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Exam 1 Blue Print
- Cancer etiology – obesity, alcohol Obesity/lack of exercise- poor nutrition; epidemic over the past 20yrs; linked to 13 distinct forms of cancer: liver, prostate, ovarian, gallbladder, kidney, colorectal, esophageal, breast (post menopause), pancreatic, endometrial, stomach, multiple myeloma, & meningioma; linked to both increased risk and increased progression of cancer Alcohol- there is strong data linking alcohol with cancer of the mouth, pharynx, larynx, esophagus, liver, colorectal, and breast.; no “safe limit” of intake Other possible causes for cancer include: Smoking, Infectious agents (mold, bacteria, viruses, parasites), Environmental exposure to sunlight, ionizing radiation, non-ionizing radiation, air/water/soil carcinogens; carcinogens in the household (drugs; personal care items), Occupational exposure to chemical and physical carcinogens, Socioeconomic, racial, geographical, and ethnic factors also affect exposures, risk, detection, and treatment
- Isotonic fluid – composition/maintenance Isotonic = 0.9% normal saline Hypertonic > 295 mOsm/kg o Can be due to water loss or solute gain, makes cells shrink. Most common cause is hypernatremia or a deficit in the ECF. o Water moves from ICF to ECF and causes hypervolemia in the vessels Hypotonic < 275 mOsm/kg o Can be due to water gain or solute loss, makes cells swell. Most common causes are hyponatremia or excess of electrolyte-free water (water intoxication) o Water moves from ECF to ICF and leads to hypovolemia. o Normal Osmolality 275-295 mOsm/kg Starling hypothesis – net filtration is equal to the forces favoring filtration minus the forces opposing filtration.
Forces favoring filtration – capillary hydrostatic pressure (BP) & interstitial oncotic pressure (water pulling into interstitial spaces) Forces opposing filtration – capillary oncotic pressure (water pulling into vessel) & interstitial hydrostatic pressure against vessel
- Know about serum potassium and sodium and clinical features related to fluctuations in Na, K Sodium 135-145mEq Hypernatremia = Na > o Hypovolemic hypernatremia – due to loss of sodium with a relatively greater loss of body water. Causes can be from loop diuretics, diuretic stages of renal disease, osmotic diuresis from diabetes mellitus, or mannitol use. o Isovolemic hypernatremia (most common) – due to loss of electrolyte-free water with a near normal body sodium level. Causes can be excessive sweating, inadequate water intake, fever with hyperventilation and increased water loss from lungs, burns, vomiting, diarrhea, lack of ADH or inadequate renal response to ADH. o Hypervolemic hypernatremia (rare) – due to and increase in TBW with a greater increase in sodium levels. Causes can be from infusion of hypertonic saline solutions, over secretion of adrenocortropic hormone (ACTH) or aldosterone from cushings syndrome or adrenal hyperplasia, deliberately high salt intake. Symptoms include weight gain, bounding pulse, increased BP, and lethargy. o Clinical Manifestations of Hypernatremia Central nervous system signs are the most serious and are related to brain cell shrinking, brain dehydration, and alterations in membrane potential. Weakness, lethargy, muscle twitching, hyperreflexia, confusion, coma, and seizures can occur. Dehydration signs and symptoms: thrist, headache, sudden weight loss, concentrated urine, hard stools, elevated body temp, soft eyeballs, sunken frontanels in infants, weak pulses, tachycardia to name a few.
In severe hyponatremia (<125), there can be lethargy, headache, confusion, apprehension, seizures, and coma. Cerebral edema! In hypovolemic hyponatremia there can be hypotension, tachycardia, and decreased urine output. In hypervolemic hyponatremia there can be weight gain, edema, ascites, and jugular vein distention. o Treatment Restriction of fluids in the case of dilutional hyponatremia. Rapid correction of chronic hyponatremia can lead to osmotic demyelination syndrome with axonal damage in the brain leading to neurological disability or death. Iso & Hypervolemic hyponatremia – ADH antagonists Potassium 3.5-5mEq o Regulation of potassium includes: o The action of aldosterone – stimulates the secretion of potassium into the urine by the distal renal tubules. Also increases the secretion of potassium from the colon and sweat glands. o The concentration gradient of K+ at the distal tubule and collecting duct – ECF potassium is detected in the peritubular capillaries and when concentrations are high more potassium is excreted to maintain homeostasis or vice versa. o The distal tubule flow rate and distal tubule sodium delivery – when flow is increased (diuretic use) the concentration of K+ is lower therefore more potassium will be secreted. o Changes in pH – hydrogen ions accumulate in the ECF creating a charge imbalance. To maintain ionic balance potassium shifts into the ECF. Acute acidosis can lead to hyperkalemia due to this. o Insulin – stimulates the Na+K+ ATPase pump, this promotes the movement of potassium into the liver and muscle cells and out of the ECF.
Hypokalemia <3.5mEq o Causes: reduced intake of potassium, an increased entry of K+ into cells, and increase losses of K+, diarrhea, GI drainage tubes, laxative overuse, diuretic use, excessive aldosterone secretion, low plasma magnesium, kidney disease o Clinical manifestations : neuromuscular excitability decrease, skeletal muscle weakness, smooth muscle atony, cardia dysrhythmias, glucose intolerance, and impaired urinary concentrating ability. Cardiac muscle cell membrane potential becomes more negative, which requires a greater stimulus to trigger and action potential. Hypokalemia delays ventricular repolarization and can lead to sinus bradycardia, AB block, paroxysmal atrial tachycardia. Decreased insulin secretion and alters hepatic and skeletal muscle glycogen synthesis. o Treatment: replacement of potassium cand correcting the underlying issues. Promotion of high potassium foods may be necessary Hyperkalemia >5.5mEq o Causes: acidosis, insulin deficiencies (DKA), whole blood admin, IV bolus of pen G, excessive replacement of K+, ACE inhibitors, ARBS, potassium sparing diuretics, aldosterone antagonists, decreased renal function. Hypoxia diminishes the efficacy of active transport and K+ can escape into the ECF. Addison’s disease decreased aldosterone secretion therefore not as much urine is being excreted so potassium can build up o Clinical Manifestations : restlessness, intestinal cramping, diarrhea, muscle weakness, loss of muscle tone, paralysis, narrow & tall T wave, short QT, depressed ST, wide QRS, ventricular fibrillation. Cells become more positive = hyperpolarized, this leads to more rapidly repolarization and hyper excitability. In extreme cases the cells can not repolarize and cannot respond to excitation stimuli. (Hypercalcemia counteracts the effects of hyperkalemia on resting membrane potential) o Treatment: calcium gluconate, glucose to stimulate insulin secretion, glucose with insulin for patients with diabetes, RASS inhibitors, potassium binders, dialysis for renal dysfunction.
- Saclike structures that originate from the Golgi
- Primary vs. secondary lysosomes Functions
- Intracellular digestion system
- Role in autodigestion and autophagy RNA mRNA- messenger RNA; takes information from DNA in the nucleus out into the cytoplasm tRNA - transfer RNA; anticodon (3 base prong) undergoes complementary base pairing with mRNA to transfer information into the sequence of amino acids rRNA - ribosomal RNA; located in the ribosome along with protein (actual site of protein synthesis)
- Transcription, translation DNA to RNA
- Mitochondria structure/functions/mutations importance Structure - Is surrounded by a double membrane. - Increased inner membrane surface area is provided by cristae. Functions - Is responsible for cellular respiration and energy production. - Participates in oxidative phosphorylation
- Barr body Inactivated X chromosome (fixed); normal females (XX) have one barr body; normal males (XY) have no barr bodies Can be the X contributed by the mother or father Individuals that have an abnormal number of X chromosomes: XXY- Klinefelter Syndrome ; males have barr body; Characteristics: Male appearance, Develop female-like breasts, Small testes—usually sterile, Sparse body hair, Long limbs XXX/XXXX- females that have multiple barr bodies (Trisomy X most common sex chromosome aneuploidy; Symptoms are variable: sterility, menstrual irregularity, and/or intellectual disability, Symptoms worsen with each additional X X- Turner syndrome ; females have no barr body; Underdeveloped ovaries (sterile), Short stature (~ 4'7"), Webbing of the neck, Edema, Underdeveloped breasts; wide nipples, High number of aborted fetuses Observable in many interphase cells- highly condensed intranuclear chromatin bodies
- Phenotype and genotype – what are the main differences?
- Respiratory acidosis and alkalosis – know how to differentiate
Anion Gap – normally 10-12 mEq/L, normal or elevated anion gap with metabolic acidosis may help determine the cause.
- Local signs of inflammation – know well Cardinal signs include redness, heat, swelling, pain, and loss of function. Systemic: fever, leukocytosis, pyrogens in the blood CELLS of inflammation / who gets there first: neutrophils first (6 or so hours), macrophages and T lymphocytes within 24 hours
- inflammation Cellular and chemical components, Nonspecific, rapidly initiated, no memory cells. 3 types of Plasma Protein Systems
- Complement System
- Clotting System
- Kinin System Complement System
o WBCs adhere to the inner walls of vessels, and they migrate through enlarged junctions between the endothelial cells lining the vessels into the surrounding tissue (diapedesis) Within seconds, arterioles near the site constrict briefly to control bleeding. o Next, vasodilation sets in and causes slower blood velocity and increased blood flow to the site.
- Cellular Mediators of Inflammation Mast cells, neutrophils, eosinophils, basophils, monocytes, macrophages, natural killer cells, lymphocytes, platelets. Biochemical mediators originate from the destroyed or damaged cell, it modulates the localization and activities of other inflammatory cells, and it helps tissue regeneration or repair. The cells can have pattern recognition receptors (PRRs) on them to help them find the source of inflammation. o Toll-like receptors recognize pathogen-associated molecular patterns (PAMPs) o Complement receptors help recognize complement fragments o Scavenger receptors promote phagocytosis Cellular Products o Chemokines or cytokines regulate innate or adaptive resistance by affecting other neighboring cells. They are either proinflammatory or anti-inflammatory and either synergistic or antagonistic. Actions are pleiotropic meaning the same molecule may have different biological activities, but it depends on the target cell it is acting on. Includes interleukins, interferons, and tumor necrosis factor. o Interleukins are made by macrophages and lymphocytes in response to microorganisms or other products of inflammation. These help regulate inflammation. o Interferons protect against viral infections, they are produced and released by the infected host cell, they do not kill viruses but prevent them from infecting additional healthy cells. o Chemokines are produced by macrophages, fibroblasts, and endothelial cells. Beta chemokines (CC) mainly affect monocytes, lymphocytes, and eosinophils. Alph chemokines (CXC) generally affect neutrophils.
- Mast cells Mast cells are cellular bags of granules located in loose connective tissues close to blood vessels. They are activated by physical injury, chemical agents, immunologic processes and TLRs. They can be
released two different ways, degranulation or synthesis of lipid-derived chemical medicator. Mast cells can be found in connective tissue and close to vessels near the body’s surfaces (Skin; GI; and respiratory tract) o Not found in the blood - basophils function like mast cells and circulate in the blood o They are also NOT found in areas of the body without blood vessels (CNS; cartilage; cornea; mineralized bone) Mast Cell Degranulation Releases histamine to cause large blood vessels to constrict and dilate postcapillary venules. o H1 receptor (proinflam) are present in the bronchi and induces bronchoconstriction. o H2 receptor (antiinflam) are present on the stomach mucosa and induces gastric acid secretion.
- Most common immunoglobulins IgG : 80-85% of antibodies in the blood; provides the most protection against infections; crosses the placenta during pregnancy & protects the child for the first 6mo of life IgM : largest antibody; first one produced in the primary response to antigens; synthesized early in neonatal life (may increase in response to infection in utero); part of BCR complex in B cells IgA : found in blood and bodily secretions (secretory IgA) IgD : also part of BCR complex in B cells- part of the antigen receptor IgE: low concentration in circulation; specialized functions: mediate common allergic responses & defense against parasitic infection
Results in large # of memory cells & sustained protective levels of antibodies, T cells, or both IgM levels similar to primary vaccination, IgG levels MUCH higher in booster than in primary vaccination Pneumonic: Mom before grandma (just a helpful way to remember) In immune response IgM (mom) responds and is elevated first, in exposure following that IgG is elevated (grandma), so if a patient has high levels of IgG then they probably have been exposed to whatever antigen it is before. If patient has high IgM levels, this is their first exposure.
- Clinical desensitization May reduce the severity of the allergic reaction but could also cause anaphylaxis Works best on common resp allergies and insect stings. Food allergies more difficult to suppress. Desensitization is effective for people 5 years of age and older
- Tumor cell markers Substances produced by both benign and malignant cells. Hormones, enzymes, genes, antigens, and antibodies Can be Used to: screen and identify individuals at high risk for cancer. (example is PSA for prostate cancer screening) help diagnose the specific kind of tumor (if certain cell marker abnormally elevated there maybe a cancer to blame) follow clinical course of cancer Estimate prognosis (medullary thyroid cancer) measure how treatment is going (CA-125 with ovarian cancer) Examples: ACTH, alpha fetoprotein (liver), PSA (prostate) catecholamines (adrenals), CEA (GI/ pancreas, lung, breast, etc), calcitonin, CA-125 (ovarian)
- TNM system T = tumor spread · T0= · T1= lesion <2cm · T2= Lesion 2-5cm · T3= invasion of skin and / or chest wall N=node involvement · N0= no node involvement
· N1=mobile nodes involved · N2 = fixed nodes involved M = metastasis to distant site · M0= no metastases · M1= demonstrable metastases · M2=suspected metastases
- Tissue regeneration in wound healing Wound healing 3 phases: inflammation; proliferation and new tissue formation; and remodeling and maturation Inflammatory phase: o vascular and cellular responses o vasoconstriction, formation of fibrin clot, and coagulation help stop blood flow o Release of inflammatory mediators o Infiltration of neutrophils and macrophages that assist in clearing debris from the wound o Debridement (fibrinolytic enzymes dissolving fibrin clots); Inflammation then reversed (assists with permeability) Proliferation and tissue formation phase: o invading macrophages release growth factors (promote angiogenesis and collagen formation) o Granulation tissue & epithelial stem cells grows into the wound from surrounding tissues o Epithelial stem cells create layers of epithelial cells o Wound closure- myofibroblasts contract to cause tension on attached cells Remodeling and maturation phase: o usually complete within 2 years (dependent on patient comorbidities, type of wound, location, and if infection is present) o scar tissue is established and remodeled o fibroblasts continue to deposit and organize collagen o wound contraction continues; o New tissue will gradually reach its maximal strength and flexibility. Usually remodeled tissues is not as good of quality as original tissue. And each injury increases risk for mutations and potential cancer, for example constant inflammation
- Adaptive immunity – memory cells Aka Acquired/Specific immunity
o Factor XIII (Fibrin-stabilizing factor)- crosslinks fibrin Vitamin K helps the liver produce clotting factors, which are proteins that cause blood to clot. Without vitamin K, the liver can't produce clotting factors II, VII, IX, and X, which means blood wouldn't clot
- Endothelial cells – know functions They participate in immune responses, inflammation, and angiogenesis. Hemostasis : Endothelial cells initiate hemostasis by constricting blood vessels to reduce blood flow at the site of injury. They release substances like von Willebrand factor (vWF) and tissue factor to activate platelets, helping in blood clot formation. Endothelial cells promote platelet adhesion by exposing collagen and vWF, promoting platelet binding. Prevention of Thrombosis : Endothelial cells prevent thrombosis through anticoagulant and antiplatelet mechanisms, ensuring clot formation only at sites of injury. These cells produce substances such as nitric oxide (NO) and prostacyclin, which inhibit blood clot formation and promote blood fluidity. Endothelial dysfunction can disrupt this balance, leading to bleeding or thrombosis, and contributing to several vascular complications. Leukocyte Interaction : Endothelial cells facilitate the movement of leukocytes from the bloodstream into the surrounding tissues. This process is necessary for immune responses and inflammation. This involves leukocyte capture, rolling, firm adhesion, and migration across the endothelium. Endothelial adhesion molecules like selectins and integrins, along with their ligands on leukocytes, help these interactions. Vascular permeability : Endothelial cells regulate the movement of substances, including fluids, electrolytes, and other molecules, between the blood and surrounding tissues. They form a selectively permeable barrier with tight junctions under normal conditions. They maintain the integrity of the vascular barrier, ensuring substances like nutrients and oxygen can pass while preventing the leakage of harmful substances into tissues. Regulation of Vascular Tone : Regulation of vascular tone refers to the adjustment of the diameter of blood vessels to control blood flow and maintain blood pressure within a normal range. This process involves the contraction (vasoconstriction) or relaxation (vasodilation) of the blood vessels. Endothelial cells release various vasoactive
substances that affect vascular tone, including vasodilators like nitric oxide and vasoconstrictors like endothelin. These molecules help regulate blood vessel diameter and blood flow. Angiogenesis : Endothelial cells are also involved in angiogenesis, the process of formation of new blood vessels from pre-existing ones. Angiogenesis is essential for processes like wound healing and is involved in various pathological conditions, like inflammatory disorders and cancer.
- Process of phagocytosis
- Recognition: the phagocyte recognizes the target particle
- Signaling: the phagocyte activates a signaling cascade to induce particle internalization.
- Phagosome formation: the phagocyte forms a phagosome by closing the phagocytic cup around the particle.
- Phagolysosome maturation: the phagosome matures into a phagolysosome, which in an acidic and hydrolytic environment that degrades the particle.
- Histamines and Leukotrienes Both are proinflammatory mediators that are released during an alergic inflammation and can cause a number of symptoms. o Histamine: responsible for many symptoms of allergic rhinitis, including sneezing, nasal itching, and rhinorrhea. o Leukotrienes: cause increased vascular permeability and nasal airway resistance. They also cause bronchoconstriction in both healthy people and those with asthma.
