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PATHO D236 Pathophysiology
Remediation Study Notes
Lesson 1: Homeostasis Concepts
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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
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.
- 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.
- 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.
- 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’.
- 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.
- 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
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.
- 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.
- 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.
- 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%.
- 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.
- 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
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.
- 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.
- 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.
- 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.
- 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
ineffective blood flow. If treated properly within the first 48 hours, the patient will have a good prognosis for recovery.
- 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.
- Endocarditis: prosthetic valves are a risk factor 2.Pericarditis:cardiac tamponade can occur 3.Pericarditis: often occurs after MI (Dressler’s syndrome)
- 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.
- 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.
- 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
- 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.
- 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.
- Lymphatic fluid circulates around the body tissues and collects ‘debris to return to the nodes to be filtered out by the lymphatic system.
- 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.
- 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.
- 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.
- Peyer’s patches are lymphatic tissue in the wall of the small
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.
- 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
- 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.
- 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?
- 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.
- 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
- 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
