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NU545 Patho Study Guide Unit 1
1. What is metabolic absorption? (p.2): • 1 of 8 cellular functions of eukaryote cell
- Chief function is to take in & use nutrients or other substances from surroundings
- Ex: kidney (fluid absorption and synthesize proteins) and Intestinal epithelial cells (fluid absorption/protein enzyme synthesis)
2. What uses oxygen to remove hydrogen atoms in an oxidative reaction? (p.8): •
Peroxisomes contain enzymes that use O2 to remove H+ in oxidative reactions that produces hydrogen peroxide which is then used by catalase to further oxidize other substances like: phenols, formic acid, formaldehyde, and alcohol
3. During cell injury what is released that is capable of cellular autodigestion? (p. 8): •
Lysosomal enzymes (hydrolases), or the digestive enzymes within the lysosome
- Autolysosomes, or autophagosomes
4. Where is the genetic info contained in the cell? (p. 2): Nucleus, specifically the
nucleolus
5. Cell membranes contain which major chemical components? (p. 12): Lipids &
Proteins in a complex lipid bilayer
6. What allows potassium to diffuse in and out of cells? (p. 31-32): • The Na+-K+-
ATP pump. Uses direct energy of ATP; found in excitable tissues (mus- cles/nerves) & also in kidneys & salivary glands. Involves the movement of Na+ & K+ against a concentration gradient.
- Protein enzyme ATPase allows potassium to move in and out of the cell.
- Mediated transport = channel protein through which ions can diffuse (K+ leak channel).
7. How is a cell protected from injury? (p.12): • Plasma membrane - Acts as a
barrier to toxic molecules, macromolecules, & foreign organisms/cells.
- Exists in a state of change & modulation. Alternates receptor numbers & patterns.
- Gating protects cells from release of Ca from injured cells by sealing off or decreasing permeability at junctional complexes.
8. In cirrhosis, what does cholesterol have to do with the erythrocytes? (p.68)-
: • Associated with chemical changes that result in structural & metabolic abnor- malities of the erythrocyte membrane leading to cell shape changes & hemolytic anemia.
- Increase in unesterified serum cholesterol owing to lecithin cholesterol acyl trans- ferase (LCAT) deficiency in cirrhosis leads to expansion of the lipid bilayer & macro- cytosis without megaloblastic changes in precursors. Substitutions of phosphatidyl choline (PC) moieties in the erythrocyte lipid bilayer lead to echinocytes (disaturated PC) or to stomatocytes (diunsaturated PC). In some patients, high density lipoprotein (HDL) abnormalities lead to erythrocyte surface changes causing rapid formation of echinocytes. (Ann Clin Lab Sci. 1990 May- Jun;20(3):169-74.Mechanisms of hemol- ysis in liver disease.Morse EE1. Department of Laboratory Medicine, University of Connecticut School of Medicine, Farmington 06032)
- Alters fluidity & function of cell membrane as well as intercellular transport
9. What is platelet-derived growth factor? (p.39): Stimulates production of con-
nective tissue cells & neuroglial cells
10. What is cell communication? How does it occur? (p.20): • Required for
homeostasis, regulate cellular growth/division & development/organization into tis- sues, & coordinate cellular function.
- Occurs in 3 ways: -via protein channels & gap junctions that directly coordinate activities of adjacent cells (must be touching) -via plasma membrane-based signaling molecules (receptors) that affect the
- Carrier returns to original shape, releasing 2 K+ ions & the leftover ATP molecule to inside of cell.
- Carrier can now repeat cycle.
14. What is active transport? (p. 31-33) ch.1: • The movement of a substance across
a membrane by a carrier protein. Requires metabolic energy (ATP) to move the molecules against the concentration gradient.
- Active transport also occurs by endocytosis (vesicle formation), where substances are engulfed by a segment of the plasma membrane, forming a vesicle that moves into the cell.
15. What are cytokines? (p.38-39)
Or cytokinesis? (p.37): • Cytokines are peptides that transmit signals within/be- tween cells to stimulate tissue growth & development.
16. Do all cells continue to replicate or divide? (p. 39): • No, all types of cells undergo
mitosis during formation of the embryo, but adult cells including: nerve cells, lens cells, & muscle cells, lose the ability to replicate.
- When a need arises for new cells, as in the repair of injured cells, previously non-dividing cells must be rapidly triggered to reenter the cell cycle.
- Neurons are fixed at birth & are unable to be replaced.
17. When normal columnar ciliated epithelial cells of the bronchial lining are replaced
by stratified squamous cells, the process is called? (p. 54): • Metaplasia: the reversible replacement of one mature cell by another, sometimes less differentiated cell type.
- However, lose protective ability, because new cells don't secrete mucus or have cilia.
- Bronchial metaplasia can be reversed if inducing stimulus is removed, such as cigarette smoking.
18. What is the relationship between ischemia and ATP? (p. 55-57): • When a hypoxic
injury occurs to myocardium, which causes an abrupt lack of contraction (caused by quick decline in mitochondrial phosphorylation), causing insufficient ATP production.
- Lack of ATP leads to increase in anaerobic metabolism, which generates ATP from glycogen when there is insufficient oxygen.
- When glycogen stores are depleted, even anaerobic metabolism ceases.
19. When does sodium enter the cell and cause swelling? (p. 57): • A reduction in ATP
levels cause the plasma membrane's Na-K pump & Na-Ca exchange to fail.
- Causes intracellular accumulation of Na & Ca & diffusion of K out of cell.
- Na & H2O enter cell freely, leading to cellular swelling.
20. What are free radicals in relation to cell damage? Progression of diseases? (p. 59-
61): Membrane damage is initiated by injury induced by free radicals, primar- ily by excess reactive oxygen species (ROS) called oxidated stress. Free radical is an electrically uncharged atom or group of atoms having an unpaired electron; thus causing the molecule to be unstable. To stabilize the molecule, it gives up an electron or steals one. This process is capable of injuries through chemical bond formation with proteins, lipids, & carbs. Free radicals aren't easily controlled & they initiate chain reactions. These reactive species are important in regard to cell injury by lipid peroxidation, alterations of proteins causing fragmentation of polypeptide chains, & alterations of DNA (breaking single strands). Diseases & disorders have been linked directly & indirectly to these reactive species.
21. Know all about lead poisoning. How does it cause damage within the cell? (p. 65-
67): • A heavy metal, primary hazard to children.
- Can cause learning disabilities, hyperactivity, & ADD
- Found in paint, soil, dust, debris from houses, baby formula mixed with lead contaminated water, newsprint, water that flows through lead pipes, hair dyes, gasoline, & tin cans or pottery made with lead based glaze.
stored in the mitochondria and endoplasmic reticulum and then pumped to extracellular space bound to calcium-binding proteins.
- Free calcium in the cytosol is caused by abnormal permeability of calcium-ion channels, direct damage to membranes, or depletion of ATP (i.e. hypoxic injury); therefore, causing uncontrolled enzyme activation causing further damage.
27. What happens to sodium and water during cell injury? (p.84): In hypoxia ATP
decreases, causing the Na/K pump & Na/Ca exchange to fail. Leading to increase of intracellular Na & Ca, & diffusion of K out of the cell; Na & water can then enter the cell freely causing swelling & dilation of the endoplasmic reticulum
28. During cell injury caused by hypoxia, what happens to osmotic pressure? (p. 30,
56, and 98): • Osmotic pressure is the amount of hydrostatic pressure required to oppose the osmotic movement of water. (P.30)
- In hypoxia you have an increase in Na in the cell and an out flow of K+ (P.56). Resulting in a deficit of Na in the ECF which decreases the ECF osmotic pressure and water is attracted to the ICF space (P.98)
29. What causes mammary glands to enlarge in pregnancy? (p. 53): • Hormonal
hyperplasia (stimulated by estrogen)
30. After ovulation what happens to uterine endometrial cells? (p. 53, 780): • Hormonal
hyperplasia occurs chiefly in estrogen dependent organs. After ovulation estrogen stimulates the endometrium to grow and thicken.
- After ovulation, then begins the secretory phase where glands in the endometrium secrete glycogen containing fluid, and if there is no ovum implantation, then we move to the ischemic phase where the endometrium sloughs off monthly (P.780) During menstruation the functional layer of the endometrium falls apart and sloughs.
31. What happens to liver cells when a portion of the liver is removed? (p.52)-
: Compensatory hyperplasia is an adaptive mechanism that allows some organs to regenerate in order to compensate for the loss. A protein, hepatocyte growth
factor (HGF) is thought to be a mediator in vitro of liver regeneration; however other growth factors and cytokines are involved.
32. Understand necrosis in relation to pulmonary TB and gangrene. (p.90-91): • TB
results in Caseous necrosis; a combination of coagulative & liquefactive necrosis -coagulative = results from protein denaturation, where protein albumin changes from gelatinous, transparent to firm, opaque like cooked egg whites -liquefactive = digestive juices eat their own hydrolases, & tissue liquefies, gets walled off from healthy tissue, & forms cysts
- Dead cells disintegrate but debris is not digested completely by hydrolases. Tissues appear soft & granular. A granulomatous inflammatory wall encloses areas of caseous necrosis.
- Gangrene is a term usually used to refer to death of tissue & results from severe hypoxic injury usually from arteriosclerosis. Hypoxia and bacterial invasion occurs.
- Dry gangrene is d/t coagulative necrosis & the skin is dry & shrinks w/color changes (black).
- Wet gangrene occurs when neutrophils invade the site & cause liquifactive necro- sis, usually in internal organs, causes site to be swollen, cold, & black. Foul odor is present produced by pus.
- Gas gangrene is caused by Clostridium that produces hydrolytic enzymes & toxins that destroy connective tissue, cellular membranes & causes gas bubbles to form in muscle cells. Can be fatal if enzymes lyse the membranes of the RBCs, resulting in shock.
33. Infants are susceptible to significant total body water loss, why? (p. 104): In
newborns, TBW is about 75%-85%, w/a decr to about 67% during first year. Infants are susceptible to significant changes in TBW because of their high metabolic rate & accelerated turnover of body fluids caused by greater BSA
sodium while urine sodium and urine osmolality are elevated.
42. During acidosis how does the body compensate for increased hydrogen ion?( Pg
123-126): • Protein buffering = H+ binds with hemoglobin & CO2. He- moglobin bound hydrogen becomes a weak acid. Venous blood (less saturated hemoglobin) = better buffer than arterial (saturated with O2).
- Renal buffering = distal tubule of the kidney secretes H+ into urine & reabsorbs HCO3.
- Ammonia (NH3) is lipid soluble and can cross the cell membrane. Ammonia binds with H+ to form ammonia ion (NH4) which is eliminated in the urine. The renal buffering of H+ requires the use of CO2 & H2O to form HCO3.
- Shifts in K+
- Bicarbonate Buffering-Carbonic Acid = in lung & kidneys. Carbonic acid is propor- tionate to PaCO
43. What is the significance of deep, rapid breathing in metabolic acidosis? (Pg 126):
- Lungs can decr carbonic acid by exhaling CO2 & leaving H2O.
44. What causes hyperkalemia? ( Pg 117-119 ): • Increased intake, a shift of K+
from ICF to ECF, or decrease renal excretion.
- Cell trauma or a change in cell membrane permeability, acidosis, insulin deficiency, cell hypoxia, burns, massive crushing injuries & extensive surgeries
- Acidosis & hyperkalemia often occur together r/t insulin promotes cellular entry of K+. Insulin deficits, such as DKA, are accompanied by hyperkalemia.
- Hypoxia diminishes the efficiency of the cell membrane
- Digitalis overdose inhibits the Na, K-ATP pump
- Potassium sparing diuretics may contribute to hyperkalemia.
- Renal failure & decrease in the secretion of aldosterone can decrease urinary excretion of K+
45. What causes hypermagnesemia? (pg. 121 table3-10): Usually caused by renal
failure or mag-containing antacids
46. What influences calcium and phosphate balances? (pgs. 119-122): • In- versely
proportional
(Na, K, H, Cl).
- Kidneys increase Na & HCO3 reabsorption & excrete H+. HCO3 is reabsorbed to maintain anionic balance since the Cl in the ECF is decreased. H+ moves to the intracellular space when K is depleted & is excreted to maintain electrochemical bal- ance. The urine is more acidic and the reabsorbed bicarbonate prevents correction of alkalosis.
50. What causes edema during inflammation? (p.107, 195): • Increases in capil- lary
permeability = proteins escape from plasma & produce edema through loss of capillary oncotic pressure & a gain in interstitial fluid proteins.
- Vasodilation
- Incr WBC accumulation
51. What is the purpose of inflammation?(p.191, 195-196): • Second line of
defense; occurs in response to tissue injury or infection; protects against further injury, prevents infection of injured tissue, & promotes healing
- Incr local blood flow; incr RBC's & leukocytes, & biochemical mediators
- kill, contain, dilute bacteria
- promote clotting & prevent extensive inflammation
52. What causes the erythema and induration during inflammation? (p. 195): •
Vasodilation - incr blood flow & RBCs at site = warmth & redness.
- Increased vascular permeability & leakage of fluid out of the vessels - biochemical mediators stimulate the endothelial cells lining the capillaries & venules to contract, creating spaces between cells which allows leukocytes & plasma to enter surround- ing tissue.
- White blood cell adherence to inner walls of vessels and migration to site of injury.
53. After prolonged antibiotic therapy, what bacterium grows in the intestine?
(p.194,1500): Clostridium difficile
54. When histamine is released from mast cells, what is the vascular effect?
(p.199,206): • Constriction of large vessel walls & dilation of post capillary venules
- results in increased blood flow into the microcirculation. (p.206)
- Increased capillary permeability and vasodilation(p.199)
55. Which leukocyte elevates when there is an early, acute inflammatory reac- tion?
(p.208): Neutrophils
56. What produces fever? (p.213): • Fever causing cytokines = endogenous py-
rogens; released by inflammatory cells after phagocytosis, exposure to bacterial endotoxin, or after exposure to antigen-antibody complexes.
- Exogenous pyrogens are pathogen-produced.
- Pyrogens act directly on the hypothalamus, which is the portion of the brain that directly controls temperature regulation
57. What is the process of repair after tissue damage? (p.215-218): • Healing begins
during acute inflammation. Resolution = return of tissue to its original struc- ture & function. Repair = replacement of destroyed tissue w/scar tissue.
- Repair begins w/phagocytosis of the particulate matter found at the site. Cleanup = debridement & involves dissolution of fibrin clots (scabs) by fibrinolytic enzymes. After debridement, the remaining debris is drained away & the vascular dilation & permeability associated w/inflammation are reversed to prepare for repair.
- Healing involves processes that: Fill in, Seal, & Shrink the wound. Primary intention are wounds that heal under conditions of minimal tissue loss, very little sealing (epithelialization) or shrinkage (contraction) is needed due to close apposition of the wound edges. Secondary intention is the healing of open wounds and requires a great deal more tissue replacement (fill in). Epithelialization, scar formation, and contraction take longer.
- Both resolution & repair occur in 2 phases:
- Reconstructive = begins 3-4 days after injury, & may last 2 wks. Injury occurs,
tion with production of many new infectious progeny. Some bacteria are intracellular pathogens and replicate in macrophages and other cells. Many extracellular bacteria form multi-cellular masses called biofilms, which provides an optimal environment for growth. (This was all I found in the book but online were answers like nutrients, oxygen, warmth, time, possibly moisture, and the correct pH)
60. How do bacteria become resistant to antibiotics? (p.310): • Antibiotic re-
sistance is usually a result of genetic mutations that can be transmitted directly to neighboring microorganisms by plasmid exchange. Microorganisms commonly develop the capacity to inactivate antibiotics.
- Other forms of resistance result from modification of the target molecule.
- A third mechanism of resistance is mediated by multidrug transporters in the
microorganism's membrane. These transporters affect the rate of intracellular ac- cumulation of the antimicrobial by preventing entrance or increasing active efflux of the antibiotic.
61. How would you clean a wound that is healing by epithelialization? (Chapter 6, p.216-
219): The ideal dressing is one that absorbs some drainage without being incorporated into the clot or granulation tissue and keeps the wound moist. Normal saline should be used to cleanse or irrigate wound as other solutions might be desiccating to the wound.
62. What is a keloid? (p.219): • A raised scar that extends beyond the original
boundaries of the wound. Caused by excessive production of collagen causing surface over healing. It invades surrounding tissue, commonly recurs after surgical removal, familial tendency common, more common in blacks than whites, do not regress over time.
63. Why do some neonates have a transient depressed inflammatory re- sponse?
(p.220): • Lack of phagocyte plasma membrane fluidity impairs pseudo- pod formation & migration resulting in neutrophils (& perhaps monocytes) being incapable of efficient chemoyaxis
- Neonates stressed by in utero infection or respiratory insufficiency - neutrophils have diminished oxidative & bacterial responses
- Partially deficient in complement (esp. components of the alternative pathway)
- Relative deficiency of factor B
- Low levels of mannose-binding lectin
- May be deficient in some of the collectins & collectin-like proteins
64. Adults? (p. 220) impaired inflammation & wound healing in older adults: - Can be
linked to chronic illness (cardiovascular disease, diabetes mellitus); Medica- tions (anti-inflammatory steroids interfere with healing process); Impaired sensation
receptors to reverse histamine's effects & cause muscle relaxation.
71. Graves Disease (p.277, 726-728): • An autoimmune disease resulting in stim-
ulation of the thyroid gland thus causing hyperthyroidism
- Generally consists of: Hyperthyroidism; Diffuse thyroid enlargement (goiter) due to increased iodide uptake and rate of metabolism; Ophthalmopathy (protrusion of the globe) double vision, irritation, pain, lacrimation, photophobia, & blurred vision; Dermopathy (shown as pretibial myexedema: subcutaneous swelling on anterior legs with indurated and erythema of skin)
- Genetic factors: major histocompatibility complex (MHC) genes associated with graves disease
- Pathology: Normal regularity mechanisms are overridden by abnormal immuno- logic mechanisms; T lymphocytes sensitized to antigens and B cells stimulated to produce IgG antibodies which bind to TSH receptors increasing release of TH; Au- toantibodies known as thyroid-stimulating immunoglobulin's (TSI) or thyroid receptor antibodies (TRAb)
- Therapy: Anti-thyroid drugs (proiouracil and methimaxole), radioactive iodine, surgery
72. Myasthenia Gravis: (p.277, 624-626): • Chronic autoimmune disease mediated by
acetylcholine receptor (AChR) antibodies that act at the neuromuscular junction with unknown etiology (although some persons may have genetic susceptibility)
- Characterized by exertional fatigue, weakness that worsens with activity, improves with rest, and reoccurs with activity
- Increases risk for other diseases such as SLE, RA, polymyositis, and thyroitoxicosis
- Subtypes of MG:
o AChR: Involves proximal musculature throughout body and has several courses
including...
- Course with periodic remissions
- Slowly progressive course
- Rapidly progressive course
- Fulminating course
- AChR further subdivided by...
- Young persons, mostly female, with thymic hyperplasis
- Older adults, both sexes, with normal or involuted thymus glands
- Persons of both sexes with thymomas
o Neonatal Myasthenia: Signs appear 1 to 3 days after birth and persist up to a
few weeks; Myasthenia immunoglobulin transferred through the placenta
o Ocular Myasthenia: Weakness of eye muscles and eyelids with swallowing diffi-
culties and slurred speech; More common in males
- Classifications by disease severity
o Grade I: Ocular disease
o Grade IIa: Generalized mild weakness
o Grade IIb: Moderate weakness
o Grade III: Severe generalized weakness
o Grade IV: Myasthenic crisis with respiratory failure
o Results from a defect in nerve impulse transmission at the junction
o Main defect is formation of autoantibodies against ACh binding site receptors
o Autoantibodies block AChR or cause loss of it
o Eventual receptor site destruction occurs causing reduced number of receptors,
diminished nerve impulse transmission, and incomplete/lack of muscle depolariza- tion
- Clinical manifestation of MG:
