:Sine-WavesThe higher the [K+], the slower the voltage-gated Na+ channels open, reflected by distinctive ECG changes:If the K+ is due to ? aldosterone effect ? principal cell dysfunctionHigh pH ? glutamate deamination, which normally produces NH4+? NH4+ reaches the thick ascending limb to be converted to NH3Less NH3 diffuses into the collecting duct to be converted to NH4+ through binding with H+ ? ? NH4+ and therefore ? H+ is excretedK+ moves into proximal tubule cells, causing H+ to diffuse out ? Intracellular alkalosis Irregular force and rhythm of cardiac muscle contraction is sensed by the patient? contraction impulse is conductedDefective electrical conduction through cardiac myocytesMore acid (H=) is retained in the body 118 kB / 357 words" title="Yu, Yan - Hyperkalemia clinical findings - Published.pptx Hyperkalemia: Clinical FindingsAuthor: Yan YuReviewers:Alexander ArnoldDavid WaldnerSean SpenceAndrew Wade** MD at time of publicationLegend:Published September 9, 2013 on www.thecalgaryguide.comMechanismPathophysiologySign/Symptom/Lab FindingComplicationsPalpitationsNotes: Symptoms usually manifest when plasma [K+] > 7.0 mmol/L, but can occur at lower [K+]s when hyperkalemia is acute.ECG changes can, but don't necessarily, correlate with a particular [K+].Initially: Excitable cells (muscle cells, neurons) undergo action potentials more readily? [K+ ] gradient between cells and the blood (K+ tends to stay inside cells, less K+ diffuses out)In the Heart:In Skeletal Muscle:[K+] >5.5 mmol/L :faster myocardial repolarization("squeezes up" T-wave)Tall, peaked T-Waves Short QT interval (<0.5 of RR interval)[K+] > 6.5 mmol/L:? atrial conduction; slow signal transmission from SA to AV nodeCells become slightly depolarized: Resting Membrane Potential (RMP) is brought closer to thresholdIn the Kidney:Muscle weakness and even paralysis (respiratory muscle weakness is rare)? reabsorption of Na+ from Cortical Collecting Duct (CCD)CCD lumen remains more positively chargedMetabolic Acidosis(normal anion gap)Over time (when patients become symptomatic): Chronic membrane depolarization desensitizes voltage-gated Na+ channels (slows their opening) ? ? membrane excitability ? ? action potential generation[K+] > 7.0 mmol/L:? ventricular conductionBradycardiaProlonged, abnormal QRSAV blocks[K+] > 9.0 mmol/L:more conduction abnormalitiesPEA with bizarre wide-QRS rhythmV-fibAsystole? urinary H+ secretion by alpha-intercalated cellsHIGH Plasma [K+] (potassium ion concentration)Dyspnea, fatigue, dizziness, syncope? cardiac output ? ? perfusion of tissues, i.e. lungs & brainCardiac arrhythmias: Conduction blocks (AV block, Bundle branch blocks), VT , V-Fib, Bradycardia, Asystole.?? PR interval ?P-wave flattens, eventually disappearsIf severe, QRS & T-waves fuse:Sine-WavesThe higher the [K+], the slower the voltage-gated Na+ channels open, reflected by distinctive ECG changes:If the K+ is due to ? aldosterone effect ? principal cell dysfunctionHigh pH ? glutamate deamination, which normally produces NH4+? NH4+ reaches the thick ascending limb to be converted to NH3Less NH3 diffuses into the collecting duct to be converted to NH4+ through binding with H+ ? ? NH4+ and therefore ? H+ is excretedK+ moves into proximal tubule cells, causing H+ to diffuse out ? Intracellular alkalosis Irregular force and rhythm of cardiac muscle contraction is sensed by the patient? contraction impulse is conductedDefective electrical conduction through cardiac myocytesMore acid (H=) is retained in the body 118 kB / 357 words" />

Hypocalcemia: Clinical Findings

Hypercalcemia: Clinical Findings

Nephrotic Syndrome: Pathogenesis and Clinical Findings

3.5g/day*? Ability of blood to retain fluids within vessels ? fluid leaks into extra-vascular spaceInjury to glomerular endothelium and epitheliumImmune complexes deposit into glomerulusDamaged glomerulus ? abnormally permeable to proteins within the blood ? plasma proteins are thus excessively filtered out? Oncotic pressure signals liver to ? albumin synthesis, only to have it filtered out by the kidneys? anabolic activity of liver ? ? lipoprotein synthesisHyperlipidemia*:(? serum LDL, VLDL, and TGs)Lipiduria(lipid/fatty casts; "Maltese cross" sign under polarized light)Since counter-balancing anticoagulant proteins are lost, clotting factors (i.e. 1, 7, 8, 10) now have more activityThrombo-embolic diseaseBlood becomes hyper-coagulable? Lipids are filtered into renal tubules, end up in urineMembranoproliferative Glomerulonephritis (MPGN)Lupus Glomerulonephritis Post-infectious GlomeruloneprhitisIgA NephropathyDamages podocytes on epithelial side of glomerulus ("podocyte effacement"; foot processes flattening)Diabetes MellitusChronic hyperglycemia damages glomeruliDeposition of Immunoglobulin light chains in glomerulusAmyloidosisAnasarca(If generalized)Peri-orbital edema (classic sign)Focal Segmental Glomerular Sclerosis (FSGS)Membranous GlomeruloneprhitisAntibodies attack podocytes, thickening glomerular basement membraneOverflow of immunoglobulin light chains into urine (More filtered than can be reabsorbed)Proteinuria >3.5g/day*The Anion Gap is mostly due to the negative charge of plasma albumin? Anion GapNotes: The four classic features (*) of Nephrotic Syndrome are PEAL (Proteinuria (>3.5 g/day), Edema, hypo-Albuminemia, and hyperLipidemia)For each 10 g/L drop in albumin below 40:Add 2.5 to the calculated anion gap (AG) to get the "correct" AG valueAdd 0.2 mmol/L to total calcium or get an ionized calcium, which is unaffected50% of serum Ca2+ is albumin-bound, so total serum calcium ? Serum total Ca2+ does not reflect ionized Ca2+ ? Blood oncotic pressure" title="Destroys charge barrier to protein filtrationNephrotic Syndrome: Pathogenesis and Clinical FindingsAuthor: Yan YuReviewers:Alexander ArnoldDavid WaldnerSean SpenceStefan Mustata** MD at time of publicationLegend:Published August 19, 2013 on www.thecalgaryguide.comMechanismPathophysiologySign/Symptom/Lab FindingComplicationsExcessive ("Nephrotic-range") loss of albumin in the urineHypo-albuminemia*Loss of anti-coagulant proteins (Antithrombin, Plasminogen, and proteins C and S) in urineMinimal Change Disease (MCD)"Underfill" edema*Proteinuria >3.5g/day*? Ability of blood to retain fluids within vessels ? fluid leaks into extra-vascular spaceInjury to glomerular endothelium and epitheliumImmune complexes deposit into glomerulusDamaged glomerulus ? abnormally permeable to proteins within the blood ? plasma proteins are thus excessively filtered out? Oncotic pressure signals liver to ? albumin synthesis, only to have it filtered out by the kidneys? anabolic activity of liver ? ? lipoprotein synthesisHyperlipidemia*:(? serum LDL, VLDL, and TGs)Lipiduria(lipid/fatty casts; "Maltese cross" sign under polarized light)Since counter-balancing anticoagulant proteins are lost, clotting factors (i.e. 1, 7, 8, 10) now have more activityThrombo-embolic diseaseBlood becomes hyper-coagulable? Lipids are filtered into renal tubules, end up in urineMembranoproliferative Glomerulonephritis (MPGN)Lupus Glomerulonephritis Post-infectious GlomeruloneprhitisIgA NephropathyDamages podocytes on epithelial side of glomerulus ("podocyte effacement"; foot processes flattening)Diabetes MellitusChronic hyperglycemia damages glomeruliDeposition of Immunoglobulin light chains in glomerulusAmyloidosisAnasarca(If generalized)Peri-orbital edema (classic sign)Focal Segmental Glomerular Sclerosis (FSGS)Membranous GlomeruloneprhitisAntibodies attack podocytes, thickening glomerular basement membraneOverflow of immunoglobulin light chains into urine (More filtered than can be reabsorbed)Proteinuria >3.5g/day*The Anion Gap is mostly due to the negative charge of plasma albumin? Anion GapNotes: The four classic features (*) of Nephrotic Syndrome are PEAL (Proteinuria (>3.5 g/day), Edema, hypo-Albuminemia, and hyperLipidemia)For each 10 g/L drop in albumin below 40:Add 2.5 to the calculated anion gap (AG) to get the "correct" AG valueAdd 0.2 mmol/L to total calcium or get an ionized calcium, which is unaffected50% of serum Ca2+ is albumin-bound, so total serum calcium ? Serum total Ca2+ does not reflect ionized Ca2+ ? Blood oncotic pressure" />

Signs and Symptoms of Hypovolemia

Placental Abruption

Contraindications to Inducing Vaginal Delivery

Active Phase Problems: Pathogenesis and Management

Normal Signs of Placental Detachment

Methods to Improve Fetal Oxygenation

Post-Partum Hemorrhage

Upper Urinary Tract infection (UUTI): Pathogenesis and Clinical Findings

Asthma: Findings on Investigations

COPD: Pathogenesis

COPD: Clinical Findings

COPD: Findings on Investigations

COPD: Complications

Bronchiectasis: Findings on Chest X-Ray and CT Scan

Cystic Fibrosis

Posterior-Anterior Chest X-Ray

Lateral Chest X-Ray

Coronal CT

Axial CT

Infant Respiratory Distress: Clinical findings

Foreign Body Aspiration

Types of Burns - Summary of Causes and Clinical Findings

Deep Partial Thickness Burns: Pathogenesis and Clinical Findings

Pericardial Effusion and Tamponade: Pathogenesis and Clinical Findings

Atherosclerosis - Pathogenesis

Atherosclerosis - Complications

Complications of Myocardial Infarction

myocardial-infarction-findings-on-investigations

myocardial-infarction-findings-on-physical-exam

MI Findings on History

Dilated Cardiomyopathy

Myocarditis

Restrictive Cardiomyopathy

Hypertrophic Cardiomyopathy

Left Heart Failure - Pathogenesis

Right Heart Failure

Left Heart Failure

Left Heart Failure - Physical Exam Findings

Left Heart Failure - Findings on History

pericarditis

Aortic Dissection

Aortic Stenosis - Pathogenesis and Clinical Findings

Aortic Regurgitation

Mitral Stenosis

Atrial Flutter

Ventricular fibrillation

1st Degree AV block

Second Degree Heart Block - Mobitz Type II - Pathogenesis and clinical findings

Atrial Fibrillation - Clinical Findings

atrial-fibrillation-complications

Second Degree Heart Block - Mobitz Type I (Wenckebach) - Pathogenesis and Clinical Findings

Third Degree (Complete) AV Block - Pathogenesis and Clinical Findings

Atrial Flutter (1)

Cardiogenic Shock

Distributive Shock

Obstructive Shock

Drugs used to treat shock

JVP-Physical Exam Features

jvp-kussmals-sign-explained

Pulsus Paradoxus

Complications of Measles Pathogenesis and Clinical Findings

Retroviral Infections Mechanisms of oncogenesis

Superficial Partial Thickness Burns - Pathogenesis and Clinical Findings

Complications of Burns

Acne Vulgaris

Androgenic Alopecia

Distinguishing between Benign and Malignant Pigmented Lesions

Seborrheic Keratosis

Basal Cell Carcinoma (BCC)

Squamous Cell Carcinoma (SCC)

Varicella Zoster (Chicken Pox)

Herpes Zoster (Shingles)

Pemphigus Vulgaris

Bullous Pemphigoid

Actinic Keratosis

Lichen Planus

Herpes Simplex Virus (HSV)

Herpes Simplex Virus (HSV)

1-and-2-syphilis-pathogenesis-and-clinical-findings

Scabies

DM I pathogenesis

Pathogenesis of Diabetes mellitus DM), Type II

Diabetic Ketoacidosis

Diabetic Polyneuropathy

GDM Complications

Hypoglycemia - Pathogenesis

Hypoglycemia - Clinical Findings and Complications

Diabetic Hypoglycemia

Acquired Disorders of Reduced Bone Strength - Pathogenesis

Primary Hypertriglyceridemia

Hypothyroidism

Hashimoto

Thyroiditis

Hyperfunctional

Central Adrenal Insufficiency - Pathogenesis and Clinical Findings

Clinical Findings of Androgen Deficiency

Hypocalcemia - Clinical Findings

Hypercalcemia - Clinical Findings

Etiologies and Physical Historical Signs of Upper GI Bleed

Infectious Large Bowel Diarrhea

Acetaminophen Overdose

Gall Bladder Disorders

Cholelithiasis

Cholestasis

signs of chronic liver disease

cirrhosis

Ascites Clinical Findings

AscitesComplications

viral hepatits

A1ATDeficiency

Hepatitis A (HAV) Infections

Hereditary hemochromatosis

Auto-immune Hepatitis

Primary Biliary Cirrhosis (PBC)

Primary Sclerosing Cholangitis (PSC)

Achalasia Pathogenesis and clinical findings

Gastroesophageal Reflux Disease (GERD) Pathogenesis and Clinical Findings

TRALI

Transfusion Associated Circulatory Overload (TACO)

Essential Thrombocytosis (ET)

Pathogenesis of thrombocytosis

Heparin Induced Thrombocytopenia

Immune thrombocytopenic purpura

hodgkin lymphoma - pathogenesis and clinical findings

Clinical Features to Describe Abnormal Lymph Nodes

Acute Myeloid Leukemia

Pathophysiology behind the leukemias

Multiple Myeloma

Overview of blood cell malignancies

Suspected Deep Vein Thrombosis

APS

TTP HUS

Polycythmia Vera

Polycythmia Overview

G6PD Deficiency

Sickle cell disease signs

Sickle cell disease

Hemolytic Anemia Signs and Symptoms

Anemia of Chronic Disease

Vitamin B12 Deficiency

Folate Deficiency

Pathogenesis of Beta Thalassemia

Beta Thalassemia Signs Symptoms Treatment

Alpha Thalassemia Pathogenesis

Iron Deficiency Anemia

CNVII_Bells Palsy

Trigger Finger

Dupuytren

Gonorrhea Pathogenesis

Cauda Equina Syndrome

Myelopathy

Radiculopathy

Spondylosis

Disc Herniations

Presentation of increased ICP

Pathogenesis of SAH

Side Effects of Opioid Medications

Non Neural Complications of Stroke

Giant Cell (Temporal) Arteritis - Pathogenesis and investigations

Giant Cell (Temporal) Arteritis - Clinical findings and Complications

Migraines and Auras Pathogenesis and Clinical Findings

Pain Pathways in the Head

Bacterial Meningitis Complications

Bacterial Meningitis Clinical Findings

Bacterial Meningitis Pathogenesis

Basal Ganglia in Huntingtons Disease

Huntingtons Disease Pathogenesis and Clinical Findings

Parkinsons Disease

Basal ganglia pathways

Lower Motor Neuron (UMN) Disease

Upper Motor Neuron (UMN) Disease

Dupuytren

Trigger Finger

Acute Compartment Syndrome

Chronic Exertional Compartment Syndrome

Patellofemoral Syndrome

Developmental Dysplasia of the Hip (DDH)

Adhesive Capsulitis

Scoliosis -Pathogenesis and Clinical Findings

Cauda Equina Syndrome

Myelopathy

Radiculopathy

Disc Herniations

Spondylolysis _and_Spondylolisthesis Pathogenesis and Clinical Findings

Representative X-ray appearance of a primary benign bone tumor

Benign Primary Bone Tumors - Pathogenesis of X-ray appearance

Representative X-ray appearance of a primary malignant bone tumor

Malignant Bone Tumors - Pathogenesis of X-ray appearance

MSK tumors complications

Avascular Necrosis - Pathogenesis and Clinical Findings

Pagets Disease Complications

Fracture Healing (and disruptors of this process)

Falls

Alcohol Use Disorder

SNRIs

Bupropion

SSRIs

MDD

BipolarDisorder

OCD

Panic Disorder

PTSD

Social Anxiety

Pathogenesis of Anxiety Disorders

3rd gen anti-psychotics

2nd generation antipsychotics

1st gen antipsychotics

Schizophrenia Pathogenesis and Clinical Findings

DSM - Axis to Formulation

Complications of Measles Pathogenesis and Clinical Findings

Kawasaki Disease

Physiologic Neonatal Jaundice

Group A Streptococci Pharyngitis Pathogenesis and Clinical Findings

AcuteOtitisComplications

Acute Otitis Media - Pathogenesis and Clinical Findings (in Children)

Asthma Exacerbation - Pathogenesis and Clinical Findings in Children

Tetralogy of Fallot-Pathogenesis & Clinical Findings

Transposition of the Great Arteries-Pathogenesis & clinical findings

21-Hydroxylase Deficiency-Pathogenesis and clinical findings

Hallux Valgus pathogenesis and clinical findings - August 15 2015

Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN) - Pathogenesis and Clinical Findings

Urticaria- Pathogenesis and Clinical Findings

High Anion Gap Metabolic Acidosis Pathogenesis

Underfill Edema Pathogenesis

Edema Pitting vs Non-pitting

Childhood Immunization Schedule-Why we immunize

Gastroenteritis-Pathogenesis and clinical findings

Hyperopia - Pathogenesis and Clinical Findings

Myopia - Pathogenesis and clinical findings

Presbyopia - Pathogenesis and clinical findings

Trachoma - Pathogenesis and clinical findings

Acute Infectious Mononucleosis-Pathogenesis and clinical findings

Age Related Macular Degeneration - Pathogenesis and clinical findings

Posterior Vitreous Detachment - Pathogenesis and clinical findings

FINAL - CREST Syndrome Pathogenesis and clinical findings

Eosinophillic Esophagitis -Kattab Yaman - Final For Publication

Raynaud Phenomenon Pathogenesis and Clinical Findings

Chan Richard - Underfill Edema - Final 210915

Pre-Renal Acute Kidney Injury Pathogenesis

High-AG Metabolic Acidosis Pathogenesis

Astigmatism Pathogenesis and Clinical Findings

Amblyopia Pathogenesis and clinical findings

Chemical Eye Injury Pathogenesis and clinical findings

Femoral Head Fracture Pathogenesis and clinical findings

PPROM - Pathogenesis and clinical findings

Septic arthitis pathogenesis and clinical findings

Family Med Slides Vitamin D Deficiency

Malignant Hyperthermia-Pathogenesis and clinical findings

Retinopathy of Prematurity - Pathogenesis and clinical findings

Orthostatic Hypotension-Pathogenesis and clinical findings

Stroke - Pathogenesis

Breast Cancer - Clinical findings

Splenomegaly - Pathogenesis and clinical findings

Chondrocalcinosis Calcium Pyrophosphate Dihydrate Deposition Disease

Graves' Disease Pathogenesis & Clinical Findings

sjogrensyndrome

Systemic Lupus Erythematosis SLE Musculoskeletal Manifestations

Hashimoto's Thyroiditis Natural History and Clinical Findings

Hashimoto's Thyroiditis Pathogenesis and Clinical Findings

Lacrimal Drainage System - Physiology

Ventricular Septal Defect (VSD)-Pathogenesis and clinical findings

Transfusion-associated Graft Versus Host Disease - Signs and Symptoms

Multiple sclerosis (MS)

Cataracts - pathogenesis and clinical findings

Keloid scar - pathogenesis and clinical findings

Overuse Tendinopathy -Pathogenesis and clinical findings

Wolff Parkinson White - Pathogenesis and clinical findings

Autonomic Dysreflexia - Pathogenesis and clinical findings

Acute Spinal Cord Injuries - Pathogenesis and clinical findings

Retinoblastoma - Pathogenesis and clinical findings

Alopecia Areata - Pathogenesis and clinical findings

Seasonal Affective Disorder - Pathogenesis and clinical findings v2

Yu, Y - Schizophrenia Pathogenesis and Clinical Findings - March 26 2016

Anterior Shoulder Dislocation - Pathogensis clinical and radiographic findings

Anterior Shoulder Dislocation - Pathogensis clinical and radiographic findings

Allergic Rhinitis - Pathogenesis and clinical findings

Allergic Rhinitis - Pathogenesis and clinical findings

Olfactory Dysfunction - Pathogenesis and clinical findings

Tinnitus

Acute Otitis Externa

Psoriasis: Pathogenesis and clinical findings

InfectiousFoodPoisoning

1st gen antipsychotics Translated

Anti-Psikotik Generasi Kedua: Mekanisme dan Efek Samping

2nd generation antipsychotics Translated

Anti-Psikotik Generasi Kedua (Atipikal): Mekanisme dan Efek Samping

Anti-Psikotik Generasi Ketiga: Mekanisme dan Efek Samping

1st gen antipsychotics Translated

2nd generation antipsychotics Translated

1st gen antipsychotics Translated

3rd gen anti-psychotics Translated

Schizophrenia Pathogenesis Translated

Pathogenesis of Anxiety Disorders Translated

SAD Gangguan Afektif Musiman Translated

PTSD Translated

Panic Disorder Translated

OCD Translated

Bipolar Disorder Translated

MDD Translated

SSRIs Translated

Bupropion Translated

SNRIs Translated

Thacker, J - Social Anxiety Translated

DSM - Axis to Formulation Translated

Alcohol Use Translated

Seasonal Affective Disorder: Pathogenesis and clinical findings

Seasonal Affective Disorder: Pathogenesis and clinical findings

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Isolated Neutropenia

Chorioamnionitis: Risk factors, pathogenesis and clinical findings

Placental Complications During Labour

Placental Complications During Labour

Acute Rheumatic Fever- Pathogenesis and Clinical Findings

Opioid Receptor Agonists

Pharmacokinetics Basic Principles

Pharmacodynamics Basic Principles

Opioid Receptor Agonists

Peds Sexual Abuse

Peds Sexual Abuse

Onset of Labour- Pathophysiology

Stages of Labour- Mechanisms

Dilatation and Curettage - Complications

myasthenia-gravis-final

horner-syndrome

Focal Seizures in the adult: Pathogenesis and Clinical Findings

Macrosomia: Maternal Complications

Pediatric Uncompensated Shock: pathogenesis and clinical findings

Type 1 Respiratory Distress Syndrome

acute-closed-angle-glaucoma

aids-and-cmv-retinitis

keratoconus

onchocerciasis

primary-open-angle-glaucoma

secondary-glaucoma

opioid-withdrawal

keratoconus

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retinitis-pigmentosa-final

xerophthalmia-final

allergic-contact-dermatitis

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cardio_lbbb_oct-15

cardio_rbbb_oct-15

cardio_ant-and-post-fascicular-blocks_oct-15

allergic-contact-dermatitis

Nephritic Syndrome: Pathogenesis and clinical findings

nephritic-syndrome

nephritic

Opioid Receptor Agonists

refeeding syndrome

Breast Cancer Risk Factors Causes and Types

Hyperosmolar Hyperglycemic State

cholesteatoma-nov-4-2016_final-edits

Ketamine

Neurotransmitters and Pharmacology behind Nausea and Vomiting

Neurotransmitters and Pharmacology behind Nausea and Vomiting

Neurotransmitters and Pharmacology behind Nausea and Vomiting

pathogenesis-of-neuropathic-pain

bn-pathogenesis

bn-signs-and-symptoms

bn-complications

Small Bowel Bacterial Overgrowth: Pathogenesis and clinical findings

slide1

menstrual-cycle-physiology-the-hypothalamic-pituitary-ovarian-axis

menstrual-cycle-physiology-correlating-the-ovarian-and-uterine-cycles

menstrual-cycle-physiology-ovarian-cycle-follicular-phase-explained

menstrual-cycle-physiology-ovarian-cycle-ovulation-explained

menstrual-cycle-physiology-ovarian-cycle-luteal-phase-explained

menstrual-cycle-physiology-the-uterine-cycle

Shoulder Dystocia: Pathogenesis and Clinical Findings

lvh-final

anorexia-nervosa

an-signs-and-symptoms

an-complications-final

als-final

alzheimers-disease-final

lewy-body-dementia-final

als-final

als-final

NSAIDs Final

NSAIDs Final

induction-of-labour-indications-and-contraindications

Stress Fracture v.5

Placenta Accreta

GDM: Risk factors and pathogenesis

BPH Final

BPH Final

ASPD FINAL

BPD FINAL

NPD FINAL

Lithium FINAL

AF FINAL

generalized-seizures-definitions

Lateral Medullary Syndrome FINAL

Subdural hematoma FINAL

Staphylococcus Scalded Skin Syndrome FINAL

Manion contraception MOAs

Manion contraception MOAs2

Common meds contra in Preg

Non hormonal

Vasa Previa

ASPD FINAL

hypertension-in-pregnancy-overview-of-definitions

Yu Yan - Pre-eclampsia pathogenesis - publish

Yu Yan - Pre-eclampsia Maternal Complications - publish

Yu Yan - Pre-eclampsia Fetal Complications - publish

Altered Metabolism in the ICU

Altered Metabolism in the ICU- Pathogenesis and clinical findings

Mental Status Exam

Addiction Long-term Consequences

Addiction Pathogenesis

Non-accidental Burns

SLE-GI Manifestations

Testicular Torsion

Acquired Hydrocephalus

Kawasaki Disease

Secondary Hemostasis: Coagulation Cascade

systemic-lupus-erythematosus-gastrointestinal-manifestations

Critical Care Malnutrition

esophageal-gastric-varices

localized-pitting-edema

Neurotransmitters-and-Pharmacology-behind-Nausea-and-Vomiting - IN

chronic-hypertensive-retinopathy-pathogenesis-and-clinical-findings

central-retinal-artery-occlusion-pathogenesis-and-clinical-findings

Fragile X Syndrome

Attention Deficit Hyperactivity Disorder (ADHD)

Oppositional Defiant Disorder (ODD)

Conduct Disorder (CD)

Down Syndrome

infectious-esophagitis-pathogenesis-and-clinical-findings

The Neuroanatomy and Physiology of Emotion

Serotonin Syndrome Pathogenesis and Clinical Findings

Side Effects of ACEi/ARBs During Pregnancy

Side Effects of Methimazole During Pregnancy

Side Effects of NSAIDs During Pregnancy

Side Effects of Valproic Acid During Pregnancy

Side Effects of Warfarin During Pregnancy

Pediatric Parasomnias and Nightmares: Pathogenesis and clinical findings

Hemolytic Disease of the Fetus and Newborn

Trigeminal Neuralgia

Mallory-Weiss Tear

Unconjugated Neonatal Hyperbilirubinemia - Complications

pathogenesis-of-select-causes-of-constipation-in-adults-and-in-elderly

1st gen antipsychotics (Slovenian translation) - FINAL VERSION

2nd gen antipsychotics (Slovenian translation) - FINAL VERSION

3rd gen antipsychotics (Slovenian translation) - FINAL VERSION

Alcohol Use Disorder (Slovenian translation) - FINAL VERSION

BMR (Slovenian translation) - FINAL VERSION

Bupropion (Slovenian translation) - FINAL VERSION

NAT), ki proizvaja aktivne metabolite. Natan'6en mehanizem delovanja (se) ni znan. znak/simptom/laboratorijska najdba DA in NE posledi6no ostaneta v sinapsah dlje Casa in okrepita 2iv6ni prenos neieleni udnki glavobol suha usta 4, tel. tee nespeEnost slabost zaprtie tahikardija epileptiEni napadi faringitis omotica hipertenziia agitacija prevedel in priredil: Jan Kejiar, dr. med., specializant psihiatrije pregledala: doc. dr. Brigita Novak Sarotar, dr. med., spec. psih. eliminacija poteka preko jeter in ledvic prilagoditev odmerka v primeru bolezni jeter in/ali ledvic bupropion lahko inhibira jetrni citokrom P4502D6 in povzrod interakcije med zdravili kontraindiciran pri boleznih, ki zmanIgajo epileptogeni prag: anoreksija/bulimija nervoza, epilepsija, odtegnitev alkohola, odtegnitev benzodiazepinov zaplet Objavljeno 30. junija 2017 na www.thecalgaryguide.com. " title="Bupropion (atipiEni antidepresiv): Mehanizem delovanja in neieleni utinki potenten antidepresiv v monoterapiji all kot dodatno zdravilo pri zdravljenju razpoloienjskih motenj okrajgave: 5-HT - serotonin DA - dopamin DAT - prenagalec DA NA - noradrenalin NAT - prenagalec NA SSRI - selektivni zaviralec ponovnega privzema 5-HT Legenda: bupropion farmakologija antidepresivni udnki uporaben pri zdravljenju "zmaniganega pozitivnega afekta" nima pomembnelgih 5-HT udnkov povzraa spolne disfunkcije v primerjavi s SSRI; lahko celo odpravi omenjeni neieleni udnek (povzraen s strani SSRI) dodatek pri zdravljenju odvisnosti od nikotina preko T iive'nega prenosa DA v nagrajevalni poti energije preko T 2ivbega prenosa NA patofiziologija mehanizem farmakokinetika farmakodinamika avtorica: JoAnna Fay, Sara Meunier pregledala: Jojo Jiang, Alexander Arnold, Aaron Mackie* * dr. med. ob objavi Nizkoafiniteten zaviralec ponovnega privzema DA in NA (DAT>NAT), ki proizvaja aktivne metabolite. Natan'6en mehanizem delovanja (se) ni znan. znak/simptom/laboratorijska najdba DA in NE posledi6no ostaneta v sinapsah dlje Casa in okrepita 2iv6ni prenos neieleni udnki glavobol suha usta 4, tel. tee nespeEnost slabost zaprtie tahikardija epileptiEni napadi faringitis omotica hipertenziia agitacija prevedel in priredil: Jan Kejiar, dr. med., specializant psihiatrije pregledala: doc. dr. Brigita Novak Sarotar, dr. med., spec. psih. eliminacija poteka preko jeter in ledvic prilagoditev odmerka v primeru bolezni jeter in/ali ledvic bupropion lahko inhibira jetrni citokrom P4502D6 in povzrod interakcije med zdravili kontraindiciran pri boleznih, ki zmanIgajo epileptogeni prag: anoreksija/bulimija nervoza, epilepsija, odtegnitev alkohola, odtegnitev benzodiazepinov zaplet Objavljeno 30. junija 2017 na www.thecalgaryguide.com. " />

PTSD (Slovenian translation) - FINAL VERSION

Lipid Physiology Slide

Subtrochanteric Femur Fracture

Ovarian Torsion

Non-Hodgkin Lymphoma

Pelvic Inflammatory Disease

Pituitary Mass Effects

10mm on MRI) vomiting Giant adenoma Extension into hypothalamus —1■• Damage to hypothalamic cells Hypothalamic (>40mm on MRI) dysfunction Obstruction of dopamine Superior tumor growth Impingement of the optic chiasma Bitemporal Loss of pituitary hemianopsia hormones ICP Suprasellar extension Occlusion of ventricles Obstruction of CSF Flow Hydrocephalus Lateral tumor growth Impingement of cranial nerves 3, 4, 5 (V1/V2) and 6 4 Pituitary stalk impingement Diplopia Inferior tumor growth Erosion into sphenoid sinus CSF leak into throat Post-nasal Obstruction of ADH drip Communication between sinus and brain Migration of bacteria from sinus flora Hyper-Diabetes Meningitis prolactinemia insipidus Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published October 1 2017 on www.thecalgaryguide.com " title="Pituitary Mass Effects Note: pituitary tumors are almost always a benign adenoma. Pituitary adenomas are very common -approximately 1 in 6 individuals. These are usually asymptomatic and are found incidentally. Symptomatic pituitary adenomas that require treatment are much less common and affect approximately 1 in 1000 individuals. Pituitary tumor Note: typically (but not always) the anterior hormones will be lost in the following order; GH, LH, FSH, TSH, ACTH, PRL. This order (with the exception of prolactin) is the order of least-essential to most-essential hormones needed for survival. A good mnemonic to remember the order the hormones are is, "Go Look For The Adenoma Please". Legend: Note: for pituitary masses of all sizes, it is important to determine whether the pituitary tumor is secreting (70%) or non-secreting (30%) as secreting tumors can be targeted with medication. The most common secreting tumors secrete prolactin (most common), growth hormone, and ACTH. Authors: Chris Oleynick Reviewers: Amyna Fidai Laura Byford-Richardson Joseph Tropiano Hanan Bassyouni* * MD at time of publication Microadenoma Small size is unlikely to cause mass effects (<10mm on MRI) Asymptomatic Macroadenoma Large size may press on surrounding structures, causing mass effects Headaches Stretching of the meninges Activation of mechanoreceptors Nausea and (>10mm on MRI) vomiting Giant adenoma Extension into hypothalamus —1■• Damage to hypothalamic cells Hypothalamic (>40mm on MRI) dysfunction Obstruction of dopamine Superior tumor growth Impingement of the optic chiasma Bitemporal Loss of pituitary hemianopsia hormones ICP Suprasellar extension Occlusion of ventricles Obstruction of CSF Flow Hydrocephalus Lateral tumor growth Impingement of cranial nerves 3, 4, 5 (V1/V2) and 6 4 Pituitary stalk impingement Diplopia Inferior tumor growth Erosion into sphenoid sinus CSF leak into throat Post-nasal Obstruction of ADH drip Communication between sinus and brain Migration of bacteria from sinus flora Hyper-Diabetes Meningitis prolactinemia insipidus Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published October 1 2017 on www.thecalgaryguide.com " />

Acute Chest Syndrome (Sickle Cell Disease)

tetanus

Anaphylaxis - Pathogenesis

Ischemia: Pathogenesis of Cellular Injury and Death

Hepatitis C (HCV) Infections: Explaining Serology Patterns

Hepatitis C (HCV) Infection: Explaining Serology Patterns

Medical Conditions Causing Mania or Mania-Like Episodes: Pathogenesis

Left Heart Failure: Pathophysiology (Neurohormonal Activation)

Primary Spontaneous Pneumothorax: Pathogenesis and clinical findings

Anksiozne motnje: patogeneza tesnobe

Depresivna epizoda/motnja: patogeneza in klinične najdbe

Obsesivno-kompulzivna motnja: patogeneza in klinične najdbe

Panična motnja: patogeneza in klinične najdbe

Sezonska depresivna motnja: patogeneza in klinične najdbe

Shizofrenija: patogeneza in klinične najdbe

Serotoninski sindrom: patogeneza in klinične najdbe

Zaviralci privzema serotonina in noradrenalina (SNRI): mehanizem delovanja in neželeni učinki

Socialna anksiozna motnja: patogeneza in klinične najdbe

Selektivni zaviralci privzema serotonina (SSRI): mehanizem delovanja in neželeni učinki

Nevroanatomija in fiziologija čustev

Diabetic Foot: Pathogenesis and clinical findings

Classification of Pelvic Ring Fractures: Mechanisms, Clinical Features and Complications

Open Fractures: Mechanisms, Clinical Features and Complications

10 cm 4, Extensive contamination Extensive comminution Type IIIA Adequate soft tissue for bone coverage Legend: Pathophysiology Mechanism Complications Open wound Contusion/Blisters Compartment syndrome Bone tenting or protruding through a wound Loss of distal pulses Amputation Type IIIC Vascular injuries, possible amputation • Type IIIB ++ soft tissue damage with periosteal stripping Sign/Symptom/Lab Finding Non- union Deep Vein Thrombosis Delayed union Infection Authors: Meaghan MacKenzie Reviewers: Annalise Abbott Usama Malik Dr. Prism Schneider* * MD at time of publication " title="Open Fractures: Mechanisms, Clinical Features and Complications Inability to weight bear Limb length discrepancy • Loss of sensation distally Deformity Gustilo-Anderson Classification Type I Wound < 1cm Typically "inside out" injury Yir Minimal comminution Type II Wound 1-10 cm 4, Possible tissue contamination Moderate comminution Note: • Open fractures can occur with low risk mechanism, typically with diseased bone Legend: *Motor cycle/car crashes, pedestrian vs. car, gun shot Direct, high energy force* Open Fractures Fractures with varying degrees of comminution Type Ill Yir Wound >10 cm 4, Extensive contamination Extensive comminution Type IIIA Adequate soft tissue for bone coverage Legend: Pathophysiology Mechanism Complications Open wound Contusion/Blisters Compartment syndrome Bone tenting or protruding through a wound Loss of distal pulses Amputation Type IIIC Vascular injuries, possible amputation • Type IIIB ++ soft tissue damage with periosteal stripping Sign/Symptom/Lab Finding Non- union Deep Vein Thrombosis Delayed union Infection Authors: Meaghan MacKenzie Reviewers: Annalise Abbott Usama Malik Dr. Prism Schneider* * MD at time of publication " />

Bronchogenic Carcinoma - Pancoast Tumors Pathogenesis and clinical findings

Polycystic Ovarian Syndrome

Nitrous Oxide

Hyperthyroidism

Hyperthyroidism

Growth Hormone Excess

Asthma Acute Exacerbation: Pathogenesis and Treatment

Bronchiectasis Pathogenesis and clinical findings

Chronic Thromboembolic Pulmonary Hypertension (CTEPH) Pathogenesis

Lung cancer clinical findings and paraneoplastic syndromes

Impetigo Pathogenesis and clinical findings

Pressure Ulcers Pathogenesis and clinical findings

Benign Prostatic Hyperplasia: Pathogenesis and medications

Erectile Dysfunction: Pathogenesis

Mixed Urinary Incontinence Pathogenesis and clinical findings

Penyembuhan Luka Akut: Patogenesis dan Temuan Klinis

Penyembuhan Fraktur: Tahapan dan Faktor Pengganggu

RICE: Mekanisme Aksi

Hemostasis Sekunder: Kaskade Koagulasi

Fisiologi sistem Renin-Angiotensin-Aldosteron (RAAS)

Gradien pO2 Alveolus-arteri: Mengapa ada, dan mengapa penting

15 mmHg) selalu menjadi tanda patologis (lihat slide terkait) Penulis: Yan Yu Penyunting: Steven Liu Amogh K. Agrawal Juri Janovcik* Penerjemah: M Harmen Reza S* * MD (dokter) pada saat publikasi Catatan: Gradien A-a yang terlalu tinggi menjadi indikasi adanya masalah dengan difusi udara antara alveolus & kapiler pulmoner " title="Gradien pO2Alveolus-arteri: Mengapa ada, dan mengapa penting Singkatan kunci: • p02: tekanan parsial 02, atau "konten 02". • Pa02: tekanan parsial 02 di arteri. Diukur secara langsung via analisa gas darah (AGD) arteri. • PA02: tekanan parsial 02 di Alveolus. (Tidak dapat langsung diukur, harus melalui perhitungan). Secara teori, pada kapiler paru yang bersebelahan dengan alveolus: 02 berdifusi dari alveolus menuju kapiler paru, dan tidak ada 02 yang hilang dari darah sampai darah mencapai arteri sistemik— maka harusnya Pa02 setara dengan PA02. 1 Tetapi dalam realitanya Darah di dalam kapiler paru sejak awal tidak sepenuhnya teroksigenasi Gravitasi menyebabkan lebih banyak darah menuju basis (dasar) paru, sehingga menyebabkan terlalu banyak darah untuk dapat sepenuhnya teroksigenasi oleh alveolus Darah yang kurang teoksigenasi dari basis paru menurunkan keseluruhan p02 darah Catatan: beberapa patologi respiratorik dapat memiliki gradien A-a normal (lihat slide terkait) Legenda: Definisi Penjelasan Darah yang kurang teroksigenasi dari vena sistemik bercampur dengan darah yang teroksigenasi dari paru ("Venous admixture"): Drainase vena dari sirkulasi bronkial bercampur dengan darah yang teroksigenasi pada kapiler paru Beberapa vena pada sirkulasi koroner bermuara menuju atrium kiri, bukan menuju sinus koroner/atrium kanan .111••••■• Maka dari itu, konten 02 darah ketika mencapai arteri sistemik (Pa02) lebih rendah dibandingkan dengan konten 02 pada alveolus (PA02) PA02 - Pa02 = "gradien" p02 antara alveolus dan arteri sistemik Gradien A-a normal: <15 mmHg Tanda/Gejala/Penunjang Gradien A-a tinggi (>15 mmHg) selalu menjadi tanda patologis (lihat slide terkait) Penulis: Yan Yu Penyunting: Steven Liu Amogh K. Agrawal Juri Janovcik* Penerjemah: M Harmen Reza S* * MD (dokter) pada saat publikasi Catatan: Gradien A-a yang terlalu tinggi menjadi indikasi adanya masalah dengan difusi udara antara alveolus & kapiler pulmoner " />

Gradien pO2 Alveolus-arteri: Penjelasan rumus (Penjelasan ringkas)

Gradien pO2 Alveolus-arteri: Penjelasan rumus (Penjelasan secara ilmiah)

Acetylcholinesterase Inhibitors

Anticholinergics

non-depolarizing-neuromuscular-blocks-ndnmbs

Propofol

Succinylcholine

Volatile Gases

non-depolarizing-neuromuscular-blocks-ndnmbs

Succinylcholine

Clavicular Fracture: Pathogenesis and clinical findings

Pediatric Pneumonia: Pathogenesis and clinical findings

Radiological findings of child abuse

Non-Accidental Head Trauma

Duchenne Muscular Dystrophy

Acquired Inguinal Hernias: Indirect + Direct

Celiac Disease: Pathogenesis and clinical findings

Celiac Disease: Complications

Orofacial Clefts cleft lip cleft palate

Cerebral Palsy clinical findings

Developmental Coordination Disorder

Sudden Infant Death Syndrome SIDS Triple Risk Model

Aplastic Anemia: Pathogenesis and Clinical Findings

Feedback Loops Growth Hormone

Kallmann Syndrome and Normosmotic Idiopathic Hypogonadotropism: Pathogenesis and Clinical Findings

Posterior Cruciate Ligament (PCL) Injury Pathogenesis and Clinical Findings

Feedback Loop: Adrenocorticotropic Hormone (ACTH)

Feedback Loop- Thyroid Stimulating Hormone (TSH)

Anaphylaxis: Signs and Symptoms

Giant Cell Arteritis: Pathogenesis and Clinical Findings

Acute Hemolytic Transfusion Reaction: Signs and Symptoms

Anaphylaxis: Treatments

Glucocorticoid Induced Osteoporosis: Pathogenesis and Clinical Findings

intrauterine-growth-restriction-iugr-pathogenesis

fetal-alcohol-spectrum-disorder-pathogenesis-and-clinical-findings

Hydrocephalus: Clinical Findings

Orbital Cellulitis: Pathogenesis and clinical findings

Periorbital Cellulitis: Pathogenesis and Clinical Findings

Child Abuse: Risk Factors and Possible Indicators

Circle of Willis: Anatomy and Physiology

Mastoiditis: Pathogenesis and clinical findings

Scarlet Fever: Pathogenesis and clinical findings

Sinusitis: Pathogenesis and clinical findings

Tonsillitis: Pathogenesis and clinical findings

Stomach Acid Reducing Medications - Mechanisms of Action

Dependent Personality Disorder Slide - Pathogenesis and clinical findings

Obsessive-Compulsive Personality Disorder Slide - Pathogenesis and clinical findings

Brain Death: Pathogenesis assessment and clinical findings

Benefits of Breast Milk: Mechanism of Action

Major Depressive Disorder: Complications

Avoidant Personality Disorder - Pathogenesis and clinical findings

Measures of Population Health

Employment as a Determinant of Health

Menopause contraindications to hormone replacement therapy

Phenylketonuria (PKU): Pathogenesis and clinical findings

Feedback Loop: Prolactin (PRL)

Vesicoureteric reflux (VUR): Pathogenesis and clinical findings

IVH Intraventricular Hemorrhage in Preterm Infants - Pathogenesis

Prader Willi syndrome: pathogenesis and clinical findings

Anticonvulsants as Mood Stabilizers: Mechanism and Side-effect

Benzodiazepine (BZD) withdrawal: clinical findings and complications

Benzodiazepines: Mechanism of Action and Side Effects

Schizotypal Personality Disorder (SPD): Pathogenesis and clinical findings

Boutonniere Deformity: Pathogenesis and Complications

menstrual-cycle-physiology-ovarian-cycle-brief-overview

Complex Regional Pain Syndrome: Pathogenesis and clinical findings

Microangiopathic Hemolytic Anemia: Pathogenesis and clinical findings

Neurogenic Claudication: Pathogenesis and Clinical Findings

Atopic Dermatitis: Pathogenesis and Clinical Findings

Rosacea: Pathogenesis and Clinical Findings

Hepatic Encephalopathy: Pathogenesis and Clinical Findings

Hypernatremia Physiology

Hyponatremia- Physiology

Coronary anatomy on ECG- Localizing Ischemia

Patent Ductus Arteriosus (PDA)- Pathogenesis and Clinical Findings

Arterial Insufficiency- Signs and symptoms

Venous insufficiency- Signs and symptoms

Takotsubo Cardiomyopathy- Pathogenesis and clinical findings

Meralgia paresthetica- Pathogenesis and Clinical Findings

Simple Febrile Seizure- Pathogenesis and clinical findings

Reactive Neutrophilia- Pathogenesis and Clinical Findings

Hypoxemia- Pathogenesis and clinical findings

Bronchopulmonary Dysplasia (BPD)- Pathogenesis and clinical findings

Neuromuscular Junction (NMJ)- Physiology and pharmacology

Biliary Atresia (BA)- Pathogenesis and clinical findings

Inflammatory-Cascade-Pathogenesis-and-Clinical-Findings

Sepsis, and Septic Shock- Pathogenesis and Clinical Findings

adrenergic-agonists-for-treating-hypotensionlow-blood-pressure

Hyperkalemia- Physiology

Torsades de Pointes (TdP)- Pathogenesis and Clinical Findings

Shoulder Dystocia: Complications

Primary Myelofibrosis pathogenesis and clinical findings

Hemorrhoids - Pathogenesis and Clinical Findings

gastroesophageal-reflux-disease-gerd-complications

autosomal-dominant-polycystic-kidney-disease-adpkd

Rickets and Osteomalacia: Pathogenesis and Clinical Findings

Polyarteritis Nodosa (PAN): Pathogenesis and Clinical Findings

dermatomyositis-dm-and-polymyositis-pm-pathogenesis-and-clinical-findings

DiGeorge Syndrome: Pathogenesis and Clinical Findings

Molluscum Contagiosum: Pathogenesis and Clinical Findings

acute-somatic-pain

Small Bowel Infarction

Crohn's Disease

Hemophilia

Signs and Symptoms of Pulmonary Embolism

Hemolytic Anemia - Pathophysiology

Wilson's Disease

chronic-myeloid-leukemia

Secondary Polycythemia

Acute Lymphoblastic Leukemia

Ulcerative Colitis

HBV Serology

Chronic Lymphocytic Leukemia

perforated-viscous

acanthosis-nigricans-pathogenesis-and-clinical-findings

HELLP syndrome pathogenesis and clinical findings

Lyme Disease Pathogenesis and Clinical Findings

intraventricular-hemorrhage-in-preterm-infants-clinical-findings-and-complications

Vitamin K Deficiency

Normocytic Anemia

Appendicitis

Acute GI Related Abdominal Pain

Operative vaginal delivery Complications of Vacuum

Ataxia Telangiectasia Pathogenesis and Clinical Findings

Diverticulosis and Angiodysplasia

Erythema Nodosum pathogenesis and clinical findings

Colorectal Carcinoma pathogenesis and clinical findings

iga-vasculitis-henoch-scholein-purpura-pathogenesis-and-clinical-findings

Negative-Pressure-Pulmonary-Edema

Thrombotic Thrombocytopenic Purpura-Hemolytic Uremic Syndrome (TTP-HUS): Pathogenesis and clinical findings

Acute-diverticulitis

virchows-triad-and-deep-vein-thrombosis-dvt

Acute-Pancreatitis

Peptic Ulcer Disease

Rapid Sequence Induction and Intubation (RSII): Clinical Approach

Priapism

Infantile Colic

Macrosomia-Fetal-Complications

intrauterine-devices-iuds-mechanism-of-action

X-linked Severe Combined Immunodeficiency (SCID)

Ischemic Colitis

Incisional-Hernia

Endometritis

Hydrocele

Varicocele

Aphasia

Slide-authoring-process-FINAL-2

A1AT-Deficiency

Viral-Hepatitis

Multiple-Myeloma

Pathophysiology-Behind-the-Leukemias

Aqueous-Humor-Production-and-Drainage

Innate-Immune-Response

vomiting-pathogenesis

Pseudogout

C5-C9-deficiency

tinea-capitis-tinea-corpora-and-tinea-pedis

Brain-Neoplasms

Umbilical-Cord-Prolapse

mechanisms-of-opioid-analgesia-in-the-peripheral-nervous-system

pharmaceuticals-under-investigation-by-who-for-treating-covid-19-proposed-mechanisms

GI-changes-during-pregnancy

Fecal-Incontinence

Placenta-Previa

Humoral-Immunity

Diabetic-Nephropathy

Infarctus du myocarde: Antécédents médicaux

Marfan-Syndrome

GU-changes-in-pregnancy

Retinal-Detachment-Pathogenesis

Retinal-Detachment-Clinical-Findings