WGU Pathophysiology Study Guide: D236 Pathophysiology

WGU Pathophysiology Study Guide: D236 Pathophysiology Lesson 1 TO Lesson 11 WGU Pathophysiology Study Guide: D236 Pathophysiology Lesson 1 TO Lesson 11: Pathophysiology Remediation Lesson 1: Homeostasis Concepts 1. Starling's Law of Capillary forces is the force behind the movements of fluid in capillary beds throughout the body. The two forces at work are hydrostatic and osmotic pressures. Homeostasis is achieved when these two forces are equal in the capillary- cell interfaces. When the hydrostatic pressure is high in the bloodstream, fluid is then pushed into the cells and overflows into the interstitial fluid, causing edema. In a case like hypoalbuminemia, there is a deficit of albumin protein in the blood. This lowers the oncotic pressure at work against the hydrostatic pressure, causing a shift in fluid change. Hydrostatic pressure pushes water into the cells, causing edema. 2. If hypotension occurs, the kidneys sense decreased perfusion and release renin. Renin stimulates the liver to release angiotensinogen. This converts to angiotensin I in the lungs. A specific enzyme, called ACE, converts it into angiotensin II in the lungs. This angiotensin II causes vasoconstriction, which increases blood pressure. Angiotensin II also stimulates the adrenal glands on the kidneys to release a hormone called aldosterone. Aldosterone helps increase blood volume by increasing sodium and water reabsorption into the body. 3. Too much potassium in the blood can cause wide QRS complexes and tall, peaked T waves. This will cause bradycardia, irregular pulse rate, and cardiac arrest. 4. If pH homeostasis is not maintained, a shift in pH either to the left (acidosis), or to the right (alkalosis) can occur. Excess H+ molecules can cause acidosis and excess HCO3- molecules can cause alkalosis. Either one of these conditions can cause cellular dysfunction and can be fatal. 5. In metabolic acidosis, the lab values would be a pH <3.5 and CO2 <22. Metabolic alkalosis lab values have a pH >4.5 and CO2 >26. With respiratory imbalances, it's opposite. With respiratory acidosis, pH is <3.5 and CO2 is >26. With respiratory alkalosis, pH is >4.5 and CO2 is <22. 6. A high AG has a value from 16-20 mEq/L and can occur with DKA or lactic acidosis. The high number of acids consume HCO3-, therefore decreasing their concentration and increasing the anion gap. In diabetic ketoacidosis, the unmeasured acids in the blood are called ketones. These ketones break apart into H+ and keto-anions. Bicarbonate buffers with the H+ ions. With this, the bicarbonate decreases in the blood, leaving the keto-anions numbers to increase. This causes the AG to increase. This is important because it can help determine the cause of certain metabolic acidosis cases since not all issues present with an elevated AG. Metabolic acidosis with an elevated anion gap is found in lactic acidosis, DKA, renal failure, overdose of aspirin, and ingestion of methanol. 7. Glucose is important to keep at normal levels within the blood because if too high, called hyperglycemia, it can cause chemical damage to the endothelial cells that line the arteries. This can cause a snowball effect of damage to the kidneys, lower extremity vessels, and retina of the eyes and can cause atherosclerosis. With that comes added risks of diseases associated with atherosclerosis like coronary artery disease, peripheral arterial disease, and cerebrovascular disease. Hyperglycemia from diabetes creates advanced glycation end products, further damaging the endothelial lining, stimulating secretion of endothelin, a vasoconstrictor. This constriction of the vessels is more common in the lower extremities, causing peripheral arterial disease. This causes ischemia of the lower extremities and feet which can cause gangrene and necrosis of the affected tissue. 8. Glucose is the primary source of energy for cells. Glucose needs insulin to help it enter the cells via insulin receptors. Type 1 Diabetics have had destruction of their insulin-producing cells, within the pancreas, making it very difficult for glucose to enter the cells. Type 1 diabetics have glucose and insulin receptors, just not enough insulin, making them insulin dependent. Type 2 Diabetics have insulin, glucose, and receptors for glucose to enter the cells. The issue with type 2 diabetics is that the receptors are desensitized to insulin, making it difficult for the insulin to enter the cells. 9. Dialysis is a treatment to help people with kidney disorders to maintain their fluids, electrolytes, and glucose homeostasis. Dialysis helps to remove wastes and harmful substances from the blood with a tubing system and a fluid called dialysate. With renal disease, the kidneys functions decrease, warranting a multitude of medications to help keep everything functioning well. When the kidney failure starts to reach a point where the loss of kidney function is irreversible, dialysis becomes necessary. Some instances for this are persistent hyperkalemia, uncompensated metabolic acidosis, and fluid volume excesses. 10. Hemodialysis draws out the patient’s blood into tubes containing dialysate that filter harmful substances out and returns the clean blood back to their patient. This is usually required a few times a week and lasts a few hours each time. Peritoneal dialysis occurs within the patient’s own peritoneum. The peritoneum is filled with a dialysis solution that also filters their blood. The fluid sits in the peritoneum for 4 hours, then is drained out from the cavity and discarded. The dialysate in the peritoneum works with diffusion to ‘draw’ the harmful substances into the peritoneum until time to drain. Hemodialysis is more common and better for patients with less kidney function, although it does have a rigorous schedule. Peritoneal dialysis can be done at the patient’s home, but must be done everyday which increases risk for peritoneal infection. *11. Homeostasis and maintaining optimal physiological health can impact your wellbeing in a positive way by developing adaptive, compensatory changes within the cells. If not maintained, you can develop maladaptive changes, resulting in dysfunctions of cells. If cells are injured too much, cell death can occur. Lesson 2: Cellular Response and Adaptation 1. Innate immunity is the body’s natural defense against pathogens. These include the skin, mucous membranes, phagocytic cells, ciliated cells, and the inflammatory response. Adaptive immunity is the body’s “learned” defense against exposed antigens, using T and B lymphocytes. These lymphocytes have memory for specific antigens. 2. The adaptive immune system recruits the innate immune system by relying on toll- like receptors on the surface of cells of the innate system that detect specific pathogens and stimulate the adaptive response. 3. B lymphocytes are naïve until they encounter antigens. Once exposed to an antigen, they are stimulated to mature into plasma cells where they can produce immunoglobulins to attack antigens. This process is why infants and children initially get sick more often. The young lack the memory cells that help the body fight off pathogens. Elderly have a decreased population of naïve T cells, decreasing the potential for strong immune responses. 4. Inflammatory mediators released by white blood cells are called cytokines. Chemokines are proteins that attract leukocytes to the area of injury, stimulating the liver to release acute phase proteins that help to destroy microbes and other foreign material at the site of injury. Kinins and prostaglandins are released with the injury response, causing the pain sensation. Histamine is released from mast cells, basophils, and platelets, which can cause vasodilation and bleeding at the site of injury. 5. If a disease is dominant, it will be expressed even if the person only has one copy for the disease. If a disease is a recessive, a person will need to have identical alleles from both parents to obtain the disease. A carrier is a person who is heterozygous for a recessive allele and doesn’t manifest it. The dominant allele overcomes the recessive allele. Since the carrier still passes the recessive allele, it can be passed down to their offspring. 6. In this example, sickle cell allele is represented with an 's'. In the case of 2 heterozygous carriers of sickle cell disease, the parents' genotypes would be Ss and Ss. With this heterozygous combination, the probability of clinical outcomes would be Ss, Ss, SS, and ss. Given these, there's a 25% chance of a genotype to definitely be sickle cell disease. 7. More than 13 alcoholic drinks per month of pregnancy, or more than 2 alcoholic drinks in one sitting, is considered more than minimal levels of alcohol before a child’s birth. Neurobehavioral Disorder Associated with Prenatal Alcohol Exposure (ND-PAE) causes thinking and memory issues, behavioral problems like tantrums, and trouble with daily living activities like bathing and dressing. 8. Some distinctive features of Down Syndrome are intellectual disability, slightly slanted eyes, epicanthic eye fold, short nose with a flat nasal bridge, palmar crease in hands, big space between first and second toes, and hyperflexible joints. Congenital heart disease and blood cancers are common with Down Syndrome. Down Syndrome is very dependent on maternal age. As a woman ages, their ability to correctly undergo meiosis can be impaired, increasing the risk for the disease. 9. Spina bifida is a disorder where some vertebrae over the spinal cord don’t fully develop and leave some exposed spinal cord. This can occur in different degrees of severity, with myelomeningocele being the most severe. The incidence of spina bifida occurring can be minimized by up to 70% when daily folic acid is taken as a prenatal. 10. Cells are adaptive to the environment you place them in until homeostasis can't be met. There are a few buffer systems that the body uses to help compensate to make things 'normal' again. If this can't be achieved, disruptions in the cells occur, causing dysfunction. Lesson 3: Musculoskeletal Pathophysiology 1. Calcium absorption via the GI tract is facilitated by vitamin D. Vitamin D's activation is dependent on kidney and parathyroid functions along with proper sunlight exposure. Hypocalcemia triggers the parathyroid to release parathyroid hormone, which stimulates the bone to release calcium into the blood. Calcitonin, a hormone, blocks excess calcium release from bone, preventing hypercalcemia. 2. Osteocytes are mature cells that maintain metabolism within the bones. They sit in an area of the bone called the lacunae. Within these lacunae are little canals that carry nutrients for the bone cells. 3. Bone remodeling is the final step in the bone healing process. Osteoclasts and osteoblasts are involved in fixing whatever stress was brought upon the bone. This process can take up to 2 months to complete. Osteoclasts function in resorbing and degrading existing bone, to help make room for new bone. Osteoblasts help to build bone up by secreting osteoid, a bone matrix. 4. Osteoarthritis (OA) is a degeneration of joints caused by aging. Articular cartilage loss is the first step in joint degeneration. Chondrocytes within the cartilage are continuously exposed to excessive force, forcing them to undergo apoptosis. Obesity and repetitive knee/shoulder injuries from athletes are some examples of excessive force on the cartilage. With loss of cartilage in the joint, subchondral bone becomes the next part to be aggravated by such repetitive force, causing osteoblasts and osteoclasts to become activated. This activation causes microscopic cracks and shearing of the microvasculature, decreasing blood flow to the subchondral bone. Inflammation of the synovial membrane within the joint causes enzymes to leech out and further attack the cartilage. 5. Rickets is a failure of osteoid calcification because of a certain genetic, nutritional, or metabolic disorder with bone development. Most cases are due to a vitamin D or calcium deficiency. These deficiencies are more common in Africa, Asia, and Europe. The incidence has been high with breastfed infants and most commonly diagnosed in children by age 2. The best treatment for Rickets is prevention of a vitamin D deficiency. Pregnant mothers should be taking prenatal vitamins that contain vitamin D and calcium. Breast fed infants should receive vitamin D supplements. Older children should drink vitamin D milk. For those with Rickets, vitamin D loading is crucial. 6. Denosumab is a monoclonal antibody that binds to the osteoclastic protein sclerostin , blocking bone resorption by osteoclasts. In people with osteoporosis, this drug helps to prevent fractures in bones. 7. ORIF is a procedure where the skin is incised down to the bone, exposing the injured bone. The bone is ‘internally fixated’ by placing a plate and screws on the bone, keeping it aligned until healing sets in. A hip replacement surgery is where certain parts of bone within the hip joint are taken out and replaced by metal parts, extending the length of the joint’s life. With ORIF, the injured bone stays within the patient, unlike replacement surgery where the injured bone is replaced with new ‘parts’. 8. With DDD, the discs between the vertebrae get compressed and impinge the spinal nerves. DDD presents with pain, weakness, or numbness in an upper extremity. DDD of lumbar vertebrae mostly presents as lower back pain. DDD of lumbar through the sacral vertebrae mostly presents with sciatica. 9. Infection in the bloodstream is called sepsis. This can be caused from complications from wounds and surgical sites. A person with sepsis will have a fever, chills, and increased pressure in the infected area. This area will also be warm to the touch, swollen, and possibly purulent with a foul odor. Treatment depends on the severity and type of bacteria that caused the sepsis. The wound will need to be debrided of infected tissue. IV antibiotics will need to be administered followed by oral antibiotics. If a surgical implant is involved, it will need to be removed. 10. Compartment syndrome can occur when tissue pressure exceeds the perfusion pressure in a closed anatomical space. The fascial membrane within the compartment can’t handle too much pressure from swelling and bleeding because it’s not flexible enough. It is most common in the anterior compartment of the leg. Dark urine is the first sign of rhabdomyolysis. An elevated creatine kinase (CK) level is the best lab test for evaluating for rhabdomyolysis. 11. A blood clot that travels through the venous system and into the pulmonary circulation is considered a pulmonary embolism (PE). It can obstruct blood flow to the lungs, causing a domino effect of symptoms. A fat embolus is similar, but instead of blood, it’s a piece of fat that is travelling throughout the venous system, causing obstruction. A patient that’s more susceptible to deep vein thrombosis (DVT) by having injuries to a blood vessel or hypercoagulability of blood, or atrial fibrillation are also at risk of a PE. A patient is at risk of a fat embolism by having a fractured long bone where the marrow of the bone enters the venous circulation. For FES, treatment is focused on hemodynamic stabilization. Infusion of fluids are used to try to flush the embolus. Corticosteroids and albumin are also used. Treatment of a PE is usually prevention of a DVT. Anticoagulation therapy will be used to try to ‘thin’ the clot. Surgery can be done with a thrombectomy or placement of a filter to catch the clot. Lesson 4: Integumentary Pathophysiology 1. The skin has many functions, some examples include temperature control and regulation, barrier protection, and vitamin D production. The skin maintains a constant body temperature of about 98.6 degrees F. Temperature sensors in the skin signal irregular body temps to the hypothalamus in the brain. If the body is too hot, messages are sent to cool the body by excreting sweat onto the skin’s surface. Then, capillaries near the skin’s surface dilate, allowing heat to escape the skin for a quicker cool-down. If the body is too cold, little erector pili muscles contract, which raises the hair on the skin, causing goosebumps. The body starts to shiver at an attempt to increase its metabolic rate and raise the temp. Those same superficial blood vessels now constrict, causing the body to retain its warmth. The skin acts as a natural barrier of protection by possessing a flora of harmless bacteria with a substance containing sweat and sebaceous secretions that all cover the skin protecting the body from infection. This layer of what sounds gross is called stratum corneum and its purpose is to stop antigens from entering the body, all while keeping the body waterproof. The skin also acts as a vitamin D producer. The sun hits the skin and the chemical 7- dehydrocholesterol is converted into a pre-form of vitamin D, cholecalciferol. This cholecalciferol furthers its transformation to vitamin D in the liver and kidneys. 2. Albinism is a genetic disorder that doesn’t allow the skin, hair, and eyes achieve pigment. The person’s vision is diminished and very sensitive to light and UV rays. Their skin tends to be pale and/or pink tinted, their hair is yellow, and their eyes are very light or even pink. These people lack melanin and should use extreme caution when in the sun. 3. Eczema, also known as atopic dermatitis, is very common. It presents with vesicles, oozing, and crusting with excoriation that can begin on the cheeks and spread to the scalp, arms, trunk, and legs. This is more common in infants. The ‘adult’ atopic dermatitis presents as dry, lichenified lesions that are hypo/hyper pigmented and can spread to the neck, hands, feet, eyelids, and behind the ears. These sores are itchy, so inflammation and infection can occur. Treatment includes allergen control, skin care, and avoidance of stress, foods, drinks, and temp changes that tend to exacerbate the eczema. Topical steroid creams are also used. Contact dermatitis often occurs because of a skin sensitivity to metals, chemicals, drugs, and poison ivy. This usually occurs days after the skin is exposed to the allergen. Emollients and topical steroids are standard treatments. 4. Urticaria is also known as hives and can present as red/pink, itchy blotches of varying size. These blotches are also known as wheals and appear suddenly on the skin. Just under half of people who experience hives also experience angioedema, which is a swelling of the face, eyes, lips, and mucous membranes. Hives and angioedema can be associated with anaphylaxis, which is an emergent situation. In the emergent situation, an epi pen should be used because the angioedema swelling can close the larynx, suffocating the person. 5. Malignant melanoma is the most lethal skin cancer. Melanocytes become cancerous, initially in the skin then metastasizing deeper affecting the dermis and other organs. Basal cell carcinoma is the most common type of skin cancer. These rarely metastasize but they can grow large and damage a lot of surrounding tissue when removed. These usually begin as a small dome-shaped bump and often covered by small blood vessels called telangiectasias. This lesion is often shiny. These can be cured with surgery. Squamous cell carcinoma can be caused by the too much UV exposure. This appears as red, crusty, scaly patch on the skin, a nonhealing ulcer, or a firm, red nodule. If detected early enough, it’s curable. If not, they can metastasize to the lymph and other organs. Treatment is similar to melanoma’s. These can be diagnosed by taking biopsies. If they can’t be treated with surgery, chemo and radiation will have to be used, along with steroids. 6. The Rule of Nines is a quick method to determine the percentage of body injured by burns. The body is divided into regions that present as 9% or multiples of nine. The perineum is only 1%. The full head is 9%, the anterior and posterior arm is 9%,front torso is 18%, back torso is 18%, and each leg is 18%. It’s a little different for children. The head is 18%, full torso is 18%, each leg is 13.5%. The American Burn Association uses the rule of nines to determine injury significance. Minor burn is less than 15 % in adults. Moderate burns are 15-25%. Major burns are over 25%. 7. People with albinism are at a very increased risk of obtaining skin cancers and should be checked routinely. Prevention is the best practice for people with albinism. They should wear a high spf sunscreen and avoid tanning beds. 8. Many complications can arise from skin burns, sometimes depending on location of the burn. Pulmonary complications can occur because of increase in respiration rate due to anxiety and pain. Increased lung capillary permeability and increased pulmonary vascular resistance can affect adequate tissue oxygenation. Airway edema and inhalation injury to the lungs are the common issues. ARDS can also occur. The patient should be intubated immediately to prevent airway obstruction. Lesson 5: Neurologic Pathophysiology 1. Ischemic strokes are caused by a thrombus or embolus blocking blood flow to the brain. A hemorrhagic stroke is caused by rupture and bleeding of a cerebral artery, which then causes compression and injury to brain cells. Both types of stroke cause damage to the brain cells and tissue, which means they share similar signs and symptoms. 2. The perimeter around the core ischemic area is called the ischemic penumbra. The penumbra can be saved by reperfusion of the surrounding area. If not reperfused quick enough, the penumbra will succumb to ischemia. 3. In a stroke, neurons within the left or right hemisphere of the brain are injured. There is an anatomical crossover of nerve tracts at the medulla which make symptoms present on the contralateral side of the hemisphere affected. For a patient who has suffered ischemia on the left hemisphere, they will most likely have muscle weakness/paralysis on the right side of the body. 4. A patient who is suspected of a CVA needs to obtain a CT head scan as soon as possible to be able to better identify the etiology of the stroke. If hemorrhage is eliminated as a possible cause, then thrombolytics can be started sooner. 5. Severe motor nerve damage can include hemiparesis, paraparesis, and quadriparesis. Sensory nerve damage can cause loss of sensation in the feet with symptoms of burning, tingling, or pain in the feet. Motor damage can also present with pain. Structural changes in the foot, like hammer toe, can occur due to sensory and motor neuronal disruption leading to abnormal muscle mechanics. Autonomic neuropathy can be damage to the sympathetic and/or cholinergic nervous systems. If it affects the cardiovascular system, it could cause resting tachycardia and postural hypotension. In the GI system, it can cause gastroparesis. 6. Damage to the cerebellum in the brain can cause lack of coordination, or imbalance, referred to as ataxia. Parkinson’s disease can cause ataxia because of the muscle rigidity and tremors associated with the disease. People with multiple sclerosis have balance issues because of damage to sensory and motor nerves, along with weak and fatigued muscles. 7. Epidural hematomas are a bleed in the space below the skull bone and above the dura mater, usually after a major injury, like a fractured skull. After the injury, there’s decreased level of consciousness followed by a calm. After the calm period, there’s rapid deterioration in physiological status of the injured person. Cushing’s triad of hypertension, bradycardia, and bradypnea are indicators of pressure on the brainstem. Subdural hematomas result from bleeding that gathers below the dura mater but above the arachnoid membrane. This can occur within 72 hours to several days of an injury, depending on severity. There are traumatic and aneurysmal subarachnoid hematomas. Traumatic SAH can result from accidents where the head is banged around, causing a rotational-acceleration injury of the brain. Aneurysmal SAH are caused by cerebral aneurysm defects that eventually ‘burst’. These SAH cause the “thunderclap headache” and a rapid decline of the patient. 8. The neurodegenerative disorders talked about were Parkinson’s, Amyotrophic Lateral Sclerosis, Multiple Sclerosis, Huntington’s Disease, Guillain-Barre Syndrome, and Myasthenia Gravis. Huntington’s Disease is an inherited, degenerative neurological disorder that causes involuntary motor symptoms, cognitive decline, and emotional and behavioral symptoms. It is a dominant CNS disorder caused by cellular deterioration. There is no treatment to slow its progression. Symptoms appear between the ages of 30-50 years of age. It is caused by a single mutated gene on a chromosome 4 that produces an abnormal repetition of DNA resulting in a mutation called huntingtin. This mutation collects within the cytoplasm of the brain cells. It is evident in areas of the basal ganglia, caudate nuclei, and the globus pallidus. These affected structures regulate coordinated movement and emotional expression. The cerebral cortex is also affected, causing problems with perception, memory, and thinking. The three common clinical manifestations involuntary motor symptoms, emotional and behavioral symptoms, and cognitive symptoms. Chorea, brief, dance-like movements are one of the symptoms. Athetosis, twisting and writhing movements, are also a symptom of HD. 9. Glaucoma is caused by increased intraocular pressure (IOP), leading to excess pressure on the optic nerve. This can cause nerve damage and blindness. Ocular fluid drainage blockage causes increases in IOP. Also, people who are born with a narrow angle between the iris and cornea are at an increased risk of primary angle-closure glaucoma. Someone with glaucoma has pain in the eye, eye redness, nausea, halos around lights, and vision loss. AMD is caused by a combination of genetic, behavioral, and environmental factors. The retina and the choroid are involved in AMD. Nonexudative is ‘dry’ macular degeneration and exudative is ‘wet’ MD. Both types involve retinal pigmented epithelium (RPE), which normally eat away old retinal cells. As the RPE cells age, they become less effective, changing the permeability of the choroid membrane with accumulated debris in the eye. Patients with AMD have decreased vision late in life, especially at night. They also have fluctuations in their vision, difficulty reading and seeing faces, and central vision is affected while the peripheral vision in intact. 10. Retinal detachment occurs when inner layers of the retina of the eye break away from the retinal epithelial cells and choroid layer. This tearing away can lead to ischemia of the retina, resulting in vision loss. 11. Otitis media is a middle ear disorder resulting from fluid accumulation. Bacteria of the nasopharynx enter the eustachian tube and middle ear. Children have shorter, wider middle ears, making them more susceptible to OM, causing inflammation. The symptoms range from earache, fever, and hearing loss. Meniere’s disease is a disorder of the inner ear with increase in endolymph that fills the membranous labyrinth. This can cause progressive hearing loss and tinnitus, ringing in the ears. It most commonly affects people from 40-50 years old. Symptoms include vertigo, tinnitus, and a feeling of pressure within the ear. Lesson 6: Cardiovascular Systems Pathophysiology 1. A thrombus is an accumulation of blood and possibly other material, like cholesterol, that sticks to the wall of a vein or artery within the vascular system, causing blockage of blood flow. An embolism is a thrombus that has broken free from the wall of the vasculature and is now going with the flow of the blood, just waiting to cause havoc on the body. 2. Aneurysms occur on weakened artery walls, causing a bulging or dilation. They are caused by chronic hypertension, atherosclerosis, and smoking. Plaque buildup in arteries weakens the walls, along with blood flow pushing on the plaque, further weakening. HTN creates a constant force of blood flow against the arterial walls that weakens the integrity of the vessel. 3. Atherosclerosis is caused by plaque build up on the walls of blood vessels, causing eventual obstruction. The endothelium of the tunica intima is where this mostly occurs. Endothelial injury to this area starts the inflammation reaction, sending in WBCs to the site of damage. They eat up lipids in the injured vessel and form lipid-laden macrophages called foam cells. This decreases the ability of the vessels to vasodilate. Excess von Willebrand factor are released, promoting platelet formation and adhesion to the endothelium. This all provides a perfect storm for vascular dysfunction and atherosclerotic plaque formation. 4. For men, angina is mostly presented as chest pain with shortness of breath. In women, it’s presented as anginal equivalents: dyspnea, diaphoresis, dizziness, extreme fatigue, or heartburn. 5. When MI is suspected, doctors usually order a serial cardiac CPK-MB and cTnI every 8-12 hours for up to 2 days. This helps to follow the progression of MI. The rise and fall of these biomarkers help to provide an indication of the extent of heart muscle cell death. 6. Ventricular fibrillation is a quivering of the ventricles in the heart, causing ineffective blood flow. If treated properly within the first 48 hours, the patient will have a good prognosis for recovery. 7. Pericarditis is inflammation of the pericardial membrane that surrounds the heart. Appears on the second or third day after MI. Endocarditis is a noncontagious infection of the cardiac endothelium that mostly affects heart valves. It’s mostly caused by bacteria. 1. Endocarditis: prosthetic valves are a risk factor 2.Pericarditis:cardiac tamponade can occur 3.Pericarditis: often occurs after MI (Dressler’s syndrome) 8. Backward effects are the result of a backup of hydrostatic pressure. Forward effects occur from decreased perfusion of the brain, kidney, and other vital organs. In LVF, HTN causes increased resistance against the left ventricle. This weak left ventricle causes backup of pressure into the left atrium, then pulmonary veins and pulmonary capillaries. This increased pressure in the pulmonary capillaries can cause pulmonary edema. 9. Two types of murmurs are pathological and physiological. Physiological are functional murmurs that may be heard in states of high blood flow within the heart caused by anxiety, stress, fever, anemia, overactive thyroid, and pregnancy. Pathological murmurs are caused by abnormalities of the heart that include valvular deformities, valvular dysfunction, and heart wall defects. A stenotic abnormality is when a valve is narrowed, not allowing blood to flow freely through it. A regurgitant valve doesn’t close properly, allowing a leakage of blood through it, causing an insufficiency. 10. Benign hypertension is a general, systemic high blood pressure reading. It can be chronic or acute. It doesn’t have a high risk for becoming fatal. Malignant hypertension is rapid and dangerous. It occurs more often in patients with a preexisting benign hypertension, making benign hypertension not so safe in the first place. Lesson 7: Lymphatic System Pathophysiology 1. The lymphatic system filters, identifies, and destroys pathogens to protect the body against infections. White blood cells play a huge role in the inflammatory process of protecting the body against infection. 2. The lymphatic system includes lymph vessels, nodes, and fluid. It also includes lymphatic tissue in the spleen, thymus, tonsils and adenoids, bone marrow, Peyer patches, and the appendix. 3. Lymphatic fluid circulates around the body tissues and collects ‘debris to return to the nodes to be filtered out by the lymphatic system. 4. Lymph nodes are small, bean-like masses of tissue located in various regions of the body, including the neck, axillary regions, central thoracic region, inguinal areas, and GI tract. 5. The spleen removes aged, lysed, and dead RBCs from blood circulation. In the spleen, RBCs are broken down into their “ingredients”, which are then recycled to make new RBCs. 6. Tonsils and adenoids help to trap bacteria and viruses that are breathed in through the mouth or the nose. They will enlarge when in contact with infections. 7. Peyer’s patches are lymphatic tissue in the wall of the small intestine that are involved in the development of immunity to antigens presented there. 8. Lymphedema is swelling of the lymph nodes due to a blockage in the lymph ducts or tissues. 9. Hodgkin’s Lymphoma occurs due to enlarged, malignant B cells that may contain EBV. It presents with fever, chills, night sweats, weight loss, or fatigue. There is also a development of binucleate Reed-Sternberg cells. Non-Hodgkin’s Lymphoma occurs due to proliferation of abnormal B cells, T cells, or NK cells. It presents with sore throat, fever, trouble swallowing, SOB, and abdominal pain. Pharyngeal edema and erythema can also be present. Both can have painless, enlarged lymph nodes and/or splenomegaly. 10. Infection can present with most or all of the cardinal signs of inflammation: rubor (redness), tumor (swelling), calor (heat), dolor (pain), and loss of function (function laesa). It can also have purulent exudate, abscesses, gangrene, or necrotic tissue. Lesson 8: Respiratory System Pathophysiology 1. Pulmonary aspiration occurs when material from the oropharynx enters the lower respiratory tract. This is more common is people who have issues clearing their lungs, like a diminished gag reflex, and people with a diminished LOC. Aspiration of contents from the oropharynx or the stomach can result in bacterial pneumonia. 2. Hypoxia is a low amount of oxygen levels in the blood. This has many causes, including pulmonary edema and chemical poisoning. Atelectasis is the deflating of a small number of alveoli, which results in a reduced gas exchange rate. Compressive forces on the alveoli cause the atelectasis. Coughing with deep-breathing help to re- inflate the alveoli. 3. Epiglottitis is the infection and inflammation of the epiglottis. When inflamed, it can obstruct the trachea, causing an emergent situation. 8. Pulmonary hypertension is abnormally high pressure within the pulmonary arteries, greater than 25 mmHg at rest and 30 mmHg with exercise. Pulmonary edema is the accumulation of fluid around the alveoli which inhibits oxygen transfer at the alveolar- capillary interface. Left ventricular heart failure is the main reason for this edema because the left ventricle can’t eject all the blood within the heart’s chamber, causing blood to accumulate in the left ventricle. This blood causes a backwards buildup of pressure into the left atrium, pulmonary veins, and pulmonary capillaries. Severe respiratory distress is the main symptom of pulmonary edema. Chronic hypoxia is the main cause of pulmonary hypertension. 9. Adult respiratory distress syndrome (ARDS) develops within 12-48 hours after an inciting event. Sudden progressive pulmonary edema is a major characteristic of ARDS. The inflammatory trigger initiates the release of cellular and chemical mediators that damage the alveolar-capillary membrane, leaking fluid into the alveolar interstitial spaces. Alveoli collapse, small airways are narrowed, and lung compliance decreases. Lungs lose the ability to ventilate, resulting in decreased LOC, tachycardia, poor peripheral circulation, sweating, restlessness, and anxiety. 10. Covid-19 enters the alveoli and replicates until the alveoli start to get injured. Macrophages and neutrophils enter the alveoli, attempting to attack the virus, in turn, more damage is done to the alveoli. The alveoli begin to breakdown, allowing fluid to rush in and block airway exchange from occurring. Our bodies can’t excrete CO2 or absorb O2. Breathing becomes difficult. This injury to the many alveoli can cause ARDS, and eventually possible death. Lesson 9: Gastrointestinal System Pathophysiology 3. Liver cirrhosis is an injured, failing liver. Cirrhosis is mostly caused by hepatitis B, C, and alcoholism. There are also occurrences of non-alcoholic liver diseases. Liver failure can be caused by viral hepatitis, drugs like acetaminophen, toxins, autoimmune hepatitis, NAFLD, alcoholic hepatitis, or a variety of other causes. Portal hypertension is the increased resistance within the portal vein. This causes a backup of pressure within all the veins of the GI system and causes the veins at the lower end of the esophagus to become distended, called esophageal varices. These veins can rupture, causing bleeding in the form of hematemesis. Decreased detoxification capability can occur due to nitrogenous wastes accumulating in the blood, causing high ammonia levels and increasing susceptibility to encephalopathy. Decreased bile synthesis will cause issues with fat digestion. Static fat in the digestive system leads to steatorrhea and decreased stores of vitamins A, D, E, and K. Decreased albumin synthesis caused by nutritional deficiency and decreased colloid oncotic pressure leads to edema in the peritoneal cavity called ascites. 4. If nausea or vomiting (N/V) is present in the patient, the clinician should review the onset of nausea, triggering factors, time frame between nausea and eating, and whether vomiting occurs. Does the emesis contain blood, mucus, or bile? Does it have a coffee-ground appearance, like in an upper GI bleed? Is blood visible? Does the patient take NSAIDs or aspirin? How much coffee do they drink? What other meds are they taking? Do they take antacids, PPIs, or histamine-2 receptor blockers? 5. One of the major risk factors for upper GI problems is the use of NSAIDs, including aspirin. These meds are often associated with gastric irritation and erosion and can be the cause of PUD. Alcohol use and smoking are associated with esophagitis, peptic ulcer, and esophageal cancer. 6. Peptic ulcer disease (PUD) is a disorder that can be associated as a side effect of many medications, like NSAIDs. Lesson 10: Renal System Pathophysiology 1. In conditions where there is a high amount of breakdown of RBCs, bilirubin accumulates in the blood (hyperbilirubinemia) and adheres to elastin, a component of connective tissue contained in the skin and sclera of the eyes. The tissues take on a yellow stain, resulting in jaundice. The 3 types of jaundice are prehepatic, intrahepatic, and posthepatic jaundice. Prehepatic jaundice is an excess of unconjugated bilirubin in the blood caused by an overwhelming amount of hemolysis occurring in the body. The bilirubin hasn’t entered the liver yet. In Intrahepatic jaundice, the liver has issues conjugating the bilirubin, causing only a portion becoming conjugated. In Posthepatic jaundice, bilirubin has been conjugated and fully processed by the liver but is backed up, caused by an obstruction in the bide duct. Bilirubin that has already left the liver can’t get to the bile duct for secretion. 2. A backup of bile is called cholestasis. Intrahepatic cholestasis occurs at the level of hepatocyte or biliary canalicular membrane. It can be caused by hepatocellular disease, drug-induced cholestasis, biliary cirrhosis, and alcoholic liver disease. 3. Biliary sludge is the precursor to gallstones, being combined of bile salts, bile acids, bile pigments, lecithin, and cholesterol. These components become highly concentrated within the gallbladder. Delayed emptying of this sludge can lead to precipitation of cholesterol and bile components to form calculi. 4. When gallstones travel farther and obstruct the common bile duct, it’s termed choledocholithiasis. When this happens, bile backs up into the liver, causing hyperbilirubinemia and intense pruritus (itching). This bile backup can also irritate the pancreas, or gallstones can move into the pancreas, causing pancreatitis. 5. Calcium stones, struvite stones, uric acid stones, and cystine stones are all types of urolithiases. Spasms of the ureter occur because of obstruction at one of 4 sites: ureteropelvic junction, the midureter at the level of the iliac vessels, the posterior aspect of the pelvis in women, and the ureterovesical junction. Calculi are mostly formed because of poor food choices, diets high in animal protein, sodium, and calcium. If a stone can’t be passed in the urine, surgical intervention with a possible laser use to break up the calculi is needed. 6. If lower UTIs persist, symptoms can progress to cloudy, strong-smelling urine and hematuria. An untreated UTI can put the patient at risk for an ascending UTI that can result in pyelonephritis, which is a kidney infection. 7. Urine acts as a natural defense against lower UTIs because it contains high osmolarity, urea, and organic acids that diminish bacterial viability in the bladder. IgA is secreted by WBCs in the urinary tract and prevents adherence of bacteria to the bladder wall. When host defenses are overcome, urine can act as a medium for bacterial growth. Uropathogenic bacteria can adhere, proliferate, and resist host defenses when in the bladder. This bacteria can also secrete hemolysins and cytotoxic necrotizing factor (CNF), which can enhance their migration up to the bladder. 8. Post-streptococcal glomerulonephritis (PSGN) is the most common cause of AGN. Infection with group A beta-hemolytic streptococcus usually begins as pharyngitis and then causes a secondary immunological reaction to the glomeruli. AGN can also occur due to other types of bacterial, viral, fungal, or parasitic infections. The streptococcus enters the body and stimulates antibody synthesis. The antibodies attack the antigen, but also form antigen-antibody complexes that float freely in the bloodstream until they deposit within glomerular membranes, damaging the structure of the glomeruli. This damage causes nephron dysfunction throughout the kidneys and hyperpermeability of the capillaries, allowing loss of albumin and RBCs in the urine. Because of this diminished albumin content in the bloodstream, decreased colloid oncotic pressure (COP) occurs throughout the body. This decreased COP causes a disturbance in hydrostatic and oncotic pressure, causing edema. 9. Transitional cell carcinoma (TCC) is the most common type of bladder cancer. TCC growth arises from the bladder’s interior surface, protruding into the bladder lumen and can penetrate to the basement membrane and then continue into the bladder muscle, where it can met. The cardinal feature of bladder cancer is painless, intermittent, gross hematuria. 10. Renal cell carcinoma is the most common type of kidney cancer. The cause is unknown in most patients, although there can be hereditary and environmental causes. RCC presents with hematuria, flank pain, and palpable abdominal mass. Most cases are asymptomatic and are discovered because a renal mass is incidentally detected on an xray. 11. The glomerulus is a tuft of capillaries within Bowman’s capsule of the kidney. It requires high hydrostatic pressure to push blood through the filtration process. The juxtaglomerular apparatus is a specialized region of the nephron within the kidney that’s sensitive to sodium. This is around the glomerulus in each nephron. They work with the RAAS system, detecting low sodium levels and triggering compensatory reactions (renin). The glomerulus is within Bowman’s capsule. It allows for water, sodium, bicarb, acids, and urea out of the blood. At the proximal tubule, large amounts of water, sodium, and potassium are reabsorbed into the bloodstream. At the descending loop of Henle, a high amount of sodium is reabsorbed, and urea is secreted from the blood into the tubule. In the distal tubule, sodium and water are reabsorbed from the tubule fluid into the bloodstream and urine is formed. 12. Bilateral renal stones can cause renal damage by scarring the tissue, which may lead to acute or chronic renal failure. Mostly, though, CRF is caused by diabetes mellitus, hypertension, glomerulonephritis, and polycystic kidney disease. 13. Chronic renal failure usually progresses to ESRD. Kidney function deteriorates to the point that the kidney is unable to excrete waste products or control volume status, making dialysis or a kidney transplant the only options to support life. ESRD can cause many adverse effects, like: encephalopathy, thrombocytopenia, electrolyte imbalances, anemia, high BUN, uremic frost, hyperparathyroidism, HTN, heart failure, infertility, ED, renal osteodystrophy, edema, and peripheral neuropathy. 14. Hemodialysis is a treatment during which the patient’s blood is drawn from their body, passed through a device to filter it, then return it to the body. A fistula is made for the patient to easily facilitate the process. The dialysis solution contains a solution of electrolytes. The patient’s entire blood volume circulates through the machine every 15 minutes. Hemodialysis is required at least 3 times a week, lasting 4-6 hours per session. Continuous renal replacement therapy is like hemodialysis but is slower. It is preferred for patients that are hemodynamically unstable and fluid overloaded. This continuous process takes smaller volumes of blood from the patient and filters it over 24 hours. Lesson 11: Endocrine Pathophysiology 1. The pituitary gland is called the master gland because it controls all other endocrine functions. If it dysfunctions, a multitude of problems can arise. Pituitary adenomas are the most common tumor of the gland. Pituitary tumors cause growth disturbances, electrolyte imbalances, and infertility. These tumors are usually benign, epithelial neoplasms. Pituitary insufficiency, called hypopituitarism, is the hyposecretion of one or more of the pituitary hormones. With this, tropic hormone production is reduced and target gland hormone production is decreased. 2. Hormonal signals are triggers in our body that relay an issue with hormones, either overproduced or underproduced. Neural signals are influenced by other neurons, not chemicals like hormones. Hormonal signals take more time to trigger a response to a low or excess amount, whereas, neural signals are almost instant. 3. Toxic multinodular goiter, Plummer’s disease, is an example of primary hyperthyroidism because the thyroid contains hyperfunctioning nodules, making an excess is T3/T4 hormones. Weight loss, sensitivity to heat, palpitations, tremors, nervousness, restlessness, and diaphoresis are possible symptoms of this disease. It presents as an enlarged thyroid or nodule, exophthalmos, tremor, lower limb weakness, a-fib, and/or an audible bruit over the thyroid gland. TSH levels are low and T3/T4 levels will be elevated. 4. Negative feedback regulates each of the hypothalamic-pituitary-hormone axes, which maintains hormone levels within a narrow range. When a person is running in a marathon, the hypothalamus receives signals from the body that the muscles and organs have extra metabolic needs. It then secretes corticotrophin-releasing factor (CRF), which stimulates the pituitary gland. The pituitary gland secretes ACTH, which stimulates the adrenal gland to secrete cortisol. When cortisol levels in the blood rise, the pituitary gland senses it, shutting off the stimulus to the adrenal gland so that it doesn’t secrete more of the cortisol. 5. DKA isn’t as much of a deal for T2DM because of there being some insulin still present. The presence of insulin allows for some glucose uptake by the cells and inhibits fat breakdown, thereby preventing the development of ketoacids. T1DM are more at risk since they have way less insulin. 6. Serum potassium levels appear normal or falsely high in HHS because of the shift of K+ from the intracellular to extracellular. As rehydration and insulin treatment ensue, potassium returns to the intracellular compartment. Serum potassium levels then decrease as the K+ ions move back into the cells. Therefore, hypokalemia results from HHS, and K+ replacement is usually necessary in the treatment plan. 7. The activation of PKC has several effects, including production of vascular endothelial growth factor (VEGF), which is implicated in diabetic retinopathy. The hyperglycemia causes damage to the fragile retinal artery endothelium. This injury incites inflammation, which attracts WBCs and platelets to the sites. This eventually occludes the retinal arterioles and capillaries, causing retinal ischemia. Injured endothelium becomes hyperpermeable, allowing fluid to leak into the tissue, causing edema. Clinical signs of retinopathy include microaneurysms, hemorrhages, macular edema, exudates, and “cotton wool spots” evident on fundoscopic exam. Lesson 12: Reproductive Pathophysiology 1. Depending on sexual reassignment surgery, a hysterectomy and oophorectomy may be involved, or the ovaries may be left in place. Because androgens are partially metabolized into estradiols, there may be estrogenic stimulation of the remaining breast tissue, which increases the risk for cancer. 2. Amenorrhea is the absence of menstrual periods. Some possible causes are delayed puberty development, birth defects of the female reproductive system, genetic disorders, lack of an opening in the membrane at the entrance of the vagina, ovarian failure, drastic weight loss, stress and anxiety, hormone birth control, and many other possible causes. 3. All 3 types of cancer are highly likely if a first-degree relative has a history of either breast, ovarian, or cervical cancer. The BRCA gene is an inherited genetic mutation that increases the risk of breast, ovarian, and other cancers. Smoking, alcohol use, drugs, and caffeine intake are important to know to determine one’s risk of cancer. 4. Obstructive causes of infertility include repeated infections, vasectomy, swelling, or defects that cause blockage of sperm from entering the ejaculate. Nonobstructive causes include deficiencies in sperm formation, motility, or concentration. Azoospermia is the name for no sperm in the ejaculate while oligospermia is the name for too little sperm. 5. Surgical excision of the prostate may be required if cancer is present. When a radical prostatectomy is done, pelvic lymph nodes are removed and examined. Radiation in the form of an implant or external beam delivery is commonly necessary. Antiandrogenic hormone chemotherapy may also be required. 6. Pelvic Inflammatory Disease is a serious STI in women. Any infection ascending from the vagina and cervix to the internal upper reproductive organs, including the uterus, fallopian tubes, or ovaries, is considered PID. 7. PID symptoms can include pelvic pain with fever and chills. In chronic PID, inflammation of the walls of the fallopian tubes leaves scars, which then create problems for egg transport. Scarred fallopian tubes can lead to infertility or ectopic pregnancy. An exquisite tenderness of the cervix on a pelvic examination is called a Chandelier sign, which is pathognomonic for PID. 8. Most cases of PID are caused by N. gonorrhoeae or C. trachomatis. Less commonly, PID is caused by aerobic and anaerobic organisms such as G. vaginalis, Prevotella sp., Haemophilus influenzae, Escherichia coli, Streptococcus agalactiae, S. pyogenes, S. pneumoniae, Cytomegalovirus, Mycoplasma hominis, and Ureaplasma urealyticum. These bacteria infect the vagina or cervix and ascend upward into the uterus, fallopian tubes, and ovary. 9. Women who are most at risk for PID are those who have a history of multiple sex partners, past STIs, intrauterine device use, or failure to use contraceptive methods. Those at increased risk are those that have had a D&C procedure, abortion by vacuum curettage, or hysterosalpingogram.