SEARCH RESULTS FOR: shock

Cardiogenic Shock

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Drugs used to treat shock

Pediatric Uncompensated Shock: pathogenesis and clinical findings

Tonsillitis: Pathogenesis and clinical findings

Tonsillitis: Pathogenesis and clinical findings Group A Streptococci (GAS) infection1,2 Authors: Amanda Marchak Reviewers: Nicola Adderley Jim Rogers Danielle Nelson* * MD at time of publication Viral pathogen1 5-15 years3 Pathogen colonizes the nasopharynx Pathogen colonizes oropharynx4 ** ↑ vascular permeability Leakage of protein and fluid into surrounding tissue Inflammatory cytokine release Inadvertent cellular injury and hemolysis Tonsillar petechiae and erythema Systemic inflammatory cytokines disrupt hypothalamic regulation Fever White blood cell (WBC) activation WBCs infiltrate site of infection WBCs kill pathogen Accumulation and deposition of cellular debris and products of inflammatory response Tonsillar exudate Note: *When GAS is the pathogen, cytokine release and WBC activation is secondary to the release of exotoxins by GAS. Swelling and irritation ↑ lymph drainage to regional nodes Enlarged anterior cervical nodes Cough Note: It is extremely important to distinguish between viral tonsillitis and bacterial tonsillitis. Viral tonsillitis is usually self-limited while GAS tonsillitis can be associated with a number of complications. Notes: Tonsillar tissue Tonsillar edema Nasal tissue6 Nasal congestion Coryza Nasal discharge irritates back of throat Complications5: Peritonsillar abscess, neck abscess, otitis media, sinusitis, pneumonia, scarlet fever, bacteremia, osteomyelitis, meningitis, arthritis, erythema nodosum, hepatitis, acute poststreptococcal glomerulonephritis, acute rheumatic fever, and toxic shock syndrome 1. In general, viral tonsillitis is more common than GAS infection. However, in the absence of cough and coryza (acute, isolated tonsillitis), GAS is more common. 2. While GAS is the most bacterial cause of tonsillitis, it can be caused by other pathogens. 3. GAS tonsillitis is most common in patients of this age group although, rarely, it can occur in adults. 4. When GAS colonizes the oropharynx, the primary location of infection determines how it’s identified. • tonsils primarily effected = tonsillitis • pharynx (throat) primarily effected = pharyngitis (See slide on Group A Streptococci Pharyngitis: Pathogenesis and Clinical Findings) • both = pharyngotonsillitis 5. The listed complications are the result of exotoxins entering systemic circulation or the bacterial infection extending beyond the tonsils. 6. While viral tonsillitis tends to be associated with more upper respiratory tract symptoms, clinical signs and symptoms are NOT reliable for diagnosing GAS tonsillitis. Throat swab or rapid antigen detection test are the standards for diagnosis. Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published November 5, 2018 on www.thecalgaryguide.com

Hypernatremia Physiology

Hypernatremia: Physiology Unreplaced H2O loss Hypodipsia H2O shift into cells Severe exercise, electroshock induced seizures Transient ↑ cell osmolality Na+ overload Inappropriate IV hypertonic solution, salt poisoning Abbreviations: H2O: Water GI: Gastrointestinal DM: Diabetes Mellitus DI: Diabetes Insipidus Na+: Sodium ion IV: Intravenous ADH: Antidiuretic Hormone LOC: Level of Consciousness Skin Sweat, burns GI Vomiting, bleeding, osmotic diarrhea Fluid [Na+] < serum [Na+] ↑ H2O loss compared to Na+ loss Renal DM, Mannitol, Diuretics Absent thirst mechanism Hypothalamic lesion impairs normal drive for H2O intake Nephrogenic ↑ renal resistance to ADH H2O Deprivation Test + no AVP response ↓ access to H2O DI Central ↓ ADH secretion H2O Deprivation Test + AVP response ↑ [Na+] 10- 15 mEq/L within a few minutes Weakness, irritability, seizures, coma ↑ thirst, ↓ urinary frequency and volume Note: Hypernatremia Serum [Na+] > 145 mmol/L Intracranial hemorrhage Headache, vomiting, ↓ LOC • Plasma [Na+] is regulated by water intake/excretion, not by changes in [Na+]. • Effects on plasma [Na+] of IV fluids or loss of bodily fluids is determined by the tonicity of the fluid, not the osmolality. Authors: Mannat Dhillon Reviewers: Andrea Kuczynski Kevin McLaughlin* * MD at time of publication Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published January 11, 2019 on www.thecalgaryguide.com

Takotsubo Cardiomyopathy- Pathogenesis and clinical findings

Takotsubo Cardiomyopathy- Pathogenesis and clinical findings emotional physical stresses other neurologic endocrine drug brain natriuretic peptide coronary artery disease takotsubo catecholamine release stimulation Beta receptors ionotropic effect alpha receptors coronary vessels metabolic contraction band necrosis edema inflammatory cell infiltration localized fibrosis coronary vasospasm microvascular dysfunction decrease oxygen supply relative to demand hypo-contraction ballooning left ventricular apex chest pain troponin BNP elevation ST ECG changes absence of obstructive CAD transient left ventricle systolic dysfunction dyskinetic apex Mitral regurgitation ventricular thrombus cardiac output low dyspnea syncope heart failure cardiogenic shock echocardiogram apex Gu gagnon Ryznar Waechter

Sepsis, and Septic Shock- Pathogenesis and Clinical Findings

Sepsis, and Septic Shock: Pathogenesis and Clinical Findings Authors: Daniel J. Lane Simonne Horwitz Reviewers: James Rogers Emily Ryznar Braedon McDonald* Christopher Doig* *MD at time of publication Sepsis Pathogen (Bacteria, Fungi, Virus, or Parasite) Comorbidities Immunosuppression or ↑ susceptibility (e.g. splenectomy) Pathogen virulence Invasion and host immune avoidance Vulnerable infection site ↑ likelihood of spread of infection & mortality Genetics ↑ Sensitivity of innate immune response Community acquired Hospital acquired Infection of host Innate immune response Fever, Leukocytosis/ Leukopenia, Left Shift/ Bandemia Compensatory response Tachypnea, Altered Level of Consciousness, Hypotension ↓ perfusion and oxygen delivery to organs Dysregulated Host Response Pro- and anti-inflammatory response Life-threatening organ dysfunction caused by a dysregulated host response to infection The Sequential Organ Failure Assessment (SOFA) or quick SOFA (qSOFA) Scores may be used to assess mortality risk Respiratory ↓ PaO2 / FiO2 (mmHg) Nervous ↓ Level of consciousness Septic Shock Cardiovascular ↓ Mean Arterial Pressure Organ Dysfunction Liver ↑ Bilirubin Kidney ↑ Creatinine, Acute oliguria Coagulation Thrombocytopenia, ↑ INR or aPTT Require vasopressors to ↑ mean arterial pressure Persistent hypotension despite adequate fluid resuscitation ↓ Mean Arterial Pressure (< 65 mmHg), ↑ Lactate (> 2 mmol/L) Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published February 12, 2019 on www.thecalgaryguide.com

Ischemic Colitis

Ischemic Colitis: Pathogenesis and clinical findings Superior and inferior mesenteric arteries (SMA and IMA) supply blood to colon Surgical repair of aorta Borders of SMA and IMA collaterals at the splenic flexure and rectosigmoid junction are vulnerable to ischemia (“watershed” areas) Atherosclerosis and narrowing of mesenteric arteries Low flow state (e.g., CHF, hypotension, arrhythmia) Underlying CAD/PVD Atrial fibrillation, endocarditis Embolic arterial occlusion of SMA and/or IMA Trauma, infection, clotting abnormalities Mesenteric vein thrombosis Vascular risk factors (e.g., smoking, hypertension) Thrombotic arterial occlusion of SMA and/or IMA Endograft coverage of IMA Nonocclusive hypoperfusion Inadequate blood flow to meet the cellular metabolic needs in the colon Ischemic Colitis Tachypnea Tachycardia Hyperthermia Hypotension Ischemic period Loss of oxygen and nutrients to bowel Reperfusion period Influx of O2àreacts to produce more oxygen free radicals Lipid peroxidation Systemic inflammatory response syndrome* Nausea and vomiting Abdominal pain (generally left sided) Peritonitis Leukocytosis Systemic shock (inadequate perfusion to tissue) Author: Audrey Caron Michael Blomfield Reviewers: Tony Gu Yan Yu* Edwin Cheng* * MD at time of publication Systemic shock (inadequate perfusion to body tissue) Hematochezia (Bloody stool) Gangrene (tissue death) Hemorrhage Tissue damage/cell death (starting from mucosa and submucosa going outwards to serosa) Mucosal ulceration Colonic inflammation Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published November 10, 2019 on www.thecalgaryguide.com

Hereditary Hemorrhagic Telangiectasia (Osler-Weber-Rendu disease)

Hereditary Hemorrhagic Telangiectasia (Osler-Weber-Rendu disease): Pathogenesis and Clinical Findings Inherited or de novo mutation in the ACVRL1, ENG, or Smad4 genes Abnormal signalling within the transforming growth factor ß (TGF-ß) pathway Unclear mechanismsàInability of vascular mural cells to stabilize and remodel newly formed blood vessels Excessive proliferation of endothelial cells and ensuing overgrowth of blood vessels Authors: Tony Gu Reviewers: Brian Rankin Yan Yu* Laurie Parsons* * MD at time of publication Formation of friable telangiectasias (small dilated vessels apparent near the surface of skin or mucous membranes) Formation of Arteriovenous malformations (AVMs): Direct connection between arteries and veins without intervening capillary bed Nasal telangiectasias Epistaxis (nosebleeds) Gastrointestinal telangiectasias Gastrointestinal bleeding Mucocutaneous telangiectasias Cerebral AVMs Hepatic AVMs Left to right shunting of blood Heart works harder to perfuse tissues Heart failure Pulmonary AVMs Rupture High flow left to right shunting of blood (the steal effect) Cerebral ischemia No oxygenation at capillaries Hypoxemia ↑ erythropoietin production Secondary polycythemia No filtering from capillaries Hemorrhage, shock, death Venous emboli enter arteries (paradoxical embolism) Stroke Venous bacteria enter arteries Cerebral abscess Iron deficiency anemia ↓ serum iron is associated with ↑ coagulation factor VIII levels (mechanism unclear) Venous thromboembolism Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published July 28, 2020 on www.thecalgaryguide.com

acute-pancreatitis-complications

Acute pancreatitis: Complications Inflammation causes vasodilation and vasculature leakage Mild, (85%): Interstitial edematous pancreatitis Local accumulation of fluid in the pancreas <2 weeks after onset Acute peripancreatic fluid collection (not encapsulated) Walled off by fibrous & granulation tissue >2 weeks after onset Pancreatic pseudocyst (completely encapsulated) Peritoneal irritation à pain Large cyst can (very rarely) compress surrounding bowel Acute Pancreatitis Inflammatory cytokines are released from damaged pancreas If recurrentàchronic pancreatitis (see relevant slide) Inflammation damages pancreatic exocrine cellsàInappropriate release of pancreatic enzymes into surrounding tissue & vasculature àdigesting pancreatic parenchyma Authors: Nissi Wei, *Yan Yu Reviewers: Dean Percy, Miles Mannas, Varun Suresh, Brandon Hisey, *Kerri Novak, *Sylvain Coderre * MD at time of publication complete resolution (most cases) Necrotic tissue is vulnerable to infection (esp. Gram neg GI bacteria) inflammation & necrosis activate cytokine cascade Severe, necrosis (15%): Necrotizing pancreatitis Local infection Severe pancreatic inflammation shifts body fluid into retroperitoneal spaceàintravascular volume depletion Systemic Inflammatory Response Syndrome (SIRS) (see relevant slide) Organ failure (may be sole feature on presentation) Stagnant fluid can more easily become infected Infection spreads to bloodstream Cardiac failure Hypovolemic shock Renal failure Local accumulation of fluid & necrosis in the pancreas < 4 weeks after onset: Acute necrotic collection (not encapsulated) Walled off by fibrous & granulation tissue > 4 weeks after onset walled-off necrosis (completely encapsulated) When treated with excess fluid resuscitation: Intra- abdominal hypertension Respiratory failure (ARDS) Disseminated intravascular coagulation (DIC) Bowel obstruction Gastric outlet (see relevant slide) obstruction Infected pancreatic necrosis Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published September 20, 2016, updated September 7, 2020 on www.thecalgaryguide.com

Beta-Blockers-Mechanism-of-Action-and-Side-Effects

Beta-Blockers: Mechanism of Action and Side Effects Two classes of “Beta-Blockers” are used clinically: Non-cardio-selective: binds Cardio-selective: binds largely beta-1 and beta-2 receptors to beta-1 receptors Authors: Tegan Evans, Davis Maclean, Yan Yu* Reviewers:, Amanda Nguyen, P. Timothy Pollak*, Sean Spence* * MD at time of publication Beta blockers bind to beta 1 and/or beta 2-receptors of various tissues throughout body, and thus competitively inhibit binding of sympathetic adrenergic molecules (such as catecholamines from the adrenal medulla, e.g. epinephrine) to these receptors, ↓ their normal adrenergic tone Beta-2 receptor antagonism Beta-1 receptor antagonism Lungs Eyes Central nervous system Heart Kidneys ↓ cAMP (intracellular messenger) productionàcomplex, tissue-specific intracellular mechanisms resulting in a variety of effects in different tissues: Throughout body tissue Epinephrine (via cAMP) indirectly ↑ the activity of the Na+/K+ pump on cell membranes (a pump that moves 3 Na+ out of cells per 2 K+ moved into cells) Blocking epinephrine from binding the beta-2 receptor and producing cAMPà↓ activity of Na+/K+ pump à↓K+ moved into cells ↑ proportion of K+ now resides in extracellular fluid, detectable in serum (total body K+ remains the same) Hyperkalemia (see Calgary Guide: Hyperkalemia – Clinical findings) Blocking sympathetic hormonesà↓ relaxation of smooth muscle circumferentially wrapped around airways ↑ resting airway muscle toneà bronchoconstriction ↑ resistance to airflow Wheezing, dyspnea, chest tightness Exacerbation of underlying airway disease (e.g. asthma) ↓ ciliary epithelium’s production of aqueous humor (fluid that fills anterior chamber of the eye) Reduced intraocular pressure Blocking adrenergic response mediated by epinephrine and norepinephrine (e.g. the physiologic “fight- or-flight” response to stress) ↓ tremor, irritability, anxiety ↓ ability to produce adrenergic symptoms in response to hypoglycemia Hypoglycemia unawareness Coronary perfusion pressure = diastolic blood pressure in aorta – LV end diastolic pressure ↓ inotropy (contractility of cardiac muscle) ↓ chronotropy (heart rate and conduction velocity) ↓ renin releaseà↓ creation of angiotensin II & aldosterone + ↓ reabsorption of Na and H2O in nephron ↑ urinary Na+ & H2O loss ↓ total blood volume Decompensation of acute heart failure Dizziness and fatigue Hypotension (Blood pressure = cardiac output x systemic vascular resistance) ↓ O2 demand of myocardial tissue Bradycardia Inability to ↑ heart rate in response to stress (e.g. shock, sepsis) ↓ stroke volume ↓ cardiac output Beta blockers ↓ diastolic blood pressure, & thus may ↓ coronary perfusion pressure Before giving beta blockers, ensure blood pressure isn’t too low Otherwise, may worsen acute myocardial ischemia Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published Jan 14, 2021, updated Feb 7, 2021 on www.thecalgaryguide.com

AAA-Clinical-Findings-and-Complications

Abdominal Aortic Aneurysm (AAA): Clinical Findings and Complications AAA = Abnormal, irreversible dilation of a focal area of abdominal aorta (area of aorta between diaphragm & aortic bifurcation) to twice the diameter of adjacent normal artery segments Asymptomatic, non-ruptured aneurysm: Most AAAs are asymptomatic until rupture or days before impending rupture Asymptomatic AAAs are only detectable on imaging or by palpation Given their structural weakness, AAAs are at risk of rupture (risk ↑ with ↑ size of aneurysm) Ruptured AAA: a medical emergency Aorta lies in between the peritoneal and retroperitoneal space Symptomatic, non-ruptured aneurysm: rarely, an unruptured AAA can cause symptoms or complications (0.1%-1% of AAAs) Authors: Olivia Genereux, Davis Maclean, Yan Yu* Reviewers: Jason Waechter*, Amy Bromley*, Sandeep Aggarwal*, Gregory Samis* *MD at time of publication Posterior aortic wall rupture Retroperitoneal hemorrhage Sudden and severe abdominal and/or back pain Anterior aortic wall rupture Peritoneal hemorrhage Peritoneal space is larger and holds larger volumes of blood Peritoneal hemorrhages are large (entire blood volume can pool in the peritoneal space in minutes) Prior to rupture, the adventitia (thin outermost collagenous layer of the aorta) may dilate significantly Adventitia is the only layer of the aorta that contains sensory innervation à nociceptors there can be activated by adventitia dilation Very rarely (0.1%), areas of stagnant blood flow within the AAA allow for blood & clotting factors to accumulate Thrombi (blood clots) develop in these aneurysms Thrombi may dislodge and travel (embolize) to distal vasculature, cutting off blood- flow to these areas This process (referred to as tamponade) is crucial in preventing catastrophic blood loss, allowing for a window of opportunity for treatment Compensated Hypovolemic Shock: Low blood pressure & poor organ perfusion, but blood loss has temporarily stopped. This state of shock is compatible with life if patient is otherwise healthy (e.g. no coronary artery disease) ↓ space for blood to accumulate in the retroperitoneal space (compared to the peritoneal space) Rapid pressure ↑ in retroperitoneal space overcomes the pressure in aorta Since blood will only travel from areas of ↑ pressure to areas of ↓ pressure, this pressure gradient prevents further blood loss from ruptured aorta Massive hemorrhage due to high blood flow volume through aorta Hypotension and rapid progression to hypovolemic shock Abdominal and/or àorgan ischemia back pain The most common symptom of a symptomatic non- ruptured aneurysm, and may be the first sign of an impending aneurysm rupture Death within minutes (rare) If low blood pressure is now (inappropriately) treated with fluid resuscitation, the blood pressure will ↑ Differential pressure gradient is reversed (aortic blood pressure > pressure in retroperitoneal space) Bleeding into retroperitoneal space resumes Decompensation of hypovolemic shock Possible death Kidney ischemia Lower limb ischemia Time exists to transfer patient to tertiary care center for surgical treatment Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Re-Published February 28, 2021 on www.thecalgaryguide.com

Fat-Embolism-Syndrome

Fat Embolism Syndrome: Pathogenesis and clinical findings Panniculitis (conditions causing inflammation of subcutaneous fat) Non-trauma related (rare) Long bone fracture Pelvic fracture Orthopedic Trauma Intraosseous access Soft tissue injuries Chest compressions Bone marrow transplant Pancreatitis Diabetes mellitus Fat from bone marrow is disrupted and leaks into bloodstream via damaged blood vessels Fat globules obstruct dermal capillaries Capillaries rupture Blood leaks into the skin Petechial rash Non-Orthopedic Trauma (less common) Fat from injured adipose tissue is released from adipocytes into bloodstream Metabolic disturbance mobilizes stored fat and moves it into circulation Fat Embolism Syndrome the presence of fat globules in circulation Fat globules damage blood vessel walls Platelets stick to damaged areas Platelet aggregation ↑ circulating free fatty acids ↑ inflammatory cytokines (TNF, IL1, IL6) ↑ serum C Reactive Protein (an acute phase reactant) C reactive protein binds to lipid vesicles in circulation ↑ formation of lipid complexes in the blood Obstruction of cerebral vasculature ↓ blood flow and oxygen delivery to brain tissue Neurological findings: ranging from ↓ level of consciousness to seizures Notes: Large quantities of fat globules can obstruct pulmonary vasculature Blood clots form throughout the body Disseminated intravascular coagulopathy Back up of blood into right heart àRight ventricular dysfunction ↓ pulmonary arterial blood flow à↓ gas exchange in the lungs Higher CO2 & lower O2 levels in blood àdetected by chemoreceptors Chemoreceptors stimulate respiratory centre in the brain to ↑ rate of respiration Dyspnea / Tachypnea Authors: Tabitha Hawes Reviewers: Hannah Koury, Alyssa Federico, Davis MacLean, Mehul Gupta, Yan Yu*, Jeremy Lamothe* * MD at time of publication • Underlined findings indicate classic triad of symptoms (petechial rash, neurologic findings, dyspnea/tachypnea) • Clinical presentation of fat embolism syndrome is variable and may present with any or all of these findings ↓ pumping of blood into systemic circulation Hypotension Obstructive shock Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published July 19, 2021 on www.thecalgaryguide.com

covid-19-pathophysiology-and-clinical-findings

COVID-19 (Corona Virus Disease 2019): Pathophysiology and Clinical Findings Authors: Ryan Brenneis, Yan Yu* Reviewers: Ciara Hanly, Yonglin Mai (􏰄􏰁􏰃)*, Stephen Vaughan* * MD at time of publication -Respiratory failure -Septic shock -Multiple organ dysfunction Critical Respiratory droplet production (cough, sneeze, talking, breathing) by human host or animal vector infected with SARS-CoV-2 Note: Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is the name of the betacoronavirus (a positive sense, single stranded RNA virus). COVID-19 is the name of the disease caused by this virus. rate, ↓ oxygen saturation -Bilateral interstitial infiltrates on Chest X-ray, progressively worsening Small droplets (<5μm in diameter) are aerosolized and become airborne Inhalation of aerosolized particles that are suspended in air Patient exposed to the virus (SARS-CoV-2) Droplet contacts the mucus membranes (eyes, nose, mouth) of recipient Live viral particles can adhere to inanimate objects called fomites (e.g. doorknobs) Symptoms are on a continuum -Worsening dyspnea: ↑ respiratory -Fever -Cough -Myalgia, fatigue -Nausea/vomiting -Diarrhea -Loss of taste/smell Recipient touching infected fomite subsequently touches any of their mucus membranes Mild Moderate Severe Virus spreads in the body via 1) mucus membrane spread to surrounding cells and 2) entering the blood Virus adheres to angiotensin-converting enzyme 2 (ACE-2) receptor on body cells, mimics ACE-2, & gains access into cell COVID-19 Symptomatic infection with SARS-CoV-2 Viral proliferation in cells of tissues with more ACE-2 receptors: lungs (type II pneumocytes); vasculature (endothelial cells), kidneys (proximal tubular epithelium), heart (myocardium), GI tract (enterocytes) Cell death and ↑ in inflammatory cytokines triggers immune response Neutrophils move to lungs, release reactive oxygen species and cytokines Alveolar/capillary damage Fluid accumulates in interstitium and alveoli ↑ Distance for O2 to diffuse from alveoli to capillaryà ↓ blood O2 saturation Cytokines induce the hypothalamus to release prostaglandins ↑ body temperature set point to fight infection Virus disassembles, releasing viral RNA, which uses host cell’s ribosomes to make new viral proteins like RNA-polymerases Newly made viral RNA-polymerases use cell’s own nucleotides to synthesize new viral RNA Bilateral ground-glass opacities (CT lung) & interstitial infiltrates on Chest X-ray Dyspnea Airway irritation Cough Myocardial cell damage ↑ Troponin ↑ skeletal muscle cell damage Viral RNA & proteins packaged into new viral particles New virus assembled and released from cell, killing the cell and contributing to disease symptoms Average incubation period (time from initial infection to symptom onset) is 4-5 days; can be up to 14 days Heart tries to compensate for Fever Myalgia hypoxemiaà↑ cardiac output Arrhythmogenic and strain on myocardium state Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published March 22, 2020, updated Aug 18, 2021 on www.thecalgaryguide.com

Ectopic Pregnancy

Ectopic Pregnancy: Pathogenesis and Clinical Findings In vitro fertilization Tubal disorders leading to infertility and unknown procedural causes Previous ectopic pregnancy Underlying tubal disorder leading to previous ectopic Pelvic inflammatory disease (PID) Endometriosis Tubal surgery or disorders Age >35 Risk factor accumulation over time Smoking Impairment in tubal motility; impaired immunity (risk factor for PID) Tubal scarring leading to adhesions, obstruction, and alteration of tubal function Ectopic Pregnancy: Implantation of developing blastocyst outside the uterine cavity, most commonly in fallopian tube (other locations: interstitial > cornual > cervical > ovarian > abdominal) Embryo releases human chorionic gonadotropin (β-hCG), which supports corpus luteum to continue producing progesterone On transvaginal ultrasound: Extrauterine gestational sac with a yolk sac or embryo Embryo & trophoblast deathàloss of hormone support for the decidua (modified endometrial lining) Progesterone maintains the endometrial lining, preventing it from shedding Missed period Penetration of ovum into muscular wall of fallopian tube Tubal distention àTubal rupture Intra-abdominal hemorrhage Pregnancy cannot survive without the uterine endometrium Maternal blood extrudes through fimbriae of fallopian tubes and into peritoneal cavity Lower abdominal pain (including peritonitis in cases of hemoperitoneum) Hemoperitoneum (blood in the peritoneal cavity) Sloughing of decidua out of the uterus through the vagina Vaginal bleeding (usually in first trimester) Cessation of human chorionic gonadotropin (β-hCG) release from embryo β-hCG plateaus or decreases Authors: Jemimah Raffé-Devine Tahsin Khan Yan Yu* Reviewers: Brianna Ghali Bishwas Paudel Mackenzie Grisdale Christina Schweitzer Ron Cusano* Jadine Paw* * MD at time of publication Syncope ↓ Level of consciousness Positive β-hCG, but rising <35% over 2 days Discriminatory zone: β-hCG >2000 + absence of intrauterine pregnancy Hypotension Shock Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published Oct 1, 2017, updated Oct 19, 2021 on www.thecalgaryguide.com

necrotizing fasciitis

Necrotizing Fasciitis: Pathogenesis and Clinical Findings Authors: Alyssa Federico, Amanda Eslinger, Matthew Harding, Mehul Gupta Reviewers: Heena Singh, Yan Yu*, Donald Graham*, Duncan Nickerson* * MD at time of publication Diabetes Loss of protective sensation in lower extremities Peripheral vascular disease Poor arterial perfusion causes necrosis of tissue Immune compromised host Increased susceptibility to infection Bacteria introduced to tissue Pharyngitis Blood carries bacteria from throat to other tissue (hematogenous spread) Laceration Recent surgery Injection Burn Blunt force trauma Childbirth Lower extremity wounds Bacteria enters tissue through open wound Infection of muscle fascia Local immune response Production of exotoxins by bacteria Disruptions of protective skin barrier Bacteria introduced into tissue during injury Necrotizing Fasciitis Type I infection: mixed aerobic and anaerobic bacteria Type II infection: group A streptococcus Type III infection: marine organisms, clostridial infections Type IV infection: fungal organisms Poor blood supply of muscle fascia allows for progressive spread of infection Systemic immune response Pyrogens produced by immune system Pyrogens travel through the bloodstream to the hypothalamus and alters the body’s thermal setpoint Transmission of bacteria from infected tissue to blood Sepsis Streptolysin (exotoxin) causes blood clot formation Blood clots in vessels Tissue ischemia in epidermis, dermis, subcutaneous fat, muscle fascia, and/or muscle Stimulation of programmed cell death Tissue destruction Pain more severe than clinical findings ↓ blood flow fails to meet tissue’s needs Tissue death Build up of gas in subcutaneous tissue from bacteria metabolism Crepitus ↑ serum creatinine kinase from protein breakdown ↑ blood flow to infected tissue Warmth Erythema Immune cells release vasoactive cytokines into the blood Capillary vasodilation Fluid and proteins shift from cells and capillaries to interstitial space Blood vessel dilation ↓ perfusion of vital organs Organ failure Hypotension ↑ heart rate to perfuse vital organs Tachycardia Bacteria releases toxins which are taken up into the bloodstream Immune cells produce inflammatory cytokines Circulating toxins activate T cells, over- activating the systemic immune response Toxic Shock syndrome Infection ↑ white blood cell production in bone marrow ↑ white blood cells Destructionof peripheral nerve endings Insensitivity to pain Tissue hypoxia à anaerobic metabolism Poor perfusion of lungs impairs gas exchange Tachypnea Cytokines affect dopamine production in the basal ganglia Acute malaise Production of non-specific acute phase reactants ↑ C reactive protein and erythrocyte sedimentation rate Fluid-filled blisters Edema Fever Compartment syndrome (see relevant Calgary Guide slide) Amputation ↑ serum lactate Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications First published Nov 20, 2013, updated Dec 19, 2021 on www.thecalgaryguide.com

sepsis-y-shock-septico-patogenesis-y-hallazgos-clinicos

sepsis-y-shock-septico-patogenesis-y-hallazgos-clinicos

Vitiligo Pathogenesis and Clinical Findings

Vitiligo: Pathogenesis and clinical findings Authors: Wisoo Shin Reviewers: Lauren Lee Stephen Williams Ben Campbell Laurie Parsons* Yan Yu* * MD at time of publication Genetic predisposition Variants in over 30 susceptibility loci Environmental exposure UV light, monobenzone, phenol, catechol Production of IgG auto- antibodies to melanocyte-specific proteins Auto-antibodies bind to melanocytes and trigger antibody-dependent cellular cytotoxicity: marking melanocytes for destruction by Fc- receptor bearing immune cells such as neutrophils Impaired mitochondrial function in melanocytes ↑ Susceptibility of melanocytes to oxidative stress ↓ E-cadherin or ↑ anti- adhesion molecule expression in melanocytes ↓ Adhesion of melanocytes to keratinocytes ↑ Clearance of melanocytes from epidermis ↑ Reactive oxygen species production within melanocytes Activation of apoptosis and senescence signaling pathways Pressure or friction Melanocytes excrete exosomes (melanocyte- specific antigens, microRNA, heat shock proteins) that, through complex mechanisms, stimulate the immune system’s CD8+ T-cells to destroy melanocytes Melanocytes enter apoptotic or senescent state ↓ Functional melanocytes ↓ Melanin production Overall loss of functional melanocytes Vitiligo Normal Skin Pigmented Epidermis Dermal- Epidermal Junction Dermis Autoimmune destruction of melanocytes Depigmented Epidermis Melanocytes Immune-mediated destruction of melanocytes (by both neutrophils and CD8+ T cells) A depigmenting skin disorder characterized by selective loss of melanocytes Depigmentation in areas of ↑ pressure, friction and/or trauma Nonsegmental vitiligo Smooth unpigmented macules or patches in bilateral, often symmetric pattern Somatic mosaicism (mutation limited to a subset of cells) in zygote during development Segmental vitiligo Smooth unpigmented macules or patches in unilateral pattern not crossing midline Vitiligo Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published February 15, 2022 on www.thecalgaryguide.com

Hypovolämischer Schock: Pathogenese, Komplikationen und klinische Befunde

Hypovolämischer Schock: Pathogenese, Komplikationen und klinische Befunde

complications-of-pulmonary-embolism

Complications of Pulmonary Embolism Authors: Sravya Kakumanu, Dean Percy, Yan Yu Reviewers: Tristan Jones, Ciara Hanly, Jieling Ma (马杰羚), Ben Campbell, Dr. Man-Chiu Poon*, Dr. Lynn Savoie*, Dr. Tara Lohmann * * MD at time of publication IF CHRONIC: Unresolved clot after 2 years leading to fibrosis of pulmonary vasculature Chronic Thromboembolic Pulmonary Hypertension (CTEPH) (<5% of PE cases) Venous Stasis Hypercoagulable state Vessel Injury Virchow’s Triad (*See Suspected Deep Vein Thrombosis slide) Deep Vein Thrombosis Clot migrates from deep limb veins à femoral àiliac veins ACUTE/MASSIVE PE: Clot obstructs pulmonary arterial or arteriolar flow Lung infarction (tissue death) from ischemia Inflammatory cells migrate to site and release cytokines ↑ Permeability of blood vessels Permeability-driven (exudate) fluid leakage into pleural space Pleural Effusion Clot migratesàinferior vena cava àright atrium (RA) of heartà right ventricle (RV) à gets lodged in pulmonary arteries/arterioles Pulmonary Embolism (PE) ↑ RV afterload ↑ RV pressure and expansion Well-ventilated (V) areas of lung do not receive adequate blood supply (Q) V/Q Mismatch Leftward shift of ventricular septum ↓ Left ventricle filling in diastole ↓ Cardiac output Obstructive Shock Impaired heart filling Pulseless Electrical Activity (ECG activity in absence of palpable pulse) Back up of pressure in systemic venous system ↑ Pressure in capillaries draining parietal pleura Pressure-driven (transudate) fluid leakage into pleural space For signs and symptoms, see the Obstructive Shock slide For signs and symptoms refer to CTEPH slide Chronic ↑ RV afterload ↑ Stretching of myocytes causing RV hypertrophy and dilation ↓ RV ejection fraction Right Heart Failure “Cor Pulmonale” For signs and symptoms, see the Right Heart Failure slide Failure to oxygenate blood Type I Respiratory Failure Hypoxemic: patient has ↓ blood [O2] IF MASSIVE PE (less common): ↑ Alveolar dead space Failure to ventilate Type II Respiratory Failure Hypercapnic: patient has ↑ blood [CO2] Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published August 7, 2012, updated Mar 31, 2022 on www.thecalgaryguide.com

burn-shock-pathogenesis-complications-and-clinical-findings

Burn Shock: Pathogenesis, Complications, and Clinical Findings Thermal burn injury > 20% Total Body Surface Area Authors: Shayan Hemmati Reviewers: Christy Chong Ben Campbell Donald McPhalen* * MD at time of publication ↑ Production of local inflammatory markers (ex. histamine, bradykinin, and prostaglandins) Endothelial cell lining in blood vessel walls is compromised ↑ Local vessel permeability Shift of plasma + proteins from vessel into interstitial space Direct vascular thermal injury (within burn wound) ↑ Production of circulating inflammatory mediators (ex. IL-1, IL-6, TNF-!) ↑ Systemic vessel permeability ↑ Circulating reactive oxygen species Damage to DNA, proteins, and lipids throughout body, including myocardium (muscle cells of the heart) ↑ Myocardial stress Myocardial dysfunction ↓ Cardiac contractility ↓ Stroke volume ↓ Cardiac output Cardiogenic Shock Refer to Cardiogenic Shock: Pathogenesis, Complications and Clinical Findings ↓ Protein concentration in vessels causes ↓ intravascular oncotic pressure Further shift of plasma from vessel into interstitial space (↑ interstitial proteins pull plasma into interstitium) ↓ Intravascular plasma ↑ RBCs per unit volume of plasma ↑ Systemic vasoconstriction to maintain blood pressure (↑ Afterload) ↓ Circulating blood volume leads to less venous return (↓ Preload) ↑ Hematocrit Pitting edema (burned & unburned tissue) ↓ Circulating blood volume Hypovolemic Shock Refer to Hypovolemic Shock: Pathogenesis, Complications and Clinical Findings Burn Shock: A complication of large burns causing end-organ hypoperfusion with resultant organ dysfunction Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published August 15, 2022 on www.thecalgaryguide.com

ascending-cholangitis-pathogenesis-clinical-findings

Ascending Cholangitis: Pathogenesis and clinical findings Authors: Brandon Hisey, Neel Mistry Reviewers: Alec Campbell, Vina Fan, Ben Campbell, Kelly Burak*, Eldon Shaffer* * MD at time of publication Reflux of biliary contents into the vascular system (cholangiovenous reflux) Bacteria ascends into biliary tract from duodenum via Sphincter of Oddi Gallstone in the common bile duct Stricture of biliary/hepatic ducts Biliary / pancreatic duct malignancy Biliary obstruction (partial bile duct obstruction) ↓ Excretion of bilirubin into bileà ↑ bilirubin in blood ↑ Serum bilirubin Deposition of bilirubin in the skin and mucous membranes Jaundice*† Parasites in bile duct (E.g. Clonorchis) Complication of endoscopic retrograde cholangiopancreatography (ERCP) Bile accumulates in biliary tract Bile duct dilation on ultrasound Sludge (bile precipitants) impact bile ducts worsening obstruction Obstruction & detergents in bile inflame ductal mucosa. Inflammation then spreads to adjacent structures Stimulates phrenic (C3-C5) and foregut autonomic nerves (T5-T8) Dull right upper quadrant pain*† radiating to back and right shoulder ↑ Intra-biliary pressure Impaired forward flowà ↑ backflow of bile Impaired bile secretion damages ductal epithelium of the biliary tract Damaged ductal epithelium leaks ALP and GGT (enzymes) into blood ↑ Serum ALP and GGT ↑ Permeability of bile ductules Reduced flushing of bile out to duodenum Inflammatory response triggered Fever*† ↑ WBCs Tachycardia Hypotension† Confusion† Oliguria Bacterial translocation from biliary tract into blood Bacteremia Massive systemic inflammatory response Septic Shock (see Distributive Shock slide) * Charcot’s triad ~20% of cases | † Reynolds’ pentad ~7% of cases Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications First published November 18, 2015; Updated August 31, 2022 on www.thecalgaryguide.com

acute-lower-gi-bleeds-pathogenesis-and-clinical-findings

Acute Lower GI Bleeds: Pathogenesis and Clinical Findings Diverticulosis Formation of diverticula (outpouchings of the bowel wall) Intestinal vessels are stretched over the domes of the diverticula Angiodysplasia Formation of dilated, thin- walled vessels in GI tract mucosa/ submucosa Colorectal Cancer Infectious Colitis Invasion of bacteria and/or bacterial toxins into intestinal wall Cell damage and cell death Sloughing off of intestinal epithelial cells Ischemic Colitis ↓ Blood flow to a portion of the colon Lack of oxygen delivery to colon wall Necrosis (cell death) in the colon wall Inflammatory Bowel Diseases (Note: these are chronic diseases and rarely present with acute lower GI bleed) New, extremely friable blood vessels develop within the tumor Malignant tissue invades the colon wall and disrupts colonic blood vessels Crohn Disease Immune- mediated full thickness inflammation of bowel wall Ulcer formation and disruption of intestinal vessels Ulcerative Colitis Recurrent immune- mediated inflammation of colon mucosa Authors: Miranda Schmidt Illustrator: Mizuki Lopez Reviewers: Vina Fan, Ben Campbell, Kerri Novak* * MD at initial time of publication Acute Lower GI Bleed ↑ Risk for vessel damage and rupture Blood travels rapidly through GI tract Hematochezia (bright red blood per rectum) May result in significant blood loss Blood from the small intestine or right colon travels a longer distance through the GI tract Bacteria in the GI tract has time to oxidize hemoglobin in the blood Oxidization makes blood a darker color Melena (rare in a lower GI bleed) (tarry black stool) Inferior Vena Cava Diaphragm Esophagus Loss of red blood cells results in a loss of hemoglobin (a component of red blood cells) Fluid from the extravascular space moves into the blood vessels to maintain vascular volume Fluid is administered in a healthcare setting to compensate for blood loss Hypovolemic Shock (rare in a lower GI bleed) (↓ Oxygen delivery to tissues due to low blood volume) See “Hypovolemic Shock” slide for signs and symptoms Lower GI Bleeds are intra-luminal GI tract bleeds that occur anywhere distal to the ligament of Treitz (transition between duodenum and jejunum) After 24 hours, the addition of fluid to the intravascular space dilutes hemoglobin in the blood Normocytic Anemia Duodenum Ligament of Treitz Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published August 31, 2022 on www.thecalgaryguide.com

ventilator-associated-pneumonia-pathogenesis-and-clinical-findings

Ventilator-Associated Pneumonia: Pathogenesis and Clinical Findings Respiratory failure or inability Risk factors: e.g. immunocompromised, poor swallowing to maintain airway ability, weakened respiratory muscles, chronic disease Insertion of endotracheal tube (ETT) for invasive mechanical ventilation to maintain respiration Paralytics and sedatives lead to inhibition of cough reflex Damage to cilia on epithelial cells of trachea during insertion of ETT ↓ Mucociliary clearance Insertion of nasogastric (NG) tube for feeding Constant opening by NG tube ↓ esophageal sphincter function Introduction of oropharyngeal microbes during intubation Severe acute illness impairs phagocytosis and dysregulates T- cells (mechanism unclear) Medications, chronic disease, or severe acute illness can weaken immune system Desensitization of pharyngoglottal adduction reflex (PAR) (PAR normally induces closure of epiglottis to protect the airway when swallowing) ↑ Reflux of gastric contents Accumulation of subglottic secretions containing microbes Microbial colonization on inside of ETT Development of biofilm on inside of ETT Dislodgement of biofilm into lower airway ↑ Age or chronic disease can weaken respiratory function Micro aspirations of subglottic and gastric contents Impaired mechanisms to remove microbes from airway Positive pressure pushes microbes down Fever/rigors ↑ White blood cell count Introduction of pathogenic microbes to airway Susceptible patient (not required for infection) Septic shock See Distributive Shock slide Sepsis Microbes descend airway and infect lungs Ventilator-Associated Pneumonia (VAP) Occurs > 48-72 hours after intubation ↑ Inflammatory response at infection site promoting immune cell extravasation and cytokine release Cytokine signalling ↑ permeability of capillaries leading to ↑ fluid leakage into interstitium and alveoli Authors: Sravya Kakumanu Reviewers: Ben Campbell *Tara Lohmann *Bryan Yipp * MD at time of publication Acute respiratory distress syndrome See ARDS pathogenesis slide Pleural effusion Lung consolidation on chest x-ray (CXR) ↑ Sputum production to clear fluid on CXR (Note: In patients with Acute Respiratory Distress Syndrome (ARDS), look for VAP consolidation in non- within alveoli/airways (may be Positive microbial culture from sputum dependent/upper regions of the lung where ARDS consolidation would be unexpected to extend to) purulent in worse infections) Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published September 2, 2022 on www.thecalgaryguide.com

syok-luka-bakar-patogenesis-komplikasi-dan-temuan-klinis

syok-luka-bakar-patogenesis-komplikasi-dan-temuan-klinis

syok-hipovolemik-patogenesis-komplikasi-dan-temuan-klinis

syok-hipovolemik-patogenesis-komplikasi-dan-temuan-klinis

Syok Obstruktif: Patogenesis, komplikasi, dan temuan klinis

Syok Obstruktif: Patogenesis, komplikasi, dan temuan klinis

Syok Kardiogenik: Patogenesis, komplikasi, dan temuan klinis

Syok Kardiogenik: Patogenesis, komplikasi, dan temuan klinis

Syok Distributif: Patogenesis, komplikasi, dan temuan klinis

Syok Distributif: Patogenesis, komplikasi, dan temuan klinis

Acute Liver Failure: Pathogenesis and clinical findings

Acute Liver Failure: Pathogenesis and clinical findings Authors: Juliette Hall Reviewers: Vina Fan, Ben Campbell, Mayur Brahmania* * MD at time of publication Acetaminophen Overdose Accumulation of toxic NAPQI (a metabolite of acetaminophen) NAPQI binds hepatocellular proteins (see Acetaminophen Overdose: pathogenesis and clinical findings slide) Drug-induced liver injury Metabolism of drugs by the liver can produce reactive drug metabolites Intracellular stress, mitochondrial injury, or immune response Viral Hepatitis (i.e. HAV, HBV, HEV, HSV) Acute infection or infection flare provokes an immune response against infected hepatocytes Autoimmune Hepatitis Autoimmune antibodies attack hepatocytes (see Auto-immune Hepatitis (AIH) slide) Ischemia (i.e. from shock) ↓ O2 delivery to the liver Hepatocellular hypoxia Wilson’s Disease Heritable mutation in the ATP7B gene ↓ Biliary excretion of copper Hepatic copper accumulation injures hepatocytes (see Wilson’s Disease slide) Accelerated rate of hepatocellular necrosis or apoptosis Hepatocyte death exceeds regeneration such that liver function is compromised within a short amount of time Acute Liver Failure An illness of <26 weeks duration in the absence of pre-existing cirrhosis, characterized by INR ≥1.5 and evidence of altered mentation (hepatic encephalopathy) Injured hepatocytes leak hepatic enzymes (AST, ALT, GGT) into circulation ↑ Liver enzymes Hepatocellular inflammation Stimulation of foregut autonomic nerves Right upper quadrant pain ↓ Toxin metabolism Toxins build up and activate microglial cells (brain macrophage) Oxidative stress and cerebral edema Hepatic encephalopathy Characteristic set of neuropsychiatric symptoms (see Hepatic Encephalopathy slide) ↓ Hepatocellular function and number ↓ Complement protein synthesis ↓ Ability to clear immune complexes and activate B cells Accumulation of pigmented bilirubin ↓ Synthesis of coagulation factors ↑ INR ↓ Conjugation of bilirubin by the liver and ↓ transport into bile for excretion ↑ Serum bilirubin Jaundice Infection Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published November 15, 2022 on www.thecalgaryguide.com

hypovolemic-shock

Hypovolemic Shock: Pathogenesis, Complications, and Clinical Findings Authors: Dean Percy Miranda Schmidt Reviewers: Yan Yu Tristan Jones Frank Spence* Ben Campbell Ayaaz Sachedina* * MD at time of publication Progressive ↓ in level of consciousness Pulseless Electrical Activity Acute Kidney Injury ↑ Reabsorption of salt and water in the kidney Oliguria (↓ urine output) Inflammation (pancreatitis, cirrhosis, post-operative, etc.) Inflammatory mediators ­ vessel permeability and fluid leaks out Trauma Ruptured vessels leak fluid into potential spaces Hemorrhagic losses (GI bleed, postpartum hemorrhage, etc.) ↓ Intravascular volume ↓ Venous return to the heart ↓ Cardiac output (blood pumped from the heart) Hypovolemic Shock ↓ Oxygen delivery to tissues due to low blood volume Insufficient organ perfusion Non-Hemorrhagic losses (dehydration, GI losses, skin losses / burns, renal losses, etc.) ‘Third Spacing’ of fluid (fluid located outside the intravascular or intracellular space; large collections can occur in the pelvis, thorax, GI tract, long bones of children, intra-abdominally, retroperitoneally) P = Q x R; less ‘flow’ in the vessels (Q), with vessels not constricting enough to maintain resistance (R)à pressure (P) will drop ↓ Blood Pressure Caution: young, healthy individuals can maintain blood pressure during circulatory collapse with ­ cardiac output and ­ vasoconstriction; do not use blood pressure as an indicator of shock severity in children Carotid sinus baroreceptors sense low blood pressure ↓ Carotid sinus inhibition of sympathetic nervous system Release of sympathetic catecholamines (epinephrine and ↓ Pressure in venous circulation Brain Heart Kidneys ↓ Blood in the right internal jugular vein ↓ Oxygen delivery to the brain ↓ Myocardial contractility (from lactic acidosis) ↓ Blood flow to kidneys ↓ Jugular Venous Pressure Catecholamines bind to beta-1 receptors in the sinoatrial node of the heart Beta-1 receptor activation causes ↑ heart rate Tachycardia norepinephrine) Catecholamines bind to and stimulate alpha-1 receptors in peripheral vessels Vasoconstriction of peripheral vessels ↓ Blood flow to peripheral tissue Catecholamines bind to and stimulate beta receptors in sweat glands Diaphoresis (sweating) In all body tissues Inadequate oxygen delivery ↓ ATP production ↑ Anaerobic metabolism ↓ Body temperature Impaired neurological functioning Renal ischemia Activation of the renin-angiotensin aldosterone system ↓ Glomerular filtration rate ↓ Clearance of lactic acid by the kidney ↑ Lactic acid production ↓ Rate of activity of clotting enzymes Lactic Acidosis Unknown mechanism Coagulopathy Hypothermia Trauma Triad of Death ↑ Capillary Cold, mottled refill time extremities Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published January 24, 2013, updated December 4, 2022 on www.thecalgaryguide.com

Wstrząs obturacyjny: Patogeneza, powikłania oraz zmiany kliniczne

Wstrząs obturacyjny: Patogeneza, powikłania oraz zmiany kliniczne

Wstrząs dystrybucyjny: Patogeneza, powikłania oraz zmiany kliniczne

Wstrząs dystrybucyjny: Patogeneza, powikłania oraz zmiany kliniczne

Wstrząs kardiogenny: Patogeneza, powikłania oraz zmiany kliniczne

Wstrząs kardiogenny: Patogeneza, powikłania oraz zmiany kliniczne

Wstrząs oparzeniowy: patogeneza, powikłania i zmiany kliniczne

Wstrząs oparzeniowy: patogeneza, powikłania i zmiany kliniczne

Leczenie wstrząsu: wyjaśnienie podstawowych mechanizmów

Leczenie wstrząsu: wyjaśnienie podstawowych mechanizmów

Burns - Full Thickness - Pathogenesis and Clinical Findings 2023

Full Thickness Burns: Pathogenesis and clinical findings Radiation Sunlight, x-ray, nuclear Emission/explosion can cause damage to keratinocytes (see Calgary Guide Slide: Superficial Thickness Burns: Pathogenesis and Clinical Findings) Author and Illustrator: Amanda Eslinger Tracey Rice Reviewers: Sunawer Aujla Alexander Arnold Duncan Nickerson* Jori Hardin* * MD at time of publication Epidermis Dermis Sub-cutaneous tissue Fire Contact Scald Chemical Electrical Transfer of heat energy causes direct injury to keratinocytes Hypoxic injury (lack of oxygen) causes ischemia-related cell death leading to necrosis Full thickness burn Non-uniform damage to the epidermal, dermal & subcutaneous layers at varying widths & depths due to unpredictable injury pattern Degraded epidermal & dermal layers cover granulated tissue Ulceration covered by eschar: a thick, dried, black (necrotic) layer Long-term risk of ulcers & infections ↑ Vascular permeability in subcutaneous layers ↑ Intravascular fluid leaves capillaries, ↓ uptake by lymph vessels Edema Compression of surrounding muscles, nerves & vessels Ischemia and/or necrosis ↓ Immunologic response due to impaired epidermal barrier function ↑ Microbial growth creating biofilm & secretion of chemicals that inhibit natural protective process Irritated, inflamed wound bed +/- exudate ↑ Risk of infection & septic shock Destruction of somatosensory structures Hypoesthesia (↓ sensation to stimuli) ↑ Risk of repeated injury due to ↓ response to noxious stimuli Destruction of cutaneous capillary beds ↓ Healing due to ↓ dermal structures throughout wound White or leathery appearance Chronic wounds require surgical interventions ↑ Risk of contractures & skin barrier weakness Legend: Mechanism of Injury Pathophysiology Sign/Symptom Complication Published December 2, 2013, updated June 26, 2023 on www.thecalgaryguide.com

Burns - Full Thickness - Pathogenesis and Clinical Findings

Full Thickness Burns: Pathogenesis and clinical findings Radiation Sunlight, x-ray, nuclear Emission/explosion can cause damage to keratinocytes (see Calgary Guide Slide: Superficial Thickness Burns: Pathogenesis and Clinical Findings) Author and Illustrator: Amanda Eslinger Tracey Rice Reviewers: Sunawer Aujla Alexander Arnold Duncan Nickerson* Jori Hardin* * MD at time of publication Epidermis Dermis Sub-cutaneous tissue Fire Contact Scald Chemical Electrical Transfer of heat energy causes direct injury to keratinocytes Hypoxic injury (lack of oxygen) causes ischemia-related cell death leading to necrosis Full thickness burn Non-uniform damage to the epidermal, dermal & subcutaneous layers at varying widths & depths due to unpredictable injury pattern Degraded epidermal & dermal layers cover granulated tissue Ulceration covered by eschar: a thick, dried, black (necrotic) layer Long-term risk of ulcers & infections ↑ Vascular permeability in subcutaneous layers ↑ Intravascular fluid leaves capillaries, ↓ uptake by lymph vessels Edema Compression of surrounding muscles, nerves & vessels Ischemia and/or necrosis ↓ Immunologic response due to impaired epidermal barrier function ↑ Microbial growth creating biofilm & secretion of chemicals that inhibit natural protective process Irritated, inflamed wound bed +/- exudate ↑ Risk of infection & septic shock Destruction of somatosensory structures Hypoesthesia (↓ sensation to stimuli) ↑ Risk of repeated injury due to ↓ response to noxious stimuli Destruction of cutaneous capillary beds ↓ Healing due to ↓ dermal structures throughout wound White or leathery appearance Chronic wounds require surgical interventions ↑ Risk of contractures & skin barrier weakness Legend: Mechanism of Injury Pathophysiology Sign/Symptom Complication Published December 2, 2013, updated June 26, 2023 on www.thecalgaryguide.com

Shock por quemaduras

Shock por quemaduras: Patogénesis, Complicaciones, y Hallazgos clínicos

Tatalaksana Syok Penjelasan dari mekanisme dasar

Tatalaksana Syok: Penjelasan dari mekanisme dasar

Overview of burns

Overview of Burns: Pathogenesis and Types Authors: Haley Shade, Amanda Eslinger* Reviewers: Christy Chong, Parker Lieb, Sunawer Aujla, Alexander Arnold*, Yan Yu*,Duncan Nickerson*, Donald McPhalen* Illustrator: Devjyoti Dutta* * MD at time of publication Contact Electrical Chemical Radiation (excluding sunburn) Less common Burns from any source can result in 3 damage zones Common Fire Scald Zone of coagulation: innermost zone; maximum damage through necrosis and irreversible tissue loss Zone of stasis: middle zone; decreased tissue perfusion, potentially salvageable Zone of hyperemia: outermost zone; tissue perfusion is increased, damage is reversible Epidermis, dermis, and subcutaneous tissue Full Thickness (3rd degree burn) Normal Skin Epidermis only Superficial Thickness (1st degree burn) Epidermis and superficial (papillary) dermis Superficial Partial Thickness (2nd degree burn) Epidermis and deep (reticular) dermis Deep Partial Thickness (2nd degree burn) Skin and deep tissues, muscle, fascia, nerves, blood vessels, bone Composite tissue injury (4th degree burn) Compartment syndrome Epidermal layer Dermal-Epidermal Junction Superficial (Papillary) Dermis Deep (Reticular) Dermis Note: The total burn surface area (TBSA) can be estimated using the rule of nines (1st degree burns are not included): Head and Neck: 9% total, Chest and Upper Back: 9% each, Arm: 9% each, Leg: 18% each (front and back), Abdomen and Lower Back: 9% each, Genital Area: 1% Refer to Complications of Burns Burn Shock Refer to Burn Shock: Pathogenesis, Complications, and Clinical Findings Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published November 8, 2023 on www.thecalgaryguide.com

Death Cardiovascular Respiratory and Neurologic Mechanisms

Death: Cardiovascular, Respiratory and Neurologic Mechanisms Mitochondria in tissues unable to utilize O2 Reduced hemoglobin in blood to carry O2 Low oxygen content in blood (CaO2) Hypoxemia (Type I Respiratory Failure): low dissolved oxygen in blood (PaO2) Lungs can’t oxygenate blood fast enough Lungs can’t rid blood of CO2 fast enough Hypercapnia / hypercarbia (Type II Respiratory Failure): elevated dissolved CO2 in blood (PaCO2) Cerebral vasodilation Toxins: e.g. cyanide, pesticides, arsenic Severe anemia Distributive problems: Systemic inflammation (sepsis, anaphylaxis, pancreatitis), adrenal insufficiency, vasodilatory drugs Obstructive problems: Cardiac tamponade*, tension pneumothorax* or massive pulmonary embolism* Hypovolemic* problems (low blood volume): Hemorrhage, dehydration, widespread skin disruption or burns Cardiac valve dysfunction Myocardial infarction* or cardiomyopathy Cardiac arrhythmia or heart block Disturbed electrical activity in cardiomyocytes Peripheral metabolic disturbances Hypokalemia*, Hyperkalemia* Acidosis* (including renal failure) Hypothermia* Toxins* (e.g. cocaine, beta blockers, tricyclics) Severe thyroid derangement Inappropriate systemic vasodilation Adjacent forces impair heart filling Low cardiac preload Low stroke volume (SV; depends on valves, contractility, preload) Decreased systemic vascular resistance (SVR) Low blood pressure (BP = CO x SVR) Decreased cardiac output (CO = SV x HR) Disseminated intravascular coagulationàwidespread thrombi that occlude blood flow (also causes hemorrhage, see relevant box at left) Methemoglobinemia: some hemoglobin gets stuck in a state that can’t carry O2 Hemoglobin has reduced capacity to carry or release O2 Drugs: e.g. dapsone, nitrates Carbon monoxide poisoning Circulatory collapse / shock: inadequate perfusion of tissue with blood Respiratory collapse: blood has insufficient useable O2 content Ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT) Hypoxia*: inadequate O2 delivery or utilization in tissues Hypoxia creates metabolic disturbances that impair cardiac cells. Alternatively, any of the preceding conditions marked with (*) can directly trigger cardiac arrest first Pulseless Electrical Activity (PEA): organized activity on ECG with no cardiac output (can be preceded or mimicked by pseudo-PEA, in which there is still some output on ultrasound) Low atmospheric pressure or oxygen content Severe lung disease Asthma, COPD, interstitial lung disease, congestive heart failure, pulmonary hypertension, pulmonary embolism, lung collapse / atelectasis Acute respiratory distress syndrome Pneumonia, aspiration pneumonitis, inhalational injury, systemic inflammation, drowning Severe hypoventilation Respiratory fatigue, advanced COPD, chest wall disorders, neuromuscular disorders, upper airway obstruction, toxins (e.g. opioids, botulism) Can degenerate at any time Asystole: no cardiac electrical activity or output Death Respiratory arrest: cessation of breathing Inability to protect airway Decreased level of consciousness Note This is a broad overview of the many scenarios that can result in death. For detailed explanations of the various disease mechanisms, refer to the corresponding slides. * = reversible causes of cardiac arrest (Hs and Ts) Author: Ben Campbell Reviewers: Yan Yu* Huma Ali* * MD at time of publication Bradycardia (low heart rate, HR) Unopposed parasympathetic stimulation of heart (can also cause vasodilation, see Distributive problems) Disruption of spinal cord sympathetic control Injury to cervical or upper thoracic spinal cord Irreversible cessation of cardiac, respiratory, and brain function Prolonged seizure initially causes increased cardiovascular activity, until the system fatigues Disruption of respiratory control center in medulla Expanding skull contents squeeze brainstem (herniation) Increased intracranial pressure Edema from intracranial hemorrhage, trauma, brain mass Edema, inflammation, hypoxia and/or metabolic derangements cause diffuse neuron dysfunction Central nervous system infection Dementia, particularly with delirium Massive ischemic stroke Seizure activity prevents or alters breathing Metabolic disturbances that affect the central nervous system Hypoglycemia Hypocalcemia, hypercalcemia Hyponatremia, hypernatremia Uremia Acute liver failure (hyperNH4) Many drugs / toxins Withdrawal (e.g. EtOH) Status epilepticus Brainstem lesion (e.g. stroke, neoplasm, inflammatory) Nervous System Insult Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published November 11, 2023 on www.thecalgaryguide.com Respiratory System Insult Cardiovascular System Insult Cardiogenic problems

Complication of MI - Acute Mitral Regurgitation

Complication of MI: Acute mitral regurgitation Authors: Victória Silva Reviewers: Juliette Hall, Raafi Ali *Angela Kealey * MD at time of publication S3 Indicates rapid overfilling of ventricle S1 S2 S3 Calcified plaque formation (atherosclerosis**) commonly in the posterior descending artery Plaque ruptures Exposed plaque contentsàPlatelet adhesion and aggregation Artery becomes partially or completely occluded Mitral Regurgitation** (Back flow of blood from left ventricle to left atrium during systole) ↑ Left atrial pressure Blood from left atrium backs up into pulmonary venous system ↑ Pulmonary venous pressure ↑ Hydrostatic pressure in alveolar capillaries ↑ Fluid leak from alveolar capillaries to interstitium (pulmonary edema**) ↓ Gas exchange Attempt at physiologic compensation à ↑ Respiratory rate Tachypnea Holosystolic murmur Heard loudest over the mitral valve (5th intercostal space, mid-clavicular line), with radiation to the axilla ↑ Volume of blood to left ventricle during diastole ↓ Blood supply to the portion of the ventricle that supports the papillary muscle à↓ Muscle movement Left ventricle dysfunction ↓ Blood supply to the posterior medial papillary muscle Cell death (myocardial infarction) Papillary muscle ischemia (muscle is intact but cannot contract) ↑ Blood in right atriumà↑ Blood in superior vena cava ↑ Blood in internal jugular vein ↑ Jugular venous pressure (JVP) Redistribution of interstitial fluid when lying flat (reduced effect of gravity) ↓ Forward blood flow from left ventricle to aorta ↓ Stroke volume (SV) ↓ Cardiac output (CO) CO = SV x HR (heart rate) Sympathetic nervous system attempts to physiologically compensate ↑ Heart rate Tachycardia ↓ Blood pressure (BP) because BP = CO X SVR (systemic vascular resistance) Cardiogenic shock** Papillary muscle rupture Papillary muscle unable to provide adequate tension on mitral valve Mitral valve unable to stay closed during systole Orthopnea Difficulty breathing Dyspnea Paroxysmal nocturnal dyspnea **See corresponding Calgary Guide slides for more details Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published November 25, 2023 on www.thecalgaryguide.com

Angioedema Bradykinin Mediated

Angioedema – Bradykinin Mediated: Pathogenesis and clinical findings Drug Induced Angiotensin converting enzyme inhibitor, dipeptidyl peptidase-4 inhibitor, or neprilysin inhibitor use Hereditary Type II Acquired Thrombolytic use Activate factor XII Factor XII initiates bradykinin synthesis Type I Type III Gain of function gene mutation in bradykinin cascade activators (factor XII) & precursors (kininogen), triggered by ↑ systemic estrogen Rheumatologic disorders & B- cell lymphoproliferative disease Complement cascade activation results in ↑ C1 protease production C1 esterase inhibitor is utilized to neutralize C1 protease, with its consumption exceeding its synthesis Plasma cell proliferation (i.e., dyscrasia/ monoclonal gammopathy) Immunoglobulin G antibodies act against C1 esterase inhibitor to render it non-functional Genetic or spontaneous mutation in C1 esterase inhibitor gene C1 esterase inhibitor deficiency C1 esterase inhibitor dysfunction Inhibition of angiotensin converting enzyme, dipeptidyl peptidase-4, or neprilysin induced metabolism of bradykinin ↓ Bradykinin (peptide hormone) degradation in plasma Misfunctioning C1 esterase inhibiter is unable to inactivate bradykinin cascade members ↓ C1 esterase inhibiter results in inadequate inactivation of bradykinin cascade members ↑ Bradykinin protein production in plasma Cutaneous Tissue Mucosal Tissue Epidermal layer Dermal-Epidermal Junction Dermal layer Subcutaneous layer Systemic bradykinin excess Bradykinin-2 receptor binding on endothelial and vascular smooth muscle cells Hyperpermeability pathway activation, with the transcription of some signalling molecules taking hours Released pro-inflammatory mediators act on venules & arterioles in subcutaneous & submucosa tissues Relaxation of vascular smooth muscle Dissociation of endothelial cell junctions ↑ Capillary blood flow ↑ Vascular permeability ↑ Plasma release into interstitial tissues (specific regions of the body hypothesized to be affected due to local differences in endothelial structure and its response to permeability inducing stimuli) Dilation & ↑ permeability of vasculature results in fluid release into surrounding tissues Mucosal Layer Muscularis mucosae Submucosal layer Muscularis externa Intestinal edema (Fluid buildup in Intestine tissues) Intestinal swelling (↑ intra-abdominal pressure) Laryngeal edema (Fluid buildup in larynx) Swelling in larynx ↓ air flow into & out of lungs Asphyxia (body is deprived of oxygen) Dyspnea (difficult in breathing) Author: Aaron Varga Reviewers: Tracey Rice Sunawer Aujla Shahab Marzoughi Maharshi Gandhi Jori Hardin* Yan Yu* * MD at time of publication Peripheral edema (Fluid buildup in extremities such as the hands, ankles, and feet) Ascites, bowel obstruction, &/or hypovolemic shock Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published Mar 21, 2024 on www.thecalgaryguide.com