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Study Guide for Midterm Exam
This study guide provides a content outline that can be used to prepare for the topic quiz. This outline may not be inclusive of all quiz content. Cellular biology and Alterations
- Compensatory hyperplasia after partial resections (mod 1) (51-53) o Ex: liver, hepatocyte growth o Adaptive mechanism that enables certain organs to regenerate o Even with removal of 70% of the liver, it will regenerate within about 2 weeks o Compensatory hyperplasia occurs in epidermal, intestinal epithelia, hepatocytes, bone marrow and fibroblasts. Some type off hyperplasia is noted in bone, cartilage and smooth muscles – Example- callus, wound healing as part of inflammation process - Tumor progress from benign to malignant (364-366) o Benign tumors are usually encapsulated and well differentiated. They retain some normal tissue structure and do not invade the capsules surrounding them or spread to regional lymph nodes or distant locations. ▪ Generally named according to the tissues from which they arise, and include the suffix –oma. o Some benign tumors can progress to cancer and are then referred to as malignant. They have more rapid growth rates and specific microscopic alterations, including loss of differentiation and absence of normal tissue organization. ▪ One hallmark is anaplasia – loss of cellular differentiation, irregularities of the size and shape of the nucleus, and the loss of normal tissue structure. ▪ May present with different degrees of encapsulation; some lack a capsule, and even if one is apparent, it’s integrity has been compromised so that tumor cells can grow to invade nearby blood vessels, lymph and surrounding structures. ▪ Most deadly characteristic is their ability to spread far beyond the tissue of origin – metastasis
Genetics
- Recurrence of autosomal diseases (152-154, 155-156) o Autosomal dominant - Affected offspring are produced by the union of a normal parent with an effected heterozygous parent ▪ Affected parent can pass either a disease gene or a normal gene to his or her children ▪ Each event has a probability of 0.5, so on average half the children will be normal and half will express the disease. o Autosomal recessive – individual must be homozygous for a recessive allele to express the disease – can survive the population one generation to the next ▪ Characterized by delay of onset, incomplete penetrance, and variable expressivity – most common is cystic fibrosis ▪ Recurrence risk for the offspring of carrier parents is 25% - Klinefelter’s syndrome (mod 1) (148, 156, 914) o Causes ▪ Chromosomal disorder XXY – genotype ▪ Genetically male – due to Y
- Male XY, female XX ▪ Random, not inherited – nondisjunction in the X chromosomes in the mother o Signs and Symptoms ▪ Both male and female sexual characteristics ▪ Decreased T more female hormones causing
- Less body and facial hair
- Gynecomastia ( risk breast CA )
- Weak muscles and bones (osteoporosis), shy (tall, lanky, shy)
- Can result in decreased IQ
- Higher risk of AI disorders ▪ Majority - Infertility BENIGN TUMORS MALIGNANT TUMORS ▪ Grow slowly ▪ Have a well-defined capsule ▪ Are not invasive ▪ Are well differentiated; look like the tissue from which they arose ▪ Have a low miotic index; dividing cells are rare ▪ Do not metastasize ▪ Grow rapidly ▪ Are not encapsulated ▪ Invade local structures and tissues ▪ Are poorly differentiated; may not be abl determine the tissue of orgin ▪ High miotic index; many dividing cells ▪ Can spread distantly; often through bloo vessels and lymphatics
o Member of Herpesviridae family
- Complement Cascade (197, 198f, 287f) o Activated by 3 pathways ▪ Classical pathway – activated by proteins of the adaptive immune system (antibodies) bound to their specific targets (antigens) - Forms antigen-antibody complex (immune complex) ▪ Lectin pathway – activated by mannose-containing bacterial carbohydrates ▪ Alternative pathway – activated by gram-negative bacterial and fungal cell wall polysaccharides o C3 deficiency blocks all three pathways ▪ People with this deficiency are at risk for recurrent life-threatening infections with encapsulated bacteria at an early age, as well as a SLE-like syndrome that may be complicated by kidney disease (glomerulonephritis) - Passive-acquired immunity (227) o Aka passive immunity o Does not involve host’s response at all o Occurs when preformed antibodies or T lymphocytes are transferred from a donor to the recipient. o Can occur naturally as in the passage of maternal antibodies across the placenta to the fetus, or artificially, as in a clinic using immunotherapy for a specific disease o Temporary immunity - IgM and IgG and IgA and IgE (229-230, 247, 254-255) o IgA (p.229)- Fungal infection skin, GI tract, Mouth Vaginal ▪ IGA in breast milk, works at GI system o IgM (p. 229) - First antibody that produced during primary response to antigen. It synthesize early in neonatal life and may be increased as response to infection in utero o IgE (p.229) primary cause of common allergies (hay fever, dust, bee stings). Complement T helper cells and immune responses ▪ IgE bind to receptors on the surface of mast cells causing release of histamine H ▪ Protects from parasites/worms o IgG (p. 229) most abundant, 80-85%, most of protective activity against infections – selective transport across the placenta, maternal IgG is also the major class of antibody found in the blood of the fetus and newborn. o Bronchial constriction (2) Edema (3) Vasodilation (4) H2 (5) Increase gastric secretions (6) Decreases the release of histamine from mast cells and basophils o IgG, IgM, and IgA bind to the surface of parasites, activate complement, generate chemotactic factors for neutrophils and macrophages, and serve as
those phagocytic cells; unique to parasitic infections, the eosinophil is a primary cell in the granuloma
- IgE-mediated hypersensitivity (263-265) o Type 1 reactions – most common allergies (i.e. pollen) o IgE can contribute to a few autoimmune and alloimmune diseases, and many common allergies (poison ivy) are not mediated by IgE. o Short life span in the blood o Individual is usually sensitized when exposed to antigen in future. o Histamine is the most potent mediator which affects several key target cells – contracts bronchial smooth muscles, causing bronchial constriction; increases vascular permeability, causing edema, and causes vasodilation, increasing blood flow into the affected area ▪ Interaction of histamine with H2 receptors results in increased gastric acid secretion and a decrease of histamine released from mast cells and basophils – action of histamine through H2 receptors suggests an important negative-feedback mechanism that stops degranulation o Mast cells are principal effector cells involved - SLE (Lupus) (mod 2) (277-278) o Antigen-antibody mediated o Type III hypersensitivity o Chronic, multisystem, inflammatory disease, most common, complex and serious of autoimmune disorders o Characterized by the production of a large variety of autoantibodies against nucleic acids, erythrocytes, coagulation proteins, phospholipids, lymphocytes, platelets, and many other self-components ▪ Most characteristic autoantibodies produced are against nucleic acids, histones, ribonucleoproteins, and other nuclear material o Occurs more often in women, age 20- o Clinical Manifestations: arthralgias or artiritis, vasculitis, rash, renal disease, hematologic abnormalities (anemia) ▪ Develops slowly and has frequent remissions and exacerbations o 11 common clinical findings (dx based on serial or simultaneous presence of 4) ▪ Facial rash confined to cheeks (malar rash) ▪ Discoid rash (raised patches, scaling) ▪ Photosensitivity ▪ Oral or nasopharyngeal ulcers ▪ Nonerosive arthritis of at least two peripheral joints ▪ Serositis (pleurisy, pericarditis) ▪ Renal disorder (proteinuria) ▪ Neurologic disorder (seizure, psychosis)
▪ Hematologic disorders (hemolytic anemia, leukopenia, lymphopenia, thrombocytopenia) ▪ Immunologic disorders ▪ Presence of antinuclear antibody (ANA) o No cure, treat symptoms, and minimize autoimmune response – NSAIDS, Steroids, immunosuppressive drugs, IVIg ▪ Protect from sunlight Fluid and Electrolytes and Acid-base
- Treatment of Hyperkalemia (mod 3) 119 o K+ > 5. o Renal Failure o Spironolactone o Hypoaldosteronism ▪ Addison’s Disease o Burns/Cell lysis o Hemolytic Anemia's o Rhabdomyolysis o Acidosis o Insulin Deficiency o Signs and Symptoms ▪ Tingling, cramps/diarrhea ▪ Weakness Flaccid Paralysis ▪ Arrhythmias Cardiac Arrest o Should be investigated when there is a history of renal disease, massive trauma, insulin deficiency, Addison disease, use of potassium salt substitutes, or metabolic acidosis o Treat contributing causes and correct imbalance o Calcium gluconate – restores normal neuromuscular irritability o Glucose – stimulates insulin secretion o Glucose + insulin – facilitates cellular entry of potassium o Buffered solutions – correct metabolic acidosis and lowers serum potassium level o Oral/rectal – exchanges sodium for potassium in the intestine o Dialysis – renal failure - Calcium and phosphate balance (119-120) o Calcium is a necessary ion for many fundamental metabolic processes ▪ Normal serum levels: 9-10. ▪ Major cation associated with the structure of bones and teeth
o Abnormal insulin secretion/action ▪ Beta cell dysfunction ▪ Insulin resistance o Increased free fatty acids and fat deposition – incr. inflammation (release of cytokines) and intracellular lipid deposits o Incr. glucagon secretion o Alteration in the production of adipokines by adipose tissue - Leptin resistance o 2 most important factors are positive family hx and obesity o See figure 22-15 page 740
- Know Autoimmune disorders (262-263, 264t-265t, 277-281, 275-276) o SEE TABLE 9-2 PAGE 264 o Hashimoto’s Thyroiditis ▪ Causes - AI, FHX ▪ Signs and Symptoms - Hypothyroidism, Painless unilateral or bilateral enlargement of the thyroid ▪ Testing - TSH, T3/4, Antibodies o Graves Disease ▪ AI Hyperthyroid ▪ Causes - Incr. F > 20, FHX, Tobacco ▪ Signs and Symptoms - Sxs of hyperthyroid exophthalmia, thyroid bruit, periorbital/ pretibial myxedema, diplopia - Goiter - Thyrotoxicosis tachycardia, HTN, delirium, N/V,D -- risk for? ▪ Testing - TSH, T3/4, Antibodies - Hormones that cause hyperglycemia (717-767, 804-834) o
- Antidiuretic Hormone (109, 696-699, 718-719) o Directly regulates water balance o Secreted when plasma osmolality increases or circulating blood volume decreases and blood pressure drops o Action is to increase permeability of renal tubular cells to water, increasing water reabsorption and promoting the restoration of plasma volume and blood pressure o Regulated by a feedback mechanism o Synthesized in hypothalamic neurons but stored and secreted by posterior pituitary o Major homeostatic function is the control of plasma osmolality as regulated by ADH o Effects may be inhibited by hypercalcemia, prostaglandin E, hypokalemia o Increase in ADH – stress, trauma, pain, exercise, nausea, nicotine, exposure to heat, drugs (morphine) o Decrease in ADH – decrease in plasma osmolality; increase in intravascular volume; hypertension; increase in estrogen, progesterone, angiotension II levels, alcohol ingestion o Causes disease of posterior pituitary – abnormal secretion of ADH o SIADH, DI - Diabetes Insipidus and associated labs (719-720) o Insufficient ADH ▪ Polyuria ▪ Polydipsia ▪ Hypernatremia o Neurogenic DI ▪ Tumors, aneurysms, thrombosis, infections, immunologic disorders o Nephrogenic ▪ Renal collecting tubules are insensitive to ADH o Dipsogenic ▪ Excessive fluid intake lowers plasma osmolality to the point it falls below the threshold for ADH secretion. o Dx: Distinguish from other polyuric states ▪ Urine Spec grav, Urine osmo, Na, Serum Osm, Serum ADH, water restriction o Tx: Desmopressin aka DDVAP o All forms are characterized by the inability of the kidney to decrease permeability to water. Causes excretion of large volumes of dilute urine and an increase in plasma osmolality. o Dehydration develops rapidly without ongoing fluid replacement. o Serum hypernatremia and hyperosmolality occur.
o Genetic ▪ First-degree relative (parent or sibling) o Environmental ▪ Viral, H.pylori, Cow’s Milk, Lack of Vit. D o Clinical manifestations ▪ Abnormal alpha and beta cell function ▪ Long preclinical period with gradual beta cell destruction, leading to insulin deficiency and hyperglycemia ▪ An 80% to 90% loss of function of the insulin-secreting beta cells in the islet of Langerhans occurs before hyperglycemia develops
- Polydipsia, Polyphagia, Polyuria, Weight loss, Fatigue **Neurology
- Fight or Flight syndrome** o Heart increases pumping action during stress or fear o Sympathetic nervous system ▪ Activates and releases norepinephrine o The adrenal medulla produces a hormonal cascade that results in the secretion of catecholamines, especially norepinephrine and epinephrine. The hormones estrogen, testosterone, and cortisol, as well as the neurotransmitters dopamine and serotonin, also affect how organisms react to stress.
- Arachnoid Villi (466) o Function as one way valves directing CSF outflow into the blood but preventing blood flow into the subarachnoid space o Villi protrude from the arachnoid space, through the dura mater, and lie within the blood flow of the venous sinuses ▪ CSF is reabsorbed by means of a pressure gradient between the arachnoid villi and the cerebral venous sinuses - Circle of Willis (467, 468f) o Intracranial Aneurysm – bifurcations in or near Circle of Willis o Also called arterial circle o Has ability to compensate for reduced blood flow from any one of its major contributors (collateral blood flow)
o Formed by the posterior cerebral arteries, posterior communicating arteries, internal carotid arteries, anterior cerebral arteries, and anterior communicating artery
- Cranial nerves functions and abnormalities associated with them (447-448, 469, 471f, 472t) o Cranial nerves are part of the peripheral nervous system (PNS) – project through the brain and pass through foramina in the skull o Cranial nerves + Function ▪ 1. Olfactory –purely sensory, carries impulses for sense of smell ▪ 2. Optic – purely sensory, carries impulses for vision ▪ 3. Oculomotor – Contains motor fibers to inferior oblique and to super, inferior, and medial rectus extraocular muscles that direct eyeballs; levator muscles of eyelid; smooth muscles of iris and ciliary body; and proprioception (sensory) to brain from extraocular muscles ▪ 4. Trochlear – Proprioceptor and motor fibers for superior oblique muscle of eye (extraocular) ▪ 5. Trigeminal – Both motor and sensory for face; conducts sensory impulses from mouth, nose, surface of eye, and dura mater; also contains motor fibers that stimulate chewing muscles ▪ 6. Abducens – contains motor fibers to lateral rectus muscle and proprioceptor fibers from the same muscle to brain ▪ 7. Facial – a) supplies motor fibers to muscles of facial expression and to lacrimal and salivary glands; b) carries sensory fibers from taste buds of anterior part of tongue ▪ 8. Vestibulocochlear (acoustic) – purely sensory; vestibular branch transmits impulses for sense of equilibrium; cochlear branch transmits impulses for sense of hearing ▪ 9. Glossopharyngeal – a) motor fibers serve pharynx (throat) and salivary glands; b) sensory fibers carry impulses from pharynx, posterior tongue (taste buds), and pressure receptors of carotid artery ▪ 10. Vagus – Fibers carry sensory and motor impulses for pharynx; a large part of this nerve is parasympathetic motor fibers, which supply smooth muscles of abdominal organs; receives sensory impulses from viscera ▪ 11. Spinal accessory – provides sensory and motor fibers for sternocleidomastoid and trapezius muscles and muscles of soft palate, pharynx, and larynx ▪ 12. Hypoglossal – carries motor fibers to muscles of tongue and sensory impulses from tongue to brain o Trigeminal Neuralgia ▪ Inflammation and demyelination of CN 5 - trigeminal ▪ Causes - MS, tumor, Structural, superior cerebellar artery
o Testing ▪ MRI – brain and spinal cord ▪ Lumbar puncture
- Myofascial pain syndrome (492-493, 1579t) o Associated with injury to muscle, fascia, and tendons and includes myositis, fibrositis, myofibrositis, and myalgia and muscle strain o Second most common pain syndrome o Pain results from muscle spasm, tenderness, and stiffness o Neuroaxonal degeneration with alterations in neuromuscular transmission may occur o Compression of the trigger points causes referred pain, motor dysfunction, and autonomic responses o During early stages pain is localized then becomes more deep and generalized ▪ Begins as a result of poor muscle tone, inactivity, muscle or tendon strain, or sudden vigorous exercise that can evolve into chronic pain state **Nephrology
- Prerenal injury (1360, 1385)** o Most common cause of acute kidney injury o Reduced effective blood volume causes renal hypoperfusion that occurs rapidly over a period of hours with elevation of BUN and plasma creatinine levels o GFR ultimately declines because of the decrease in filtration pressure ▪ Poor perfusion can result from renal artery thrombosis, hypotension related to hypovolemia or hemorrhage, renal vasoconstriction and alterations in renal regional blood flow, microthrombi, or kidney edema that restricts arterial blood flow o Possible causes: hypovolemia, hemorrhagic blood loss (trauma, GI bleed, complications of childbirth), loss of plasma volume (burns, peritonitis), water and electrolyte loss (severe vomiting or diarrhea, intestinal obstruction, uncontrolled DM, inappropriate use of diuretics), systemic hypotension or hypoperfusion, septic shock systemic inflammation, cardiac failure or shock, massive PE, stenosis or clamping of renal artery, increased intra-abdominal pressure (abdominal compartment syndrome) --- most common: dehydration, hemorrhage, sepsis - IgG nephropathies (glomerulonephritis) (1352-1358) o Associated with Nephritic Syndrome ▪ Rapidly progressive or crescentic glomerulonephritis
- Type 1: Formation of IgG antibodies against pulmonary capillary and glomerular basement membrane (Goodpasture
syndrome);
diagnosis
- BRCA1 and BRCA2 mutations (174, 831) o Associated with familial ovarian cancer o BRCA1 – chromosome 17; BRCA2 – chromosome 13 o Women who inherit a mutation experience a 50-80% lifetime risk of developing breast CA o BRCA1 mutations also increase risk for ovarian cancer (20-50%), also confer a modestly increased risk of prostate cancer and colon cancer o BRCA2 mutations confer an increased risk of ovarian cancer (10-20%); 6% of males who inherit BRCA2 will develop breast cancer o Most common cause of breast cancer - Cancer treatment symptoms (392, 395) o Box 12-2 page 396 o Fatigue is the most frequent reported symptom of cancer and cancer treatment r/t sleep disturbances, various biochemical changes o Leukopenia and thrombocytopenia r/t toxic chemotherapy drugs o Infection r/t being predisposed from advanced disease and chemotherapy causing immunosuppression o GI – decreased cell turnover leading to oral ulcers (stomatitis), malabsorption, diarrhea, disruption of flora o Hair and Skin – alopecia can result from chemo effects on hair follicles, skin breakdown and redness, and dryness - Human papillomavirus and cancer (382, 423-424) o Causes almost all cervical cancer, infects basal skin cells and commonly causes warts o HPV 16,18,31, 45 are associated with highest risk of developing cervical, penile, and anogenital cancer o Most HPV can be handled by the immune system and doesn’t cause cancer o When it does causes cancer, typically people are infected with HPV for a decade or longer and the viral DNA becomes integrated into the genomic DNA of the infected basal cell of the cervix and directs the persistent production of viral oncogenes o Detected by PAP o Cofactors: smoking, oral contraceptives, decreased immunity, multiple children, poor oral hygiene use, chronic inflammation o Once an HPV virus enters an epithelial cell, the virus begins to make proteins that can interfere with normal functions in the cell, enabling the cell to grow in an uncontrolled manner, and avoid apoptosis o Most common sexually transmitted disease in US
