Midterm Review 3

HIV is a type of retrovirus which contains RNA as its genetic material.

CD4+ T cells are a type of white blood cell that are crucial for the adaptive immune system and are the primary targets of HIV infection.

After HIV has attached to a host cell, it uses the enzyme reverse transcriptase to convert its RNA into DNA. This DNA can then be integrated into the host's genome.

The period after initial infection when HIV replicates quickly and destroys host cells, leading to a high viral load and a rapid decline in CD4+ T cells.

The immune response to HIV leads to a temporary decrease in viral replication and an increase in CD4+ T cell numbers.

The final stage of HIV infection, characterized by a severe depletion of CD4+ T cells, making the body highly susceptible to opportunistic infections.

An abnormal energy balance where energy intake doesn't meet the body's needs. Can be caused by decreased energy input, increased energy output, or both.

Inflammatory cytokines like TNF-α and IL-1 contribute to energy imbalance in cachexia, promoting muscle breakdown and further reducing energy intake.

A rapid and non-specific response to tissue injury, aimed at containing damage, eliminating pathogens, and initiating healing. It involves vascular changes, cellular events, and the release of signaling molecules called cytokines.

The initial stage of inflammation, characterized by redness, swelling, heat, pain, and loss of function. Key processes include vasodilation, increased vascular permeability, and leukocyte recruitment.

The process of attracting immune cells to the site of injury using chemical signals.

Immune cells that engulf and destroy pathogens and cellular debris.

Specialized signaling molecules that regulate the immune response. They can either amplify (pro-inflammatory) or dampen (anti-inflammatory) the response.

A long-lasting inflammatory process that can result from unresolved acute inflammation or persistent triggers like infections or autoimmune diseases. It can lead to tissue destruction and scar formation.

A type of chronic inflammation characterized by the formation of granulomas, which are collections of macrophages and other cells that wall off and isolate a foreign body or infected area.

Immune cells that are part of the innate immune system, responsible for the first line of defense against pathogens.

The time during which the heart muscle relaxes and allows blood to fill the chambers.

The time during which the heart muscle contracts and pumps blood out of the chambers.

The amount of blood in the ventricle at the end of diastole, before the heart contracts.

The resistance the heart has to overcome to eject blood during systole. For the left ventricle, this is determined by the pressure in the aorta.

The intrinsic ability of the heart muscle to contract, independent of preload and afterload.

States that the force of ventricular contraction increases as the myocardial fibers are stretched, up to a certain limit. This means more blood in the ventricle leads to a stronger contraction.

A disease that causes the buildup of plaque in the arteries, narrowing them and reducing blood flow.

Factors that increase the risk of developing atherosclerosis, such as smoking, high blood pressure, and high cholesterol.

A type of right-sided heart failure specifically caused by lung disease, where persistently high pressure in the pulmonary arteries overloads the right ventricle, leading to its enlargement and eventual failure.

A hormonal system that regulates blood pressure and fluid balance by constricting blood vessels, retaining sodium and water, and stimulating the sympathetic nervous system.

An enzyme released by the kidneys when blood pressure or blood flow is low, initiating the RAAS cascade.

A protein produced by the liver, serving as the precursor to angiotensin I in the RAAS.

A vasoconstrictor that increases blood pressure and stimulates the adrenal glands to release aldosterone.

A hormone that promotes sodium and water retention by the kidneys, further increasing blood volume and pressure.

The process where angiotensin II binds to these receptors, resulting in vasodilation, decreased remodeling, anti-inflammatory effects, and antioxidant properties, counteracting RAAS actions.

The mechanism that prevents excessive activation of the RAAS by inhibiting renin release when blood pressure and sodium levels increase.

A genetic disorder caused by mutations in the CFTR gene, leading to thick and sticky mucus buildup in the lungs, pancreas, and other organs.

A protein responsible for transporting chloride ions across cell membranes, crucial for regulating fluid balance.

The primary symptom of CF, characterized by thick, sticky mucus accumulating in the airways, leading to breathing difficulties and recurrent infections.

White blood cells that fight infection but can also damage lung tissue by releasing destructive enzymes in CF patients.

Inflammation of the lung tissue, often caused by bacterial, viral, or fungal infections. A common complication of CF.

Immune cells that reside in the air sacs (alveoli) and play a key role in defending against inhaled pathogens.

Proteins on the surface of immune cells that recognize specific molecules from pathogens, triggering an immune response.

Powerful chemical messengers released by immune cells, including alveolar macrophages, that orchestrate the inflammatory response.

An infection of the bladder, commonly caused by E. coli.

An infection of one or both kidneys. It can be caused by bacteria ascending from the bladder or entering the bloodstream.

The most common cause of UTIs (including cystitis and pyelonephritis).

Fimbriae allow E. coli to stick to the bladder lining, resisting the flushing action of urine.

Inflammation of the filtering units in the kidneys, causing damage to the glomerular filtration membrane. Can be acute or chronic.

Glomerulonephritis caused by systemic diseases like diabetes or lupus.

Glomerulonephritis that originates within the glomeruli themselves, often triggered by infections.

Inflammation of the renal pelvis, calyces, and medulla. Can lead to abscess formation.

Located near epithelial surfaces and blood vessels, they immediately release histamine upon activation, causing vasodilation and increased vascular permeability. They also release chemokines, attracting other immune cells.

Resident in tissues and recruited from the bloodstream, they engulf pathogens and cellular debris. They also release pro-inflammatory cytokines and present antigens to T helper cells, initiating the adaptive immune response.

A specialized type of macrophage (antigen-presenting cells (APCs)) that bridge the innate and adaptive immune systems. They capture antigens in tissues, migrate to lymph nodes, and present antigens to T cells.

Primarily involved in defense against parasites, they also regulate vascular mediators released by mast cells. They are implicated in allergic reactions and can contribute to tissue damage.

The body's first line of defense against injury and infection. It provides an immediate, non-specific response to a wide range of threats, and consists of:

Amplify inflammation, promote leukocyte recruitment, and induce systemic effects like fever.

Composed of DNA and antimicrobial peptides, which can trap pathogens but also contribute to inflammation and tissue damage.

The deepest layer of skin, composed of connective tissue, containing structures like hair follicles, sweat glands, blood vessels, and nerves.

Cells responsible for producing connective tissue and collagen, which provide structural support to the dermis.

The subcutaneous layer is mainly composed of adipose tissue (fat), providing insulation, cushioning, and energy storage.

The primary cell type in the subcutaneous layer, storing fat for insulation, cushioning, and energy.

A bacterial skin infection that infects the hair follicles, often caused by Staphylococcus aureus. It manifests as papules, pustules, and surrounding redness.

A bacterial infection of the dermis and subcutaneous tissue, commonly caused by Staphylococcus aureus and group A Streptococcus. It presents as erythema, warmth, edema, and pain without a defined border.

The amount of blood in the ventricle at the end of diastole (relaxation) before the heart contracts.

The resistance the heart has to overcome to eject blood during systole (contraction). It's mostly determined by the pressure in the aorta for the left ventricle.

The intrinsic ability of the heart muscle to contract, independent of preload and afterload.

The force of ventricular contraction increases as the myocardial fibers are stretched, up to a certain limit. This means more blood in the ventricle leads to a stronger contraction.

A form of arteriosclerosis caused by lipid-laden macrophages building up in the artery wall, leading to plaque formation.

Factors that increase the risk of developing atherosclerosis, such as smoking, high blood pressure, and high cholesterol.

Injured endothelial cells become inflamed, attracting macrophages and other inflammatory cells. These cells release inflammatory cytokines like TNF-α, interferons, interleukins, and C-reactive protein.

A diet high in saturated and trans fats can raise cholesterol levels, increasing the risk of atherosclerosis.

Stones form when salts in the urine become supersaturated, precipitate, and grow into crystals. They are most commonly made of calcium oxalate and calcium phosphate.

An obstruction in the lower urinary tract can be caused by prostate enlargement, urethral stricture, or severe pelvic organ prolapse.

A dysfunction in bladder control due to nerve damage, which can cause lower urinary tract obstructions. This can happen due to lesions in the spinal cord or sacral peripheral nerves.

When one kidney is obstructed, the unaffected kidney may try to compensate by increasing in size and function.

After an obstruction is relieved, there may be a period of increased urine production as the body restores fluid and electrolyte balance.

Urine leakage with sudden increases in intra-abdominal pressure, such as during coughing, sneezing, laughing, or exercise.

Urine loss accompanied by a strong, sudden urge to urinate.

Involuntary urine loss due to bladder overdistention. It can be caused by neurologic lesions, polyneuropathies, urethral obstruction, or detrusor underactivity.

The immune response during asthma involves Th2 cells, which secrete cytokines IL-4, IL-5, IL-8, and IL-13.

IgE antibodies bind to receptors on mast cells, triggering their degranulation and the release of inflammatory mediators like histamine, bradykinin, prostaglandins, and leukotrienes.

Histamine, released from mast cells, leads to bronchoconstriction, increased vascular permeability, and edema of the airway. These factors result in airway narrowing and impaired airflow.

Over time, untreated chronic inflammation or repeated asthma exacerbations can cause airway remodeling. This involves changes like increased muscle mass, thickening of the airway wall, and goblet cell hyperplasia, making it difficult to breathe.

Cystic Fibrosis (CF) is an autosomal recessive genetic disorder that affects epithelial cells that produce mucus, sweat, and digestive juices.

A mutation in the CFTR gene leads to thick and sticky mucus buildup in the airways, pancreas, and other organs, causing breathing difficulties, recurrent infections, and digestive problems.

Neutrophils, white blood cells designed to fight infection, can also damage lung tissue in CF by releasing destructive enzymes when they try to control bacterial infections in the airways.

Mucus plugging, the thick mucus buildup in the airways, is a primary symptom of CF. This can lead to breathing difficulties and increased susceptibility to respiratory infections.

Characterized by excessive protein loss in urine (more than 3.5 g per day), low blood protein levels, swelling, high lipid levels in blood and urine. The underlying cause is increased permeability of the glomerular membrane.

A sudden decrease in kidney function, marked by reduced filtration rate and buildup of waste products in the blood.

Caused by direct damage to the kidney structures, particularly the nephrons. It includes acute tubular necrosis often caused by lack of blood flow or toxins, as well as glomerulonephritis and inflammation of the kidney tissues.

A type of AKI caused by an obstruction in the urinary tract, which increases pressure within the kidneys and impairs their function.

Characterized by blood in the urine with red blood cell casts, high blood pressure, swelling, and decreased urine output. It often occurs with infections, rapid kidney damage, and lupus.

A type of AKI caused by reduced blood flow to the kidneys, often due to dehydration, heart failure, or bleeding.

Massive proteinuria (>3.5g/day), hypoalbuminemia, edema, hyperlipidemia, lipiduria.