Blueprint Module A Pain & Oxygenation Exam Topics PDF

Blueprint Module A Pain Oxygenation IIIT (Infection, Immunity, Inflammation, Thermoregulation) Spring 2025 Total: 60-63 questions Pain 8-10; Oxygenation 20-22; IIIT 28-32 Pain Iden...

Blueprint Module A Pain Oxygenation IIIT (Infection, Immunity, Inflammation, Thermoregulation) Spring 2025 Total: 60-63 questions Pain 8-10; Oxygenation 20-22; IIIT 28-32 Pain Identify special populations of people and people across the people that may have special needs regarding pain. -​ Neonates: nonverbal, but research shows they have intact neural pathways of pain transmission -​ Children: response by crying, anxiety and stress; may not know how to ask for treatment; develop a memory that influences future experiences -​ Adolescents: emotional functioning influences coping -​ Adults: chronic pain is widespread problem; women > men -​ Older Adults: persistent pain is common; may be undertreated; slower metabolism to drugs (greater risk for higher blood levels and adverse effects) -​ People unable to self-report pain: many conditions affect a patient’s ability to report pain -​ Patients with substance abuse problems: use the American Society for Pain Management Nursing guidelines -​ Patients in CCU: intubated patients are challenging for pain or neuro assessment Discuss risk factors for pain conditions and risk factors for under-treatment of pain. -​ Risk factors for pain conditions: -​ Neonates, young adults in sports, individuals at risk for nerve disorders (neuropathies), older adults, individuals vulnerable to stress and impaired cortisol response, medical conditions involving traumatic injury, surgical procedures, critically ill. -​ Risk factors for undertreatment: -​ Cultural and societal attitudes, lack of knowledge, fear of addiction, exaggerated fear of respiratory depression Describe the withdrawal reflex. -​ powerful reflex stimulated by a nociceptive stimulus which causes the quick movement of the body part away from the offending stimulus, usually by flexing a limb. -​ I.E. burning your finger, and quickly pulling your hand back Describe physiological consequences of pain, including effects of unrelieved pain. -​ stress response causes the endocrine system to release excessive amounts of: cortisol, catecholamines, & glucagon -​ unrelieved pain: increased levels of nosocomial infections increased tumor growth -​ respiratory system is affected, decreased tidal volume, decreased lung capacity, pneumonia, atelectasis -​ CV system is affected, increased HR, increased BP, increased myocardial O2 consumption  -​ affects mobility and hinders recovery → may lead to impaired muscle function, muscle atrophy and joint contraction -​ unrelieved pain (nociceptive, acute) can lead to chronic pain through central sensitization Describe nociceptive pain, neuropathic pain, phantom limb pain, and breakthrough pain. -​ nociceptive pain: pain resulting from an external stimuli on an uninjured fully functional nervous system; warns of tissue damage -​ neuropathic pain: pain caused by a lesion or disease of the somatosensory nervous system; widespread pain that is not otherwise explainable; may involve few or many damaged axons -​ phantom limb pain: a type of neurologic pain following limb or body part amputation -​ breakthrough pain: a sudden increase in pain that may occur in patients who already have chronic pain from cancer, arthritis, fibromyalgia, or other conditions Differentiate between nociceptive and neuropathic pain. -​ refer to nociceptive pain pathophysiology if chronic pain is related to normally functioning nervous system -​ refer to neuropathic pain pathophysiology if pain is related to nerve impairs Explain the pathophysiology of nociceptive pain (transduction, transmission, perception and modulation). -​ transduction: the conversion of painful, tissue damaging stimuli to an electrical impulse through peripheral nerve fibers, known as nociceptors. -​ tissue damage results in the release of neurotransmitters. when these neurotransmitters attach to the membrane of the nociceptor → opening of ion channels → generation of an action potential -​ transmission: the process by which pain signals are relayed from the periphery to the spinal cord and then to the brain. pain impulses travel from the periphery, from the site of tissue injury, along the A and C nerve fibers into the dorsal horn of the spinal cord where neurotransmitters regulate it -​ perception: awareness of pain occurs when pain is recognized, defined, and assigned meaning by the person experiencing the pain. perception occurs in various areas of the brain, with influences from thought and emotional processes -​ modulation: refers to the process by which the body alters a pain signal as it is transmitted along the pathway. What are action potentials and ion channels, and how do they relate to the pathophysiology of pain? -​ action potential: a rapid change in voltage across a cell membrane. it is a nerve impulse that travels along the surface of an axon, affecting the entire excitable membrane. -​ it relates to the pathophysiology of pain in that the generation and propagation of action potentials within pain sensory neurons (nociceptors) is a critical step. -​ ion channel: a protein embedded in a cell membrane that acts as a pore, allowing specific ions to flow across the membrane according to their electrochemical gradient → a controlled pathway for charged particles to move in and out of the cell. -​ it relates to the pathophysiology of pain in that by acting as a key component in the transmission of pain signals from the site of injury to the central nervous system where pain is perceived → when activated by noxious stimuli, ion channels allow ions to flow across the cell membrane generating electrical pulses that travel as pain signals to the brain. Explain the pathophysiology of chronic neuropathic pain (peripheral sensitization, central sensitization, allodynia, hyperalgesia, neuroplasticity). -​ peripheral sensitization: injury to a peripheral nerve results in prolonged, intense, stimulation of nerves (lower threshold for activation), resulting in enhanced response. -​ central sensitization: an exaggerated response is generated to painful stimuli (hyperalgesia) and contributes to allodynia (the brain perceives mild stimuli as painful) -​ allodynia: when the brain perceives a mild (typically non-painful) stimuli as painful -​ hyperalgesia: an exaggerated response to painful stimuli, extreme sensitivity -​ neuroplasticity: processes that allow neurons in the brain to compensate for injury and adjust their responses to new situations or changes in the environment; it CAN contribute to adaptive mechanisms for reducing pain, but can also result in MALadaptive mechanisms that enhance pain sensitivity → the brain’s ability to change its structure and function in response to new experiences and learning Differentiate between acute/chronic pain; somatic (superficial cutaneous and deep), visceral pain, and referred pain. -​ acute: < 3 months, nociceptive, serves as a warning system (protective), increased HR and BP, anxiety, grimacing, moaning, etc. -​ chronic: > 3 months, nociceptive or neuropathic, no real purpose, depression, fatigue, sleep disturbance, disability, muscle spasms, limited mobility or groaning with movement -​ somatic cutaneous: superficial (skin and mucous membranes), sharp pain – abrupt or slow in onset, easily localized, sunburn or skin contusions -​ somatic deep: from nociceptors in muscles, tendons, joints, blood vessels, connective tissue; sharp pain associated with swelling, cramping, or bleeding; localized or diffused and radiating, arthritis or tendonitis -​ visceral: nociceptive, origin in visceral organs (kidney, stomach, pancreas, gallbladder), caused from strong contractions, distention, or ischemia affecting walls of viscera; pain is deep, dull, or aching; well or poorly localized -​ referred: nociceptive, pain that is perceived at a site different from its point of origin but innervated by same spinal segment; occurs when nerve fibers that innervate the injured region and nerve fibers from other regions converge at the same level in the spinal cord and the brain can’t identify the original source; pain is poorly localized; MI, gallbladder Distinguish between clinical manifestations of acute & chronic pain. -​ acute: autonomic → increased HR and BP, dilated pupils, increased muscle tension, decreased GI motility and salivation, N/V, rapid, shallow respirations, diaphoresis, pallor; behavioral → anxiety, grimacing, moaning, flinching, guarding, decreased ADLs -​ chronic: physiologic → absence of autonomic response (vs usually not affected or lower than normal), appetite changes or loss; behavioral → depression, fatigue, sleep disturbance, decreased functioning ability, disability, withdrawal from outside interests; may include → compensatory posturing, muscle spasms or tense muscles, limited mobility or groaning with movements, clenched teeth Describe risk factors and etiology of peripheral neuropathy. -​ risk factors: diabetes, age, alcohol, genetics, autoimmune diseases, infections (herpes–shingles), toxins, meds, injuries, nutritional deficiencies (B), trauma or injury, chronic kidney disease and hypothyroidism -​ etiology: metabolic conditions, toxins and drugs, infections, autoimmune diseases, trauma or compression, genetic disorders, nutritional deficiencies Discuss the etiology and clinical manifestations of mononeuropathy & polyneuropathy. -​ mononeuropathy (damage to a single nerve causing local pain, weakness, and numb) -​ etiology: direct trauma or injury, nerve compression, systemic diseases, infections, tumors, autoimmune diseases, vitamin deficiencies, toxins/meds -​ clinical manifestations: sharp, burning, or aching pain; numbness or tingling, weakness, loss of reflexes, muscle atrophy, discomfort with touch, paralysis -​ polyneuropathy (damage to multiple nerves, symmetrically) -​ etiology: diabetes mellitus, autoimmune diseases, infections,toxins and drugs, nutritional deficiencies, hereditary conditions, chronic kidney disease,thyroid disorders, alcoholism, metabolic disorders, cancer, idiopathic (unidentified) -​ clinical manifestations: sensory → numbness, tingling, pain, allodynia, loss of coordination; motor → muscle weakness, muscle atrophy, foot drop, clumsiness; autonomic → orthostatic hypotension, digestive issues, excessive sweating or heat tolerance, urinary issues; reflex changes → diminished, impaired proprioception; progression of patterns → often in distal limbs, typically symmetric to both sides Explain the following terms: pain threshold & pain tolerance. -​ pain threshold: the point at which a stimulus is perceived as painful by a person -​ pain tolerance: the amount of pain a person is willing to bear; also the response to a drug due to repeated drug administration Discuss pharmacologic management of pain; how do NSAIDs (Aspirin & Ibuprofen), and Tylenol (alternative to NSAIDs) work to control pain. Discuss indications for opioid analgesics (Morphine). What are adjuvant (co-analgesic) medications (examples include antidepressants and anticonvulsants). -​ NSAIDs: inhibit COX enzymes which interfere with prostaglandin synthesis, decrease sensitivity of blood vessels to bradykinin and histamines, reverse vasodilation, decrease release of inflammatory mediators from mast cells and basophils -​ indications for opioid analgesics: manages acute or chronic pain, but requires careful monitoring due to potential side effects (respiratory depression or LOC) and risks of addiction -​ adjuvant medications: have analgesic properties, potentiate the effects of pain medications, relieve other discomforts, or reduce the side effects of analgesic drugs Describe non-pharmacologic treatment of pain. -​ cognitive behavioral interventions -​ relaxation → slow rhythmic breathing -​ distraction → makes pain more tolerable -​ imagery → using imagination to develop a mental picture -​ massage → aid in acute or chronic pain -​ biofeedback → learning to make the person aware of their body functions and modifying these functions at a conscious level (temp, BP, muscle tension) -​ physical agents -​ heat, cold, TENS unit, acupuncture Describe the effects of pain across the lifespan. -​ neonates → nonverbal but have intact neural pathways of pain transmission -​ children → respond by crying, anxiety and stress; may not know how to ask for treatment; develop a pain memory that influence future pain experiences -​ adolescents → emotional functioning influences coping -​ adults → chronic pain is widespread; more prevalent in women -​ older adults → persistent is common, may be undertreated, metabolize drugs slower so are at greater risk for high BP levels and adverse effects Describe the gate control theory of pain. -​ a mechanism within the spinal cord acts like a “gate” which can either allow or block pain signals from reaching the brain -​ when open → pain signals can be sent up to the brain and is PERCEIVED -​ when closed → pain signals do not reach the brain IIIT General: Define specific terms involved with infection, immunity, inflammation and thermoregulation. -​ infection -​ pathogen: an organism, such as a bacterium, virus, or fungus, that causes disease by invading the body. -​ bacteremia: the presence of bacteria in the bloodstream, which can lead to infection in other parts of the body. -​ viremia: the presence of viruses in the blood, which can spread infection to various organs. -​ Sepsis: a life-threatening condition caused by the body's response to infection, leading to widespread inflammation and potential organ failure. -​ carrier: an individual who harbors a pathogen but does not show symptoms of infection, though they can still spread it. -​ immunity -​ innate immunity: the body’s first line of defense, non-specific and present at birth. it includes physical barriers like skin, as well as immune cells like macrophages and neutrophils. -​ adaptive immunity: a specific immune response that develops over time after exposure to pathogens. this involves T cells, B cells, and antibodies. -​ antigen: any substance that triggers an immune response, typically parts of pathogens like proteins or polysaccharides. -​ antibody: proteins produced by B cells in response to antigens; they bind to pathogens to neutralize them or mark them for destruction. -​ immunization: the process of inducing immunity through vaccines or exposure to an antigen, helping the immune system recognize and fight future infections. -​ inflammation -​ inflammatory response: the body’s reaction to infection or injury, involving redness, heat, swelling, pain, and sometimes loss of function. -​ cytokines: signaling proteins released by immune cells that help regulate inflammation and immune responses.  -​ histamine: a compound released by mast cells during inflammation, causing blood vessels to dilate and increase permeability, leading to swelling and redness. -​ phagocytosis: the process by which immune cells (like macrophages) engulf and digest pathogens, dead cells, and debris. -​ exudate: fluid that leaks from blood vessels during inflammation, containing immune cells, proteins, and sometimes pathogens or debris -​ thermoregulation -​ hypothalamus: the part of the brain that regulates body temperature, balancing heat production and loss. -​ pyrexia (fever): an increase in body temperature often caused by infection or inflammation, as a response to kill or inhibit the growth of pathogens. -​ vasodilation: the widening of blood vessels, which allows more blood to flow near the skin surface to release heat and cool the body. -​ vasoconstriction: the narrowing of blood vessels to reduce heat loss when the body is cold. -​ sweating: the process by which the body releases moisture through the skin, which cools the body when it evaporates. -​ shivering: rapid muscle contractions that generate heat to raise body temperature during cold exposure. -​ thermoregulatory set point: the target body temperature that the hypothalamus attempts to maintain, typically around 37°C (98.6°F) in humans. Describe the function of cells involved with inflammation and immunity including endothelial cells, platelets, neutrophils, monocytes, eosinophils, basophils and mast cells. -​ endothelial cells: Regulate blood flow and immune cell migration. -​ platelets: Promote clotting and release inflammatory mediators. -​ neutrophils: First responders to infection, phagocytize pathogens, and release antimicrobial agents. -​ monocytes: Differentiate into macrophages or dendritic cells that clear pathogens and initiate adaptive immunity. -​ eosinophils: Defend against parasitic infections and contribute to allergic inflammation. -​ basophils: Release histamine and other mediators, contributing to allergic responses and inflammation. -​ mast cells: Release histamine and other substances in response to allergens, playing a central role in allergic reactions. General Infection: Describe people at increased risk to develop an infection. -​ age, socioeconomic status, geographic location, compromised host: immunodeficiency, compromise host: chronic disease, environmental conditions Discuss the etiology and pathophysiology of infections. -​ etiology: -​ bacteria, viruses, fungi -​ pathophysiology: -​ modes of transmission/portal of entry, susceptible host, pathogen, reservoir, portal of exit How do virulence factors (endotoxins and exotoxins) play a role in disease?  -​ Endotoxins: are part of the outer membrane of Gram-negative bacteria. When released, they trigger inflammation, fever, and can cause septic shock and organ failure through immune system activation. -​ Exotoxins are secreted proteins that directly harm host cells. They can: -​ Cytotoxins kill cells. -​ Neurotoxins affect nerves (e.g., tetanus). -​ Enterotoxins cause diarrhea (e.g., cholera). -​ Some exotoxins cause severe immune reactions, like toxic shock syndrome. -​ Both endotoxins and exotoxins contribute to the severity of infections by damaging tissues, triggering immune responses, and potentially leading to shock or organ failure. Discuss the chain of infection, mechanisms (process of infection) and symptomatology (clinical picture). -​ infectious agent -​ definition: the microorganism that causes the disease (bacteria, viruses, fungi, parasites). -​ examples: E. coli, Influenza virus, Malaria parasite. -​ role: this is the start of the chain. without the pathogen, infection can't occur. -​ reservoir -​ definition: the place where the pathogen lives, grows, and multiplies. this could be a human, animal, or environmental source (like soil or water). -​ examples: ​ humans (carriers or infected individuals) ​ animals (e.g., rabies in bats or rodents) ​ environmental sources (e.g., water containing Vibrio cholerae). -​ role: the reservoir is essential for the pathogen’s survival and spread. It can be asymptomatic or symptomatic hosts. -​ portal of exit -​ definition: the path the pathogen takes to leave the reservoir and spread to others. -​ examples: ​ respiratory tract (cough, sneeze) ​ gastrointestinal tract (vomit, diarrhea) ​ blood (via open wounds or insect bites) ​ urinary tract (urine) -​ role: this allows the pathogen to exit the reservoir and reach a new host. -​ mode of transmission -​ definition: how the pathogen travels from the reservoir to a susceptible host. -​ types: ​ direct contact (e.g., skin-to-skin, sexual contact) ​ indirect contact (e.g., contaminated objects like doorknobs, towels) ​ droplet transmission (e.g., cough, sneeze) ​ airborne transmission (e.g., TB, measles) ​ vector-borne transmission (e.g., mosquitoes transmitting malaria or dengue). -​ role: the mode of transmission determines how easily a pathogen spreads. -​ susceptible host  -​ definition: the individual who is at risk of being infected by the pathogen. the degree of susceptibility depends on factors like age, immune status, and underlying health conditions. -​ examples: ​ infants, elderly, immunocompromised individuals (e.g., cancer patients or people with HIV). ​ people who have not been vaccinated or have low immunity to specific pathogens. -​ role: the host must be vulnerable for the infection to take hold and spread. -​ breaking the chain of infection -​ to prevent the spread of infection, interrupting any of these links is crucial. for example: ​ vaccination (reduces susceptibility). ​ handwashing and sanitation (breaks transmission through direct or indirect contact). ​ using masks (prevents droplet transmission). ​ antibiotics or antivirals (can target pathogens directly). Identify the stages in the disease course. -​ incubation period: the phase during which the pathogen begins active replication without producing symptoms -​ prodromal stage: initial appearance of symptoms, with vague clinical presentation -​ acute or illness stage: host experiences maximum impact of symptoms -​ convalescent period: containment of infection Describe signs and symptoms (clinical manifestations) of infection across the lifespan. -​ infants and newborns: -​ Symptoms: poor feeding, lethargy, irritability, fever or hypothermia, respiratory distress (rapid breathing or grunting), jaundice, and dehydration. -​ Note: infections can be subtle or non-specific. -​ children (toddlers to adolescents) -​ symptoms: fever, fatigue, irritability, loss of appetite, rashes (e.g., chickenpox), respiratory symptoms (cough, wheezing), localized pain (e.g., ear pain), and vomiting/diarrhea. -​ note: children may show more behavioral signs (crying or irritability) due to inability to communicate symptoms. -​ adults -​ Symptoms: fever, fatigue, localized pain (e.g., abdominal pain), respiratory symptoms (cough, shortness of breath), gastrointestinal issues (nausea, diarrhea), and rashes. -​ note: infections often present more classically here, but can still vary depending on the pathogen. -​ older adults -​ symptoms: low-grade fever or absence of fever, confusion/delirium, fatigue, decreased appetite, unexplained pain, and respiratory distress. -​ note: cognitive changes (e.g., confusion) can be a major sign, and symptoms may be less obvious. -​ general signs across all ages:  -​ common symptoms: fever, chills, pain, swelling, redness, fatigue, and decreased function. -​ note: symptoms can be less pronounced or atypical in infants and older adults. Differentiate between primary and secondary infection. -​ primary: -​ Definition: a primary infection is the initial infection caused by a pathogen (bacteria, virus, etc.) that enters the body and causes disease for the first time. -​ cause: it is the first infection in an otherwise healthy individual. -​ example: a person develops influenza after being exposed to the flu virus, or a person gets a sinus infection caused by a primary bacterial infection. -​ characteristics: the pathogen directly causes the symptoms and the infection. -​ secondary: -​ definition: a secondary infection occurs after the primary infection, often because the body’s immune system is weakened or compromised by the initial infection. -​ cause: it is typically caused by a different pathogen that takes advantage of the body's weakened defenses, which were already taxed by the primary infection. -​ example: after having the flu (primary infection), a person might develop pneumonia (secondary infection) due to a bacterial infection like Streptococcus pneumoniae. another example is a skin infection that develops after a cold sore (herpes simplex virus). -​ characteristics: secondary infections often complicate the course of the primary infection and may result in more severe illness. -​ key differences: -​ order: primary infection occurs first; secondary infection happens after the primary infection. -​ pathogen: primary infections are caused by the initial pathogen; secondary infections are caused by a different pathogen, often opportunistic. -​ impact: secondary infections usually arise when the immune system is weakened, typically by the primary infection, treatments (e.g., antibiotics), or other factors like comorbidities. Describe specific ways infections are diagnosed. Discuss general categories of medications used to treat infections. -​ culture: -​ blood, urine, feces, sputum, spinal fluid, wound, abscesses, sinus tract, skin lesions, GU tract -​ ID based on microscopic appearance; gram stain, shape/texture/color of colonies and biochemical reactions -​ serology: -​ indirect; identifying infectious agents by measuring serum antibodies in the diseased host -​ antibody titer rises during the acute phase; falls during convalescence -​ DNA/RNA sequencing -​ assess patients response to infection and response to therapy  -​ wbc count and differential, procalcitonin, antibiotic peak/trough levels, radiologic examination, lumbar puncture, ultrasound, lumbar puncture Identify common healthcare acquired infections; describe the pathophysiology of a CAUTI. -​ common infections: -​ CLABSI: central line associated bloodstream infection -​ CAUTI: catheter associated urinary tract infection -​ SSI: surgical site infection -​ VAP: ventilator associated pneumonia -​ hospital-acquired pneumonia -​ pathophysiology of a CAUTI: -​ bacteria adhere to surface of catheter → initiate growth of biofilms to catheter surface → biofilm protects the bacteria from the host response and antibiotic action UTI: Discuss urinary tract infection including risk factors for developing a UTI, etiology, patho- physiology, and clinical manifestations in adults, pregnant women, and older adults. -​ risk factors: -​ females, older adults, alkaline urine, indwelling urinary catheters, stool incontinence, bladder distension, urinary conditions (anomalies, stasis, calculi, residual urine), disease (diabetes) -​ etiology: -​ pathogenic bacteria → E. coli and K. pneumoniae -​ urinary obstruction and reflux -​ urinary catheterization (nosocomial UTI) -​ most are caused from bacteria entering the urethra -​ bacteria entering via bloodstream -​ bacteria colonizes urethra, vagina, or perianal area -​ pathogen virulence -​ pathophysiology: -​ obstruction → outflow obstruction causes urine to remain in the bladder = medium for bacterial growth. (causes may be anatomic or functional) -​ anatomic: associated with stasis of urine flow -​ urinary tract stones, prostatic hyperplasia, pregnancy, malformation of ureterovesical junction -​ functional: -​ neurogenic bladder, infrequent voiding, detrusor (bladder) muscle instability, constipation -​ reflux: -​ urethrovesical reflux: occurs mostly in women → related to activities that increase intra-abdominal pressure; causes urine to be squeezed into the urethra and then flow back into the bladder -​ vesicoureteral: this junction normally closes during bladder contraction, preventing reflux of urine to the ureters and kidneys; may results from congenital defects of the ureter that force urine into the ureter during micturition; may occur in adults with bladder outflow obstruction (as with benign hyperplasia)  -​ clinical manifestations: -​ adults: -​ lower UTI symptoms: (related to bladder storage or emptying) -​ dysuria, frequency, urgency, suprapubic discomfort, hematuria (visible blood) or sediment (cloudy appearance), usually does NOT have systemic symptoms -​ upper UTI symptoms: (involve the renal parenchyma and pelvis) -​ fever, chills, flank pain -​ pregnant women: asymptomatic bacteriuria (presence of bacteria without symptoms) — common, but can lead to UTI → pyelonephritis and other complications -​ older adults: confusion or impaired cognition, incontinence, general abdominal discomfort instead of dysuria or suprapubic or flank pain, loss of appetite, nocturia, fever and chills may be absent -​ children: -​ newborns: fever, feeding problems, vomiting, diarrhea, irritability, apneic episodes, lethargy, foul-smelling urine -​ infants: fever, feeding problems, vomiting, diarrhea, and foul-smelling urine -​ toddlers: fever, abdominal pain, vomiting, diarrhea, foul-smelling urine -​ older children: fever, frequency, dysuria, suprapubic pain Describe diagnostic testing, and treatment of UTIs. -​ diagnosis: -​ H&P -​ urinalysis diagnosis — presence of: 100,000+ CFUs, nitrites (bacteria reduce nitrates to nitrites), leukocyte esterase (leukocytes secrete esterase [enzyme]) -​ urine culture and sensitivity to guide treatment -​ x-ray, ultrasound, CT and renal scans to identify causative factors -​ treatment: -​ most lower UTIs from E. coli are treated by antibiotics -​ treatment with antibiotics based on culture and sensitivity -​ bladder analgesic -​ forcing fluids may be relieve → adjunct to antibiotic -​ recurrent lower UTIs -​ remove causative agent, education on pathogen transmission measures, cranberry juice may reduce bacterial adherence to epithelial lining of tract -​ chronic UTIs – more difficult to treat -​ correct underlying problems, such as enlarged prostate -​ probiotics > antibiotics (if effective) Describe host defense mechanisms against a UTI. -​ women: are protected by the normal flora of the periurethral area, which consists of organisms such as Lactobacillus, which provides defense against the colonization of uropathic bacteria -​ men: are protected by prostatic fluid General Immunity: Compare and contrast innate and adaptive immunity. What are 2 components of innate  immunity? -​ innate: present at birth; provides nonspecific response, not antigen specific. can distinguish self from non-self; early; more rapid response. -​ neutrophils, macrophages, dendritic cells, natural; killer cells -​ adaptive (acquired): final line of defense. involves humoral and cellular mechanisms that respond to antigens ; recognizes antigens on repeat exposure Compare and contrast cell-mediated and humoral immunity; and the types of cells involved in each. -​ cell-mediated immunity: -​ key cells: ​ cytotoxic T cells (CD8+): directly kill infected or cancerous cells. ​ helper T cells (CD4+): assist in activating cytotoxic T cells, macrophages, and B cells. ​ regulatory T cells (Tregs): regulate immune responses and prevent autoimmunity. -​ mechanism: ​ targets intracellular pathogens (viruses, certain bacteria) and abnormal cells (cancer). ​ cytotoxic T cells destroy infected cells by recognizing antigens on MHC Class I molecules. ​ helper T cells release cytokines to activate macrophages and T cells. ​ macrophages are activated to engulf pathogens. -​ memory: ​ forms memory T cells that remember and respond faster to future infections. Compare antigens and antibodies. -​ antigens: -​ definition: foreign molecules (e.g., proteins or polysaccharides) that trigger an immune response. -​ source: found on pathogens (viruses, bacteria), allergens, or abnormal cells (e.g., cancer). -​ function: stimulate immune system to produce antibodies or activate T cells. -​ types: exogenous (outside the body), endogenous (inside the body), autoantigens (body’s own cells mistaken for foreign). -​ antibodies: -​ definition: proteins produced by B cells to neutralize or mark antigens for destruction. -​ structure: Y-shaped with a variable region that binds to antigens. -​ function: neutralize pathogens, mark them for phagocytosis, and activate the complement system. -​ types: IgG, IgA, IgM, IgE, IgD. -​ key differences: -​ antigens: trigger immune response, found on pathogens or abnormal cells. -​ antibodies: produced by the immune system to target and neutralize antigens. Discuss the key features and mechanisms of autoimmune disease and risks for altered immunity.  -​ key features: -​ self-tolerance — ability of body’s immune system to differentiate between foreign and self antigens; in autoimmune disorders there is FAILURE of self-tolerance -​ mechanisms: -​ gender: more frequent in women likely related to estrogen influencing the immune system -​ heredity: high concentration in 1st degree relatives -​ environmental factors: viral infection, exposure to chemicals, (i.e. type 1 diabetes mellitus; diabetes) -​ risks for altered immunity: these individuals have unusual antibodies circulating in their blood that target their own body tissues → (increased susceptibility to infections, autoimmune flares, overactive immune response, impaired immune regulation) Describe why infants and elderly have decreased immune system function. -​ infants: have weaker immune systems because it is still developing and lacks exposure to pathogens. while they receive passive immunity through breast milk, their own immune responses are not fully functional yet -​ elderly: experience decreased immunity due to immunosenescence—a decline in immune system function with age. this includes slower immune responses, reduced production of immune cells, and weakened reactions to vaccines. chronic conditions and medications also contribute to their increased vulnerability to infections. Describe active and passive immunity, and give examples. -​ active: acquired when the host mounts an immune response to an antigen either through the process of vaccination or from environmental exposure (active because it requires the host’s own immune system to develop an immunological response including the development of memory) -​ examples: immunity to a virus after having a cold; immunity to polio after having the vaccine -​ passive: immunity transferred from one source to another; occurs also by introduction of preformed antibodies -​ examples: mother to fetus; immunoglobulins Rheumatoid Arthritis Describe risk factors for RA, etiology and pathophysiology of RA, and diagnostic testing. -​ risk factors: -​ age (frequency increases) -​ gender (women 3:1 over men) -​ 1st degree relatives -​ family hx -​ individuals with the HLA-DR4 marker -​ smoking -​ bacterial or viral infection (particularly Epstein-Barr virus) -​ obesity, physical/emotional stress, or exposure to environmental toxins -​ etiology:  -​ the etiology is unknown; however evidence suggests it results from a combination of genetics and environmental triggers, most likely an autoimmune case. a key genetic factor → HLA-DR4 -​ exposure to the antigen (bacteria, viruses, such as Epstein-Barr) may play a role in initiating the autoimmune response -​ in genetically predisposed individuals, exposure to HLA-DR4 antigen causes unusual immune response -​ with long-term exposure to the antigen, normal antibodies become autoantibodies (rheumatoid factors) that attack the host -​ rheumatoid factor (RF) is a self-antibody present in 70-80% of pts. with RA -​ pathophysiology: -​ genetically predisposed person is exposed to virus → exposed to antigen → unusual immune response → activation of T helper cells → release of cytokines and antibody formation → autoantibodies react with IgG to form immune complexes which deposit on synovial membranes or superficial cartilage → inflammatory response, neutrophils, macrophages, and lymphocytes arrive → begin phagocytosis of immune complexes → lysosomal enzymes are released → destruction of joint cartilage → attraction of additional inflammatory cells and intensifies response → warmth, redness from vasodilation and increased blood flow → joint swelling from increased capillary permeability → reactive hyperplasia (abnormal reproduction of synovial cells) an abnormal thickened layer of granulation tissue develops (PANNUS) -​ pannus: destructive vascular granulation tissue → destroys adjacent cartilage and bone → develops between joint margins → reduced joint motion → ankylosis. **destructive changes are irreversible -​ diagnostic testing: -​ made when: -​ all three criteria are met: -​ inflammatory arthritis of 3 or more joints, positive RF and/or anti-citrullinated peptide antibody, elevated c-reactive protein levels or ESR -​ differential diagnosis rules out psoriatic arthritis/acute viral polyarthritis/gout or systemic lupus erythematosus -​ duration of symptoms is greater than 6 weeks -​ joints have soft spongy feeling along with signs of inflammation. body movements may be guarded to prevent pain -​ the RF test are not diagnostic for RA but can be of value differentiating RA from other forms of arthritis Discuss clinical manifestations, including articular (joint) manifestations and extra-articular manifestations. -​ clinical manifestations: -​ insidious (gradual onset): fever, weakness, anorexia, weight loss, general aching and stiffness, characterized by exacerbations and remissions -​ articular (joint) manifestations: -​ spinal involvement is limited to cervical region -​ symmetric, bilateral movement  -​ redness, warmth, pain, and swelling of affected sites -​ INITIAL limitation of motion RT pain; LATER fibrosis/sclerosis -​ joint swelling and deformity -​ joint stiffness, more pronounced in the morning -​ most common in fingers, hands, wrists, knees, and feet -​ pain at rest and with movement -​ hands and fingers: -​ bilateral, symmetric involvement of PIP and MCP joints; DIP joint affected later -​ progressive damage can lead to dislocation of joint causing misalignment of bone ends, instability of joint, limitation of movement -​ swelling and thickening of synovium stretches the joint capsule and ligaments, causing joint deformities -​ ulnar deviation of fingers when extensor tendons in MCP joints slip to ulnar side -​ swan neck deformity of fingers -​ boutonniere deformity -​ knee: one of the most common joints affected -​ active synovitis is seen as visible swelling -​ bulge sign -​ joint contractures, instability and knock-knee deformity -​ baker cyst -​ ankle: limited flexion and extension -​ can cause walking difficulty -​ toe: metatarsophalangeal joint involvement -​ hallux valgus and hammer toe -​ neck: discomfort common -​ rare → neurologic complications such as occipital headaches, muscles weakness, numbness, and tingling in upper extremities -​ extra-articular manifestations: outside the joint -​ fatigue, weakness, anorexia, weight loss, low grade fever -​ elevation of ESR -​ anemia (of chronic disease) -​ rheumatoid nodules -​ vasculitis (inflammation of small and medium arteries) -​ episcleritis and scleromalacia -​ splenomegaly -​ lymph node enlargement (less common) Discuss the goals of treatment of RA; discuss actions and side effects of Methotrexate and Sulfasalazine. What is the action of corticosteroids in general? -​ treatment goals: -​ pharmacologic: reduce joint pain, decrease inflammation, maintain or restore joint function, prevent bone and cartilage destruction -​ non-pharmacologic: to prevent and/or reduce pain, decrease stiffness and swelling, maximize mobility, and possibly halt the process of RA -​ methotrexate: DMARD  -​ actions: 1st line of treatment, potent –improvement in around 1 month; by interfering with pure metabolism, a potent anti-inflammatory compound is released -​ side effects: bone marrow suppression, (leukopenia, anemia, thrombocytopenia); mouth ulcers; urinary retention; severe skin reactions; hepatotoxicity -​ sulfasalazine (azulfidine): DMARD -​ actions: acts as an immune system suppressant; also as an aminosalicylate which reduces inflammation and swelling; inhibits transcription factor and suppresses pro-inflammatory genes, including tumor necrosis factor; prescribed in combination with Methotrexate -​ side effects: leukopenia, abnormal liver function tests, dyspnea. also may cause serious skin reactions such as exfoliative dermatitis, Steven-Johnsons syndrome, toxic epidermal necrolysis, and generalized exanthematous pustulosis. -​ action of corticosteroids: -​ used to reduce discomfort, interrupt inflammatory and immune response; they do NOT modify the disease or prevent joint destruction General Inflammation: ompare acute and chronic inflammation, including what is happening in the body. -​ acute: -​ duration: short-term (minutes to days) -​ cause: triggered by an immediate injury, infection, or irritation (e.g., cuts, infections, burns). -​ what’s happening in the body: ​ the body’s immune system reacts quickly to neutralize the threat. ​ blood vessels dilate (increase in size) to increase blood flow to the affected area, which causes redness and warmth. ​ white blood cells, such as neutrophils, move toward the site of infection or injury to fight off pathogens or clear damaged tissue. ​ the release of chemicals like histamines and prostaglandins causes swelling (edema), pain, and sometimes fever. -​ outcome: in an ideal scenario, the inflammation resolves once the threat is neutralized, tissue is repaired, and the immune response subsides. -​ chronic: -​ duration: long-term (weeks, months, or even years) -​ cause: can be caused by unresolved acute inflammation, persistent infections, autoimmune diseases, or ongoing exposure to irritants (e.g., smoking or environmental toxins). -​ what’s happening in the body: ​ the inflammatory response doesn’t resolve and continues, often at a low level but with significant long-term effects. ​ the immune system remains activated, with the body sending immune cells like macrophages and T-cells to the site of inflammation. ​ tissue damage and scarring may occur due to prolonged inflammation (e.g., fibrosis, organ damage)\  ​ ] ​ chronic inflammation can lead to the release of cytokines and other molecules that promote further inflammation and even the development of disease (e.g., cardiovascular disease, arthritis, cancer). -​ outcome: chronic inflammation is linked to a range of serious conditions, including autoimmune diseases (like rheumatoid arthritis), cardiovascular diseases, and some cancers. It can also contribute to tissue degeneration. -​ key differences: -​ duration: acute is brief, while chronic is prolonged. -​ cause: acute inflammation is often caused by an injury or infection, while chronic inflammation can result from continuous irritation or immune system dysfunction. -​ symptoms: acute inflammation has clear signs like redness, heat, swelling, and pain. Chronic inflammation is often silent or has subtle, long-term symptoms. -​ tissue damage: chronic inflammation can cause ongoing damage, while acute inflammation is meant to resolve once the issue is dealt with. Compare local and systemic inflammation, including clinical manifestations (sign/symptoms). -​ local: -​ Scope: Restricted to a specific area or tissue. -​ Causes: Typically triggered by injury, infection, or irritation in a localized region (e.g., a cut, sprain, or infected wound). -​ Clinical Manifestations (Signs/Symptoms): ​ Redness (erythema) ​ Heat (increased blood flow) ​ Swelling (edema from fluid accumulation) ​ Pain (due to pressure from swelling and chemicals like prostaglandins) ​ Loss of function (possible limitation of movement or function in the affected area, e.g., a sprained ankle) -​ systemic: -​ scope: affects the entire body. -​ causes: often triggered by widespread infections (like sepsis), autoimmune diseases, or chronic conditions (e.g., inflammatory bowel disease or rheumatoid arthritis). -​ clinical manifestations (signs/symptoms): ​ fever (increased body temperature) ​ fatigue (feeling generally unwell or exhausted) ​ increased heart rate (tachycardia) ​ elevated white blood cell count (leukocytosis) ​ malaise (general sense of discomfort or illness) ​ increased inflammatory markers (e.g., C-reactive protein, ESR) -​ key differences: -​ local inflammation is confined to one area, with symptoms like redness, swelling, and pain, while systemic inflammation affects the whole body, often with fever, fatigue, and increased inflammatory markers. -​ local is more direct and obvious (e.g., a swollen ankle), while systemic may be harder to pinpoint, involving general symptoms like fever and fatigue that can be caused by underlying diseases or infections. Describe the vascular phase of acute inflammation including vascular changes that occur. -​ vasodilation: blood vessels widen, increasing blood flow to the affected area, causing redness and heat. -​ increased permeability: blood vessel walls become more porous, allowing proteins (like antibodies and clotting factors) and immune cells to leak into the tissue, leading to swelling (edema). -​ exudation: fluid, proteins, and white blood cells move out of the bloodstream into the tissue. -​ stasis: blood flow slows, making blood thicker and allowing white blood cells to stick to vessel walls (margination). this phase results in classic inflammation signs: redness, heat, swelling, and pain, all aimed at containing the injury and starting immune response and repair. Describe the effect of vasodilation during inflammation from infection or injury. -​ increased blood flow: causes redness and heat, delivering more oxygen and nutrients to the area. -​ enhanced immune response: white blood cells (e.g., neutrophils) reach the site to fight infection and aid in repair. -​ increased permeability: blood vessels become "leaky," allowing proteins to enter tissues, which helps isolate pathogens and support clotting. -​ swelling (edema): fluid leaks into tissues, causing swelling and contributing to pain. -​ nutrient delivery: supplies oxygen and nutrients to support tissue repair and immune activity. Discuss how inflammation can be harmful with an exaggerated or inadequate response. -​ exaggerated inflammation: -​ tissue damage: chronic inflammation (e.g., rheumatoid arthritis) can destroy healthy tissues. -​ autoimmune diseases: the immune system attacks the body’s own tissues (e.g., lupus, MS). -​ chronic diseases: linked to conditions like cardiovascular disease and cancer. -​ increased risk of infection: damaged tissues make the body more susceptible to infections. -​ inadequate inflammation: -​ impaired infection control: weak immune response leads to chronic infections (e.g., HIV). -​ delayed healing: slower tissue repair, leading to chronic wounds. -​ increased risk of sepsis: infections may spread without proper inflammation, risking sepsis. -​ cancer progression: inability to detect and destroy abnormal cells, allowing cancer to develop. Describe the cells involved in inflammation: endothelial cells, platelets, neutrophils (including segs and bands), monocytes, eosinophils, basophils, and mast cells. -​ endothelial cells: regulate vascular changes, allowing immune cells and proteins to enter tissues. -​ platelets: release mediators that help in clotting and inflammation. -​ neutrophils: first responders, engulfing pathogens and contributing to pus formation. -​ monocytes: differentiate into macrophages, clear debris, and regulate inflammation. -​ eosinophils: fight parasitic infections and contribute to allergic inflammation. -​ basophils: release histamine and other mediators, involved in allergic responses. -​ mast cells: release histamine and other inflammatory mediators, critical in allergic reactions. each of these cells has a specific role in initiating, maintaining, and resolving inflammation, and they interact with each other to ensure the appropriate immune response. What are inflammatory mediators and how are they involved with inflammation? -​ molecules that regulate the inflammatory response. they can be proteins, lipids, or small molecules, and they help initiate, amplify, and resolve inflammation -​ histamine: one of the first mediators to be released during an acute inflammatory reaction -​ found in platelets, basophils, and mast cell granules -​ causes dilation of arterioles and increases permeability of venules -​ arachidonic acid metabolites: prostaglandins, leukotrienes -​ prostaglandins: lipids with hormone-like actions produced as a result of tissue injury; act as vasoconstrictors or vasodilators. cause inflammation, which is associated with pain, redness, swelling, and fever. synthesized via the cyclooxygenase pathway -​ leukotrienes: contract airway smooth muscle, increase vascular permeability, increase mucus secretion, and attract and activate other inflammatory cells Appendicitis: Describe the pathophysiology of appendicitis. -​ exact mechanism is unknown -​ most likely believed to be resulting from obstruction of the lumen with stool, gallstones, tumors, parasites, or lymphatic tissue, with resulting bacterial infection -​ obstructed lumen does not allow drainage of the appendix -​ mucosal secretions continue → luminal pressure increases → decreases mucosal blood flow → hypoxia → ulceration → infection and inflammation -​ gangrene could develop if there is thrombosis of the luminal blood vessels followed by perforation Describe clinical manifestations. -​ abrupt onset -​ pain initially vague in location, then referred to the epigastric or periumbilical area -​ caused by stretching of the appendix -​ pain becomes colicky  -​ pain is persistent and continuous. when inflammation reaches the serous layer of the appendix and peritoneum, the pain becomes localized to RLQ -​ abdomen is tender to palpation -​ rebound tenderness and spasm of the overlying abdominal muscles are common -​ possible low grade fever -​ nausea frequently accompanies pain -​ wbc count may be elevated, but not in all cases Describe diagnostic testing and treatment. -​ diagnostic testing: -​ based on hx and physical exam findings -​ ultrasound or ct may be used to confirm the diagnosis -​ treatment: -​ surgical removal — antibiotics can be used for treating uncomplicated appendicitis -​ complications — peritonitis General Thermoregulation: Discuss the role of the hypothalamus in regulating temperature. -​ controls processes to balance heat loss and gain Discuss sources of heat loss (radiation, conduction, convection, and evaporation), and list examples for each. -​ radiation: heat is emitted as infrared radiation from the body to the surrounding environment. -​ example: the body radiating heat away into a cooler room -​ conduction: heat transfer through direct contact with cooler object -​ example: sitting on a cold metal bench -​ convection: heat is carried away by the movement of air or water -​ example: wind chill or warm air rising in a heated room -​ evaporation: heat is lost when liquid (like sweat) turns into vapor -​ example: sweating during exercise Discuss causes of fever. What is the purpose of fever? -​ causes: -​ pyrogens (fever-producing substances) -​ formed from breakdown or bacteria and bacterial toxins -​ phagocytic cells engulf and digest these bacterial products and release cytokines which are transported to the hypothalamus -​ they induce formation of prostaglandin E2 – binds to receptors in the hypothalamus to cause an increase in the thermostatic set point -​ hypothalamus initiates shivering and vasoconstriction to raise the body’s core temperature to a new set point and fever is established -​ purpose: -​ may signal the presence of infection or other condition that warrants treatment -​ resolves when the causative process is removed -​ some evidence supports that small temperature elevation enhances T cell proliferation. many microbes that cause fever grow best at normal body temperature; thus their growth is inhibited by a rise in temperature  -​ however, mild temperature elevations can have a negative effect, i.e. older adults with chronic or pulmonary disease (increases O2 demand). fever may also produce confusion -​ cell damage can occur when temperatures are elevated greater than 108 with life-threatening acidosis, hypoxia, and hyperkalemia Discuss risk factors for altered thermoregulation. -​ age: infants and the elderly are more vulnerable due to immature or weakened thermoregulatory systems. -​ chronic illnesses: conditions like neurological disorders (e.g., Parkinson’s), cardiovascular disease, and endocrine disorders (e.g., hypothyroidism) impair temperature regulation. -​ medications: drugs like antipsychotics, beta-blockers, and alcohol can disrupt the body’s ability to regulate temperature. -​ environmental factors: extreme temperatures, humidity, and prolonged exposure to heat or cold overwhelm the body’s thermoregulatory mechanisms. -​ dehydration/nutrition: lack of hydration and essential nutrients can impair thermoregulation, especially in hot conditions. -​ body composition and fitness: obesity and low body fat can hinder heat regulation, while physical fitness generally improves temperature tolerance. -​ infections: fever during infections can disrupt normal thermoregulation. -​ acclimatization: lack of acclimatization to extreme temperatures increases risk for heat stroke or hypothermia. -​ lifestyle: physical exertion, improper clothing, or alcohol use can impair heat management and increase susceptibility to temperature-related illness. in short, altered thermoregulation is influenced by age, health conditions, environment, medications, hydration, and lifestyle factors. Identify populations at risk for alterations in thermoregulation. -​ infants and young children: -​ thermoregulatory systems are still developing, making them more sensitive to extreme temperature -​ limited ability to communicate discomfort leading to a higher risk of heat stress or hypothermia -​ elderly individuals: -​ reduced metabolic rate, slower circulation, and diminished sweat response make them less able to regulate body temperature -​ increased risk of heat-related illnesses during hot weather or hypothermia in cold water -​ people with chronic medical conditions: -​ neurological disorders: conditions like parkinson’s disease, multiple sclerosis, and spinal cord injuries can disrupt the hypothalamus’ ability to regulate temperature -​ cardiovascular diseases: heart failure or peripheral vascular disease can impair circulation reducing the body’s ability to adjust to temperature changes -​ endocrine disorders: hypothyroidism, diabetes, and other metabolic conditions can impair thermoregulation, especially in extreme temperatures  -​ individuals with mental health disorders: -​ people with conditions like schizophrenia or depression may have altered perceptions of temperature and may not seek help in extreme environments -​ cognitive impairments can also affect their ability to recognize or respond to temperature threats -​ pregnant women: -​ hormonal changes during pregnancy can affect the body’s thermoregulatory processes, making them more susceptible to ​heat stress -​ homeless or displaced persons: -​ lack of shelter or appropriate clothing increases vulnerability to both cold and heat-related illnesses -​ limited access to hydration and food exacerbates the risk -​ outdoor workness and athletes: -​ people who work or exercise in extreme environments (e.g. construction workers, athletes in hot climates) are at higher risk for heat exhaustion, heat stroke, or dehydration -​ people with obesity or low body fat: -​ obesity: excess body fat can act as insulation, making it harder for the body to cool down in hot environments and harder to generate heat in cold conditions -​ low body fat: insufficient body fat can impair heat conservation, increasing the risk of hypothermia in cold weather -​ people with substance use issues: -​ alcohol: alcohol impairs temperature perception and thermoregulation, increasing the risk of hypothermia in cold weather and heat stress in hot weather -​ drugs: certain drugs, especially stimulants, can raise body temperature, increasing the risk of heat stroke -​ immunocompromised individuals: -​ people undergoing treatments like chemotherapy or those with HIV/AIDS may have altered thermoregulation due to the effects of their conditions or treatments, making them more vulnerable to infections and temperature extremes -​ people living in extreme climates -​ those in very hot and cold climates are at constant risk for heat stroke, heat exhaustion, or hypothermia, especially if they adequate housing, clothing, or access to cooling/heating systems Fever, Hypothermia, Hyperthermia, Malignant Hyperthermia Compare fever and hyperthermia. -​ fever: -​ definition: fever is a controlled increase in body temperature that is regulated by the hypothalamus in response to an infection or other pathological condition. -​ cause: fever is typically caused by the body's response to infection (e.g., bacterial, viral) or inflammation (e.g., autoimmune diseases). It can also be triggered by certain medications or toxins. -​ mechanism: the hypothalamus resets the body's "set point" temperature higher in response to pyrogens (fever-inducing substances). Pyrogens can be either exogenous (e.g., bacterial toxins) or endogenous (e.g., cytokines released by the immune system).  -​ this rise in set point causes the body to generate heat through mechanisms like shivering, increased metabolic rate, and vasoconstriction (narrowing of blood vessels). -​ characteristics: ​ typically occurs in response to infection or inflammation. ​ the body can regulate temperature through sweating and vasodilation (widening of blood vessels) once the fever “breaks.” ​ fever is often accompanied by chills, sweating, and a feeling of being cold despite the elevated temperature. -​ treatment: -​ treatment generally focuses on treating the underlying cause (e.g., antibiotics for infection). Fever-reducing medications (antipyretics) like acetaminophen or ibuprofen can help lower the set point and alleviate discomfort. -​ body temperature range: -​ typically, a fever is defined as a body temperature above 100.4°F (38°C). Discuss clinical manifestations of fever across the lifespan. -​ infants/young children: -​ decreased or immature immune system -​ body mechanisms to control temp not as well developed -​ < 3 months: -​ mild temp increases (100.4) can be due to serious infection -​ infants from 1 to 28 days: -​ consider that they have bacterial infection that can cause bacteremia or meningitis -​ S/S of toxicity — lethargy, poor feeding, hypoventilation, poor tissue oxygenation, cyanosis -​ < 1 y/o and girls 1-2 y/o: -​ consider UTIs -​ older adults: -​ slight increase in temp can = serious infection -​ fever not recognized due to lower baseline body temp. -​ weaker immune system -​ S/S of infection in elderly -​ unexplained change in functional status -​ worsening mental status -​ weakness -​ fatigue -​ weight loss -​ method of temp. measurement: oral may not be accurate due to mouth breathing, tongue tremors, agitation Discuss goals of pharmacologic treatment of fever. What are nonpharmacologic methods to treat Fever? -​ pharmacologic treatments goals: -​ antipyretics are used to reset the point of the hypothalamus to a lower level; block activity of COX (enzyme) which interferes with prostaglandins synthesis -​ used to alleviate discomfort of fever and protect vulnerable organs (brain) from extreme temperature elevation → aspirin, ibuprofen, acetaminophen Discuss malignant hyperthermia and possible causes. -​ malignant hyperthermia: -​ a metabolic disorder -​ heat is generated by uncontrolled skeletal muscle contraction -​ genetic component -​ the muscle contraction is caused by abnormal release of intracellular calcium which leads to sustained elevated metabolic rate -​ in susceptible people this is triggered by exposure to stresses or general anesthetic agents -​ treatment: -​ measures to cool the body — administration of Dantrolene → a muscle relaxant drug that blocks the release of calcium Discuss alcohol and the relation to hypothermia. -​ alcohol can dull senses and inhibits shivering Discuss risk factors for altered thermoregulation. -​ age: infants and the elderly are more vulnerable due to immature or weakened thermoregulatory systems -​ chronic conditions: neurological disorders, cardiovascular diseases, and endocrine disorders (i.e. hypothyroidism, diabetes) impair temperature regulation -​ medications: drugs like antipsychotics, beta-blockers, and alcohol disrupt thermoregulation, making individuals more prone to heat or cold stress -​ environmental exposure: extreme temperatures (heat or cold), humidity, and prolonged exposure overwhelm the body’s thermoregulation -​ dehydration and poor nutrition: lack of fluids or essential nutrients impairs sweating and circulation, increasing vulnerability to temperature extremes -​ body composition: obesity limits heat dissipation, while low body fat reduces heat retention, both increasing risk in extreme temperatures -​ physical fitness: low fitness levels can hinder temperature regulation, while high fitness levels generally improve tolerance to extremes -​ pregnancy: hormonal changes during pregnancy can increase the body’s heat load, making it harder to cool down -​ substance use: alcohol and drugs like stimulants can impair the body’s ability to regulate temperature, increasing the risk of heat stroke or hypothermia -​ mental health disorders: cognitive impairments may prevent individuals from recognizing or responding to temperature extremes -​ immune suppression: immunocompromised individuals are more susceptible to infections that cause fever or disrupt thermoregulation -​ lack of acclimatization: people not used to extreme heat or cold are at higher risk of temperature-related illnesses Discuss the physiological response to hyperthermia/hypothermia. -​ hyperthermia: -​ increase in body temperature that occurs without a change set point -​ thermoregulatory mechanisms are overwhelmed -​ continued muscle exertion in warm weather; at risk: -​ people who work outdoors (athletes, construction workers) RT prolonged muscle exertion  -​ elderly and those with CV disease are at risk RT impaired circulation to dissipate heat -​ infants left in a closed car for a short time -​ excessive heat production -​ inadequate ability to cool -​ hypothalamic regulator dysfunction -​ hypothermia: -​ core temperature < 95 -​ may be accidental – prolonged exposure to cold environment -​ no problem with the temperature regulating center -​ may be RT underlying conditions -​ malnutrition -​ people with hypothyroidism, CV disease, spinal cord injury at risk -​ dulled senses (alcohol or sedative drugs) -​ alcohol inhibits shivering -​ symptoms: -​ poor coordination, slurred speech, stumbling, irrationality and poor judgment, hallucinations, blueness and puffiness of skin, pupil dilation, decreased respiratory rate, weak, irregular pulse, stupor Discuss treatments for hypothermia and hyperthermia. -​ hyperthermia: -​ prevention is best treatment -​ move to a cooler environment -​ apply ice packs, cold, wet towels or sponges, cooling blankets -​ immerse in cold water -​ oral hydration or IV fluids -​ anti-inflammatory drugs (NSAIDs) -​ hypothermia: -​ remove from cold environment -​ warm person gradually -​ use warm, dry, blankets or sleeping bags -​ drink warm, non-alcoholic, non-caffeinated fluids -​ use warm packs -​ immerse in warm water -​ heated blankets Oxygenation Respiratory: Define specific medical terms involved with the respiratory system and oxygenation, including lung compliance and airway resistance. -​ gas exchange: the process by which oxygen from the air is transferred into the blood and carbon dioxide, a waste product of metabolism, is transferred from the blood into the lungs to be exhaled → primarily occurs in the alveoli -​ ventilation: the mechanical process of moving air in and out of the lungs to facilitate gas exchange. it includes both inhalation and exhalation -​ ischemia: a condition where there is a reduced or restricted blood flow to tissues or organs, leading to a lack of oxygen and nutrients, and potential tissue damage. it often results in impaired function of the affected area (i.e. myocardial ischemia, where blood flow to the heart muscle is reduced) -​ hypoxia: a condition in which tissues or organs are deprived of adequate oxygen supply, even though the partial pressure of oxygen in the blood may be normal. hypoxia can occur in different body regions, such as brain hypoxia, and it can result from a variety of causes like poor circulation or respiratory failure -​ hypoxemia: a state in which there is low oxygen concentration in the blood, specifically in the arterial blood. hypoxemia is often measured by the partial pressure of oxygen or oxygen saturation and is a key indicator of respiratory dysfunction -​ transport: the process by which oxygen and carbon dioxide are carried by the blood from the lungs to the tissues (via hemoglobin) and from the tissues back to the lungs. this involves both the circulatory system and the respiratory system -​ perfusion: the process by which blood flows through the capillaries to deliver oxygen and nutrients to tissues and remove waste products. proper perfusion is essential for tissue survival and function -​ lung parenchyma: the functional tissue of the lungs, including the alveoli, blood vessels, and connective tissue. it is where gas exchange takes place. damage to lung parenchyma, such as in diseases like emphysema or pneumonia, can impair gas exchange -​ diffusion: the movement of gases across a membrane (such as the alveolar-capillary barrier in the lungs) from an area of higher concentration to an area of lower concentration. in the lungs, oxygen diffuses from the alveoli into the blood and carbon dioxide diffuses from the blood into the alveoli to be exhaled -​ pulmonary interstitium: the space and tissue between the alveoli and the blood vessels in the lungs, which included connective tissue, lymphatics, and small blood vessels. it plays a role in supporting the alveolar structures and facilitating gas exchange by acting as a medium for the exchange of gases between the alveoli and blood Describe the components that make up the respiratory system and their function, including upper and lower airways, mechanics of breathing and muscles involved in breathing, conducting airways and gas exchange airways. -​ conducting airways -​ nose and nasal passages, mouth, pharynx, larynx, trachea, bronchi and bronchioles -​ nose warms, filters, and humidifies air passing through nasal passages -​ larynx: functions in speech and protecting the lungs from substances other than air  -​ lines with ciliated epithelial mucosa that warms and humidifies inspired air -​ goblet cells (mucus-secreting cells) produce a “mucociliary blanket” to protect the respiratory system -​ nose is preferred route for entrance of air; mouth serves as an alternative airway when the nasal passages are plugged or when a greater need exists for air -​ tracheobronchial tree: -​ trachea: (windpipe) tube that connects the larynx and major bronchi -​ bronchi and bronchioles -​ gas exchange airways: -​ lobules: smallest functional units of the lung, consisting of a cluster of alveoli, bronchioles, and small blood vessels. they are organized within larger structures called lobes of the lungs. each lobule is supplied by a terminal bronchiole, and it functions as a unit for gas exchange -​ terminal bronchioles: smallest branches of the bronchial tree that lead to the respiratory bronchioles. they mark the end of the conducting zone of the respiratory system, which is responsible for air conduction but not gas exchange. they are lined with ciliated epithelial cells and have no alveoli attached, but they are crucial for air distribution to the alveolar regions where gas exchange occurs -​ alveoli: tiny air sacs that the ends of the respiratory bronchioles where gas exchange takes place. they are lined with a thin epithelial membrane, allowing oxygen to diffuse from the air into the blood and carbon dioxide to diffuse from the blood into the air. the alveolar-capillary membrane is where the exchange of gases between the lungs and blood happens -​ alveolar ducts: small, tubular structures that connect the respiratory bronchioles to the alveolar sacs. these ducts are lined with alveolar openings and are important for distributing air to the alveoli for gas exchange. the walls of the alveolar ducts are made up of alveoli, which facilitate the exchange of gases -​ alveolar sacs: clusters of alveoli at the end of the alveolar ducts. these sacs resemble a cluster of grapes and represent the terminal portion of the respiratory zone, where the greatest part of gas exchange occurs. they contain many alveoli, each surrounded by a network of capillaries that allow for efficient oxygen and carbon dioxide exchange -​ mechanics of breathing and muscles used: -​ diaphragm and external intercostal muscles are used (normally) -​ during inspiration, the diaphragm contracts and moves down, increasing the volume of the thoracic cavity, creating negative pressure that draws gas into the lungs through upper airways and trachea -​ during expiration, the diaphragm relaxes and moves up, allowing elastic recoil of the lungs to deflate the lungs -​ accessory muscles used: sternocleidomastoid, abdominal and internal intercostal Describe the process of gas exchange (ventilation and perfusion). -​ ventilation: -​ air enters the body through the mouth and nose, to the pharynx, to the larynx and enters the trachea which bifurcates into 2 branches (left and right bronchus) -​ each bronchus divides many times into smaller branches (bronchioles) which leads to alveoli, which inflate during inhalation and deflate during exhalation  -​ perfusion: -​ deoxygenated blood enters the lung through the pulmonary artery, which branches. the small pulmonary arteries accompany the bronchi as they move down to the lobules, and supply the capillary network that surrounds the alveoli Asthma: Describe risk factors for asthma. -​ genetics: predisposition toward developing an IgE-mediated response to common allergens (ATOPY) -​ family hx -​ smoking and second-hand smoke exposure -​ gender: females after adolescence have increased risk persisting to adulthood; males are at increased risk before puberty -​ environmental allergies -​ antenatal exposure to tobacco smoke and pollution -​ older adults have decreased pulmonary reserves; more susceptible to infections -​ GERD Discuss factors affecting asthma severity. Describe the term atopy. -​ intermittent → < 2 times a week, asymptomatic between attacks -​ mild (persistent) → > 2 times a week, < 1 time per day -​ moderate (persistent) → daily symptoms, exacerbations > 2 times per week, may last days, may affect activity -​ severe (persistent) → continual symptoms, limited physical activity, frequent exacerbations Discuss asthma triggers. -​ allergens: cockroaches, furry animals, fungi, pollen, molds -​ cigarette smoke: smoking and passive smoke -​ air pollutants: vehicle exhaust, wood smoke -​ respiratory tract infections -​ GERD: reflux disease -​ drugs and food additives/dyes: aspirin, NSAIDs, beta-blockers -​ exercise Describe the role of alpha and beta airway receptors, especially in people with asthma. -​ smooth muscle is under involuntary control. alpha receptors in bronchial walls send message to smooth muscle to constrict -​ alpha 1 receptors are activated to a greater degree in people with asthma by triggers -​ allergen is inhaled → it binds to alpha 1 receptors → histamine is released → edema of bronchial walls -​ beta 2 receptors cause relaxation; beta adrenergic meds cause smooth muscle relaxation Describe the etiology and pathophysiology of asthma, as well as involvement of mast cells, histamines, leukotrienes. -​ etiology: -​ atopy and triggers -​ pathophysiology: -​ first exposure: genetically predisposed → exposed to trigger → t2 tells b-cell to make IgE → IgE sit on mast cells → mast cells line lungs and airways  -​ second exposure: allergen inhaled → remembered and body is told to quickly make IgE → attach to mast cells → mast cell is now primed → degranulation of mast cells → release of granules → airway obstruction, edema, inflammation and mucus plugging -​ release of cytokines: attract other inflammatory cells (everything gets worse) Describe the terms hyper-responsiveness, inflammation, bronchospasm, and bronchoconstriction. -​ hyper-responsiveness: an exaggerated reaction to stimuli, often seen in conditions like asthma, where the body or airways overreact to triggers, causing inflammation or constriction -​ inflammation: swelling and irritation of the airways, making them narrower and more sensitive. this leads to wheezing, coughing, and difficulty breathing -​ bronchospasm: the tightening or narrowing of the muscles around the airways, which makes it harder to breathe. its a common feature of asthma and can cause wheezing and shortness of breath (dyspnea) -​ bronchoconstriction: narrowing of the airways in the lungs, making it difficult to breath. it happens with the muscles around the airways tighten, often triggered by conditions like asthma What is meant by airway remodeling? -​ long-term changes in the structure of the airways due to ongoing inflammation. these changes can include thickening of the airway walls, increased mucus production, and fibrosis (scarring). over time, airway remodeling can make asthma symptoms worse and harder to control Describe clinical manifestations of asthma and presentation; what people experience, and what happens with progression of asthma, and during a prolonged attack. -​ mild attack: feelings of chest tightness, slight increase respiratory rate with prolonged expiration and dyspnea, mild wheezing, coughing -​ severe attack: dyspnea, tachypnea, use of accessory muscles, air trapping with distant breath sounds, loud wheezing, cyanosis, retractions -​ progression of the condition: fatigue, moist skin, signs of anxiety, apprehension, restlessness, breath sounds become inaudible with diminished wheezing, ineffective cough, possible respiratory failure -​ prolonged attack: air trapping, increased energy requirement, accessory muscle use, dyspnea and fatigue Discuss presentation of asthma in children. -​ leading cause of chronic illness in children -​ onset at any age -​ symptoms may worsen at night → airway patency decreases -​ symptoms vary with the stage and severity of the attack -​ may develop a cold with rhinorrhea, quickly followed by irritability, a tight and nonproductive cough, wheezing, tachypnea, dyspnea, and use of accessory muscles -​ cyanosis and tachycardia indicate worsening Discuss prevention of asthma and nonpharmacologic measures. -​ prevention: -​ control exposure to irritants or triggers -​ evaluate any hx of aspirin sensitivity -​ medical conditions: -​ nasal polyps -​ GERD -​ immunizations for influenza -​ nonpharmacologic measures: -​ relaxation techniques -​ controlled breathing -​ desensitization for triggers that cannot be avoided (i.e. dust) -​ skin testing to ID antigens; injections to stimulate production of IgE antibodies to block IgE response -​ allergen immunotherapy Discuss the function of short-acting beta agonists in treatment of asthma. -​ SABA (bronchodilator) -​ relaxes the bronchial smooth muscle -​ prompt relief of symptoms (30 minutes) -​ inhalation and used for acute attacks -​ administered by metered-dose inhaler or nebulizer -​ example: albuterol and xopenex Discuss how asthma is diagnosed. -​ hx and physical exam -​ laboratory tests: ABGs, sputum, cultures, allergy testing -​ diagnostic tests: chest x-rays, pulmonary function tests -​ spirometry to measure lung volumes -​ **pulmonary function tests and spirometry are most reliable Pneumonia:​ Discuss risk factors for developing pneumonia. -​ age (infants, young children, older adults) -​ compromised immunity -​ history of splenectomy -​ lack of current immunization -​ chronic lung disease -​ recent viral respiratory infection -​ alcoholism -​ inactivity and immobility -​ conditions that increase the risk of aspiration -​ altered consciousness -​ dysphagia -​ smoking -​ mechanical ventilation -​ residence in a nursing home Discuss respiratory defense mechanisms and how impairment can contribute to development of pneumonia. -​ glottic and cough reflexes: protect against aspiration into tracheobronchial tree -​ impair effectiveness: loss of cough reflex RT stroke, neural lesion, neuromuscular disease, sedation, anesthesia, NG tube -​ mucociliary blanket: removes secretions, microorganisms, and particles from resp. tract -​ impaired effectiveness : smoking, viral diseases, chilling, inhalation of irritating gases -​ phagocytic and bacterial action of alveolar macrophages: removes microorganisms and foreign particles from lung -​ impaired effectiveness: tobacco smoke, chilling, alcohol, oxygen intoxication -​ immune defenses (IgA and IgG and cell-mediated immunity): destroy microorganism -​ impaired effectiveness: congenital and acquired immunity states Compare community-acquired pneumonia and hospital-acquired pneumonia. -​ community-acquired: -​ infections from organisms found in the community not hospital or nursing home -​ defined as beginning outside the hospital or diagnosed within (less than) 48 hours after admission of the hospital -​ bacterial or viral, typical or atypical -​ hospital-acquired: -​ defined as a lower respiratory tract infection that was not present or incubating on admission to the hospital -​ infections occurring 48 hours or more after hospital admission -​ most are bacterial, typical -​ many have acquired antibiotic resistance What is lung consolidation? -​ when the lung tissue becomes filled with liquid or solid material (pus, blood, mucus) instead of air, making the lung tissue firmer. it often occurs in conditions like pneumonia and can cause symptoms such as cough, difficulty breathing, and chest pain Compare typical pneumonias and Atypical pneumonias, including pathophysiology and clinical presentation. -​ typical: -​ people aspirate small amounts of organisms from their upper airways, particularly during sleep -​ respiratory tract defense mechanisms normally prevent them from entering distal air passages -​ loss of cough reflex, damage to ciliated endothelial cells or impaired immune system may lead to infection -​ epithelial cells may be receptive to bacterial adherence, increases colonization -​ lung consolidation -​ pathophysiology: -​ three ways organisms reach lungs: -​ aspiration from nasopharynx or oropharynx -​ inhalation of microbes released into the air from coughing, sneezing, talking -​ hematogenous spread from primary infection elsewhere in body  -​ decreased cough and epiglottal reflexes may allow aspiration -​ organism evades upper airway defense mechanisms and colonize the alveoli → airway epithelial cell and alveolar macrophages activate T and B cells → inflammatory response initiated → toxins released cause damage to bronchial mucous membranes and alveolar-capillary membranes → terminal bronchioles fill with infectious debris and exudate → consolidation of lung tissue -​ clinical manifestations: -​ sudden onset of malaise, severe shaking chills, and fever -​ tachypnea, dyspnea, congestive stage with coughing and watery to yellow-tinged sputum, crackles -​ progressively sputum becomes blood-tinged, rust-colored, purulent -​ pleuritic pain and chest discomfort RT coughing -​ atypical: -​ caused by M. pneumoniae (most common), viruses and Chlamydia pneumoniae -​ also caused by viruses (influenza, RSV, adenoviruses, rhinoviruses, rubeola, and varicella viruses) -​ common in children and young adults, college students, and military recruits -​ highly contagious -​ characterized by lack of consolidation; patchy involvement, alveolar septum and pulmonary interstitium; production of moderate amounts of sputum; moderate elevation of wbc, and lack of alveolar exudate -​ pathophysiology: -​ infection of respiratory epithelium → inflammation and immune response → mild or non-productive cough → exudation into the alveolar interstitium → alveolar damage and impaired gas exchange → clinical presentation -​ key features: patchy infiltrates on imaging rather than lobar consolidation, non-productive cough and mild symptoms, interstitial inflammation instead of alveolar exudate, less severe hypoxia and respiratory distress than typical pneumonia -​ clinical manifestations: -​ usually has a milder presentation of symptoms (“walking pneumonia”) -​ fever, headache, muscle aches and pains -​ cough, if present is dry, hacking, nonproductive Describe the specific pathophysiology of pneumococcal pneumonia (including red and gray hepatization. -​ streptococcus pneumoniae is the most common cause of bacterial pneumonia -​ virulence is enhanced by its capsule, which prevents or delays digestions by phagocytes -​ classified as “typical” -​ individuals who do not have a spleen (functional asplenia) are at risk -​ pathophysiology: -​ edema: alveoli become filled with protein-rich fluid containing organisms -​ red hepatization: marked capillary congestion → massive outpouring of RBCs and neutrophils. the lung “resembles a liver”  -​ grey hepatization: macrophages arrive → phagocytosis of fragmented neutrophils, RBCs and cellular debris -​ resolution: alveolar exudate is removed and lung returns to normal Discuss clinical manifestations of pneumonia based on type of pneumonia. -​ typical: -​ sudden onset of malaise, severe shaking chills, fever -​ tachypnea, dyspnea -​ congestive stage with coughing and watery to yellow-tinged sputum, crackles -​ progressively sputum becomes blood-tinged, rust-colored, purulent -​ pleuritic pain and chest discomfort RT coughing -​ atypical: -​ usually has a milder presentation of symptoms (“walking pneumonia”) -​ fever, headache, muscle aches and pains -​ cough, if present is dry, hacking, nonproductive Discuss how pneumonia is diagnosed. -​ history and physical exam -​ chest x-rays -​ sputum specimens (culture and sensitivity) and gram stain -​ cbc and blood cultures -​ serum procalcitonin Discuss general categories of medications used to treat pneumonia. -​ antibiotics -​ given to destroy organism (penicillins and cephalosporins) -​ oral versus iv therapy -​ medications for cough, bronchodilators, mucolytics -​ medications to relieve pain/fever ​ RSV/Bronchiolitis: Describe what bronchiolitis is. -​ a generic term applied to various inflammatory processes that affect the bronchioles -​ most often caused by respiratory syncytial virus (rsv) in infants and children; less common in adults. rsv is highly contagious -​ usually occurs in the first two years of life, with peak incidence between 3-6 months of age -​ may be mild and require minimal treatment, or more severe, requiring hospitalization Discuss risk factors for developing RSV/bronchiolitis. -​ prematurity -​ low birth weight -​ chronic pulmonary disease and defects of airways -​ immunodeficiency -​ in utero exposure to tobacco smoke -​ not being breastfed Describe the diagnosis of RSV/bronchiolitis. -​ history and physical -​ chest x-rays -​ antigen testing for rsv in nasal washings Discuss pathophysiology and presentation of RSV/bronchiolitis. -​ pathophysiology: -​ viral infection → necrosis of bronchial epithelium and destruction of ciliated epithelial cells -​ bronchioles become infiltrated with lymphocytes → release of inflammatory substances (lymphokines) → activation of eosinophils, neutrophils, monocytes -​ mucosa becomes edematous; cellular debris and fibrin form plugs within the bronchioles -​ bronchiolar edema, accumulation of mucus and cellular debris and bronchospasm narrow the airways; may become occluded → atelectasis and/or hyperinflation -​ presentation: -​ infection produces inflammatory obstruction of the small airways and necrosis of the cells lining the lower airways -​ insidious onset of cough and dyspnea -​ minimal finding on chest x-ray -​ may start with mild uri; symptoms usually last several days then progress to respiratory distress Describe clinical manifestations of RSV/bronchiolitis. -​ initially significant rhinorrhea, thick discharge, followed by a tight cough, sneezing and possible pharyngitis -​ decreased appetite, lethargy and irritability -​ intermittent fever, up to 102 -​ tachypnea (normal newborn rr 30-60; infants 24-30) -​ severe coughing -​ respiratory distress: grunting, wheezing, crackles, retractions of lower ribs and sternum, nasal flaring -​ air trapping and atelectasis -​ progression if not responsive → cyanosis, pallor, listlessness, diminish