infection & Gastrointestinal conditions Flashcards
(4 cards)
What is the Pathophysiology of Sepsis and
Septic Shock?
Sepsis is a life-threatening condition resulting from a dysregulated host response to infection, leading to widespread inflammation, tissue injury, and organ dysfunction. The pathophysiology begins when pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs) activate pattern recognition receptors (such as toll-like receptors) on immune cells. This triggers the release of pro-inflammatory cytokines (e.g., TNF-α, IL-1, IL-6) and other mediators, causing a systemic inflammatory response.
This inflammation damages the endothelium, increases vascular permeability, and activates the coagulation cascade, resulting in microvascular thrombosis and impaired tissue perfusion. Simultaneously, anti-inflammatory mediators are released, which can lead to immunosuppression in later stages. The combined effects of vasodilation, capillary leak, and microthrombi cause hypoperfusion, tissue hypoxia, and ultimately multi-organ dysfunction.
Septic shock, a severe subset of sepsis, is characterized by persistent hypotension and cellular/metabolic abnormalities despite adequate fluid resuscitation. It involves profound circulatory failure, metabolic disturbances, and often progresses from an initial hyperdynamic phase (increased cardiac output, vasodilation) to a hypodynamic phase (decreased cardiac output, refractory hypotension, and irreversible organ failure)
What is the pathophysiology of Meningitis?
Meningitis is characterized by inflammation of the protective membranes (meninges) surrounding the brain and spinal cord, most commonly due to infection by bacteria, viruses, or other pathogens. The pathophysiology typically begins when pathogens enter the bloodstream (bacteremia, viremia) and cross the blood-brain barrier, or spread directly from adjacent infections (e.g., sinusitis, otitis media), or via defects in the skull or spine. Once in the subarachnoid space, pathogens multiply in the cerebrospinal fluid, which lacks robust immune defenses.
The presence of pathogens or their components triggers a strong inflammatory response, with immune cells releasing cytokines such as TNF-α and IL-1, increasing blood-brain barrier permeability and attracting large numbers of neutrophils to the CSF. This leads to cerebral edema (vasogenic, interstitial, and cytotoxic), increased intracranial pressure, and decreased cerebral perfusion, causing symptoms like headache, fever, altered mental status, and, in severe cases, neuronal injury and death. The inflammatory process and immune cell activity can also damage brain tissue, cranial nerves, and blood vessels, leading to complications such as hydrocephalus, infarcts, and, if untreated, potentially fatal brain herniation
What is the Pathophysiology of a Upper Urinary
Tract Infection?
An upper urinary tract infection, such as pyelonephritis, typically begins when bacteria-most often from the gastrointestinal tract-ascend from the urethra to the bladder and then travel up the ureters to infect the kidneys. The most common causative organism is Escherichia coli, which uses specific adhesins (like P-fimbriae) to attach to and colonize the urinary tract lining. Once in the kidney, the bacteria trigger an inflammatory response, leading to infiltration of immune cells (especially neutrophils), tissue injury, and sometimes the formation of microabscesses. If severe or left untreated, this inflammation can cause renal scarring, impaired kidney function, and may allow bacteria to enter the bloodstream, resulting in sepsis. Factors such as urinary obstruction, catheter use, or anatomical abnormalities increase the risk and severity of infection
What is the Pathophysiology of Cholecystitis?
Cholecystitis is inflammation of the gallbladder, most commonly caused by obstruction of the cystic duct by gallstones (calculous cholecystitis), which accounts for about 90–95% of cases. This blockage leads to bile stasis and increased pressure within the gallbladder, resulting in distention, compromised blood flow, and lymphatic drainage. The stagnant bile and ischemia trigger an inflammatory response, causing the gallbladder wall to become edematous and potentially necrotic. In some cases, secondary bacterial infection occurs, further exacerbating inflammation. If untreated, this process can lead to complications such as gangrene, perforation, or chronic cholecystitis. Acalculous cholecystitis, which occurs without gallstones, is less common and is often seen in critically ill patients, with mechanisms involving bile stasis, ischemia, and direct injury to the gallbladder wall
