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NSG | 533 |Adv |Pathophysiology |Exam | 1 |
questions |with |answers
What |are |the |five |components |of |pathophysiology? |- |CORRECT | ANSWERS |✔✔etiology pidemiology pathogenesis clinical |manifestations outcomes Etiology |- |CORRECT |ANSWERS |✔✔Causative |factor -simple -complex -idiopathic -iatrogenic Epidemiology |- |CORRECT |ANSWERS |✔✔Patterns |in |populations |of | people |and |their |characteristics -incidence -prevalence Incidence |- |CORRECT |ANSWERS |✔✔New
Prevalence |- |CORRECT |ANSWERS |✔✔Existing |and |new; |total Pathogenesis |- |CORRECT |ANSWERS |✔✔Sequence |of |events |from | stimulus |of |disease |and |manifestations Clinical |manifestations |- |CORRECT |ANSWERS |✔✔Signs | (assessment, |definitive) Symptoms |(experienced |by |pt, |subjective) Outcomes |- |CORRECT |ANSWERS |✔✔Cure, |remission, |chronicity, | or |death -not |specifically |treatment Primary |prevention |- |CORRECT |ANSWERS |✔✔Preventing |initial | occurrence Secondary |prevention |- |CORRECT |ANSWERS |✔✔Detection |and | screening Tertiary |prevention |- |CORRECT |ANSWERS |✔✔Treating |or |reducing | relapse/disability/chronicity What |are |the | 4 |common |mechanisms |of |cell |injury |and |death? |- | CORRECT |ANSWERS |✔✔1. |ATP |depletion
- |O2 |and |oxygen-derived |free |radicals
Pyknosis |- |CORRECT |ANSWERS |✔✔Clumping |of |nuclear |material | as |a |result |of |a |drop |in |pH Karyorrhexis |- |CORRECT |ANSWERS |✔✔Fragmentation |of |nuclear | material Karyolysis |- |CORRECT |ANSWERS |✔✔Dissolution |of |nuclear | material What |are |free |radicals? |- |CORRECT |ANSWERS |✔✔Unstable | compounds |with |an |unpaired |electron |and |high |affinity |for |lipids, | normal |byproduct |of |cellular |metabolism What |is |lipid |peroxidation? |- |CORRECT |ANSWERS |✔✔Binding |of | free |radicals |to |phospholipid |bilayer |membrane |around |the |cell | and |its |organelles |causing |dissolution |or |a |hole What |are |reactive |oxygen |species |(ROS) |- |CORRECT |ANSWERS | ✔✔Chemically |reactive |molecules |formed |as |natural |oxidant | species |in |cells |during |mitochondrial |respiration |and |energy | generation How |does |the |body |handle |free |radicals |and |ROS |to |prevent | tissue |injury |- |CORRECT |ANSWERS |✔✔Antioxidants |remove problems |occur |when |free |radicals |are |produced |in |amounts |that | overwhelm |antioxidants
How |can |membrane |permeability |defect? |- |CORRECT |ANSWERS | ✔✔Inherited |/ |genetic acquired |/ |exposure |to |mutagenic |or |carcinogenic |environmental | factors lysis |by |enzymes, |virus, |or |direct |injury |from |stressors What |is |bilirubin? |- |CORRECT |ANSWERS |✔✔Pigment |released | when |RBC's |breakdown What |is |unconjugated |bilirubin? |- |CORRECT |ANSWERS |✔✔Type |of | bilirubin |that |is |fat-soluble |and |can't |be |excreted What |is |conjugated |bilirubin? |- |CORRECT |ANSWERS |✔✔Type |of | bilirubin |that |is |water-soluble |and |able |to |be |excreted What |is |the |role |of |glucuronic |acid |in |bilirubin |metabolism? |- | CORRECT |ANSWERS |✔✔It |is |required |from |liver |cells |to |convert | unconjugated |bilirubin |to |conjugated |bilirubin What |is |hemolytic |hyperbilirubinemia? |- |CORRECT |ANSWERS | ✔✔Excessive |hemoglobin |breakdown |that |the |liver |can't |keep |up | with
-protein |kinases -phospholipidases -proteases | -endonuclease Liquefactive |necrosis |- |CORRECT |ANSWERS |✔✔Brain |tissue ischemic |injury |to |neurons |and |glial |cells brain |liquefies, |walled |off |from |healthy |tissue, |and |forms |cysts Coagulative |necrosis |- |CORRECT |ANSWERS |✔✔Kidneys, |heart, | adrenal |glands caused |by |hypoxia/ischemia |due |to |chemical |injury protein |denaturation |—> |gelatinous Caseous |necrosis |- |CORRECT |ANSWERS |✔✔Combination |of | coagulative |and |liquefactive commonly |tuberculosis dead |cells |disintegrate |but |debris |not |fully |digested; |resembles | cheese
Fat |necrosis |- |CORRECT |ANSWERS |✔✔Breast, |pancreas, |other | abd |structures lipases |break |down |triglycerides |releasing |fatty |acids |creating | opaque/chalk |white |"soaps" What |is |gangrenous |necrosis? |- |CORRECT |ANSWERS |✔✔Death |of | tissues |from |severe |hypoxic |injury What |are |the |characteristics |of |dry |gangrenous |necrosis? |- | CORRECT |ANSWERS |✔✔Result |of |coagulative |necrosis; |No | infection; |Clear |demarcation |of |live |and |dead |tissue; |Dry |and | shrunken, |mummified What |are |the |characteristics |of |wet |gangrenous |necrosis? |- | CORRECT |ANSWERS |✔✔Result |of |liquefactive |necrosis; |Infection | present |with |exudate, |malodor, |inflammation; |Unclear | demarcation |between |live |and |dead |tissue What |is |gas |gangrene? |- |CORRECT |ANSWERS |✔✔Caused |by | clostridium |and |creates |crepitus Necrosis |- |CORRECT |ANSWERS |✔✔-Pathologic -Nasty, |violent, |disorganized |sequence | -Stimulates |inflammatory |process -initiated |by |ischemia/toxins/physical |stimuli
Hypertrophy |- |CORRECT |ANSWERS |✔✔Increased |cell |and | functional |component |size |due |to |increased |work |demands Hyperplasia |- |CORRECT |ANSWERS |✔✔Increased |number |of |cells | due |to |increased |work |demands Metaplasia |- |CORRECT |ANSWERS |✔✔Substitution |of |one |normal | cell |type |with |another |not |normally |found |in |that |tissue -replacements |are |better |able |to |survive |vs |original Dysplasia |- |CORRECT |ANSWERS |✔✔Abnormal |cell |growth |and | differentiation |(variable |size, |shape, |appearance) |within |specific | tissue -precursor |to |cancer What |is |aging? |- |CORRECT |ANSWERS |✔✔Decrease |in |functional | reserve |and |reduced |ability |to |adapt |to |environmental |demands How |does |DNA |and |metabolic |damage |contribute |to |aging? |- | CORRECT |ANSWERS |✔✔DNA |repair |mechanisms |are |faulty Metabolic |(free |radical) |damage |is |excessive | Decreased |antioxidants
What |are |some |origins |of |aging? |- |CORRECT |ANSWERS | ✔✔Genetic, |epigenetic, |inflammatory, |oxidative, |stress, |metabolic |origins Frailty |- |CORRECT |ANSWERS |✔✔Someone |vulnerable |to |falls, | functional |decline, |disability, |disease, |death involves |oxidative |stress, |inflammation, |malnutrition, |physical | inactivity, |muscle |changes How |does |acidosis |effect |potassium? |- |CORRECT |ANSWERS | ✔✔Excess |H+ |in |blood |shift |into |cell K+ |moves |out |of |cell |to |balance |ionic |concentration Hyperkalemia |develops How |does |alkalosis |effect |potassium? |- |CORRECT |ANSWERS | ✔✔H+ |moves |into |bloodstream |to |balance | excess |bicarbonate/lack |of |acid K+ |moves |into |cell |to |balance |ionic |concentration Hypokalemia |develops
Calculation |of |water |deficit |- |CORRECT |ANSWERS |✔✔Liters |of | water |to |be |given |= |Ideal |total |body |water |- |current |total |body | water Calculation |of |ideal |total |body |water |in |water |deficit |- |CORRECT | ANSWERS |✔✔(Current |Na |X |TBW) |/ | 140 Calculation |of |current |total |body |water |in |water |deficit |- |CORRECT |ANSWERS |✔✔Weight |(kg) |X |___ 0.4 |for |women 0.5 |for |men 0.6 |for |infants Calculation |of |water |excess |- |CORRECT |ANSWERS |✔✔Liters |of | water |to |be |removed |= |Current |total |body |water |X |Ideal |total | body |water Calculation |of |current |total |body |water |in |water |excess |- | CORRECT |ANSWERS |✔✔Weight |(kg) |X |__ 0.5 |for |women 0.6 |for |men 0.7 |for |infants Calculation |of |ideal |total |body |water |in |water |excess |- |CORRECT | ANSWERS |✔✔ 1 |- |(Na/125)
Hyponatremia |- |CORRECT |ANSWERS |✔✔< Normally |hypotonic, but |normal |tonicity |(pseudohyponatremia) |and |hyperosmolality | exist | Therefore, |may |need |to |calculate |adjusted |sodium |levels Pseudohyponatremia |- |CORRECT |ANSWERS |✔✔Low |serum |Na, | serum |osmolality/tonicity |normal |or |elevated Calculation |for |corrected |sodium |in |hyperglycemia |- |CORRECT | ANSWERS |✔✔1.6 |mEq/L |X |((current |glucose |- |100) |/ |100) |= |X Current |sodium |+ |X |= |corrected |sodium Calculation |for |serum |osmolality |- |CORRECT |ANSWERS |✔✔OSM | = | 2 |X |[sodium |concentration] |+ |[glucose |concentration/18] |+ | [BUN/2.8] Osmolality |vs |Tonicity |- |CORRECT |ANSWERS |✔✔Osmolality: | determined |by |total |solute |concentration |in |a |fluid |compartment Tonicity: |refers |to |the |ability |of |the |combined |effect |of |all |solutes | to |generate |an |osmotic |driving |force |that |causes |water | movement
Pitting |edema |- |CORRECT |ANSWERS |✔✔Edema |fluid |contains |few | protein -increased |capillary |hydrostatic |pressure -decreased |capillary |oncotic |pressure Non |pitting |edema |- |CORRECT |ANSWERS |✔✔Edema |fluid | contains |a |lot |of |protein -increased |cap |permeability -lymphatic |obstruction Normal |bicarbonate |- |CORRECT |ANSWERS |✔✔22- Metabolic |acidosis |- |CORRECT |ANSWERS |✔✔pH<7.35 |and | bicarbonate< -loss |of |bicarbonate -increase |of |metabolic/nonvolatile |acids | -decrease |in |acid |excretion characterized |by |normal |anion |gap |or |elevated |anion |gap Anion |gap |- |CORRECT |ANSWERS |✔✔Difference |between |total | cations |in |ECF |and |total |anions |in |ECF
Normal: |10- Anion |gap |= |Na |- |(Cl+HCO3) Metabolic |acidosis |with |elevated |anion |gap |- |CORRECT |ANSWERS | ✔✔Abnormal |numbers |and |types |of |anions, |due | to |retention/addition |of |acid -deranged |metabolism |(DKA, |LA) -exogenous |ingestions Metabolic |acid |with |normal |anion |gap |- |CORRECT |ANSWERS | ✔✔Cause |of |metabolic |acid |is |due |to |loss |of |bicarbonate When |bicarbonate |is |lost, |chloride |is |reabsorbed |keeping |gap | normal therefore, |also |called |"hyperchloremic |metabolic |acid" What |is |Renal |Tubular |Acidosis |(RTA)? |- |CORRECT |ANSWERS | ✔✔Renal |cause |of |metabolic |acidosis What |is |the |characteristic |of |Type | 1 |Distal |RTA? |- |CORRECT | ANSWERS |✔✔Decrease |in |distal |nephron |to |produce |new | bicarbonate, |resulting |in |hypokalemia
PLUMSEEDS |- |CORRECT |ANSWERS |✔✔Mnemonic |for |causes |of | elevated |anion |gap |metabolic |acidosis Paraldehyde Lactic |acidosis Uremia Methanol Salicylates Ethanol Ethylene |glycol DKA Starvation Why |is |acidosis |associated |with |hypercalcemia? |- |CORRECT | ANSWERS |✔✔Increases |the |fraction |of |ionized |calcium |and | promotes |the |effects |of |calcium |onto |cells |(bad) Metabolic |alkalosis |- |CORRECT |ANSWERS |✔✔pH>7.45, | bicarbonate |>
- |Addition |of |bicarb
- |Contraction |alkalosis |(hypochloremic)
- |Loss |of |H+ |(mineralocorticoid |like |aldosterone |or |Cushing's) Saline |responsive |vs |saline |resistant |metabolic |alkalosis |- | CORRECT |ANSWERS |✔✔Saline |responsive/sensitive: |associated |
with |hypovolemia |and |corrected |once |ECF |is |expanded |with |NaCl | and |K+ Saline |resistant: |associated |with |excessive |mineralocorticoids | (aldosterone) What |is |the |percentage |of |prerenal |kidney |failure? |- |CORRECT | ANSWERS |✔✔60-70% What |causes |prerenal |kidney |failure? |- |CORRECT |ANSWERS | ✔✔hypotension/shock |leading |to |poor |renal |blood |flow What |are |types |of |damage |that |can |lead |to |prerenal |kidney | failure? |- |CORRECT |ANSWERS |✔✔CV |dysfunction |(MI, |HF), | vasodilation, |hypovolemia/hemorrhage, |vascular |resistance | (surgery), |abdominal |compartment |syndrome, |PE What |is |the |percentage |of |Intrarenal |/ |Intrinsic |kidney |failure? |- | CORRECT |ANSWERS |✔✔25-40% What |causes |of |Intrarenal |/ |Intrinsic |kidney |failure? |- |CORRECT | ANSWERS |✔✔Direct |kidney |damage |from |inflammation/infection, | toxins/drugs, |reduced |blood |supply What |are |the |types |of |damage |that |can |lead |to |Intrarenal |/ | Intrinsic |kidney |failure? |- |CORRECT |ANSWERS |✔✔Glomerular | inflammation, |vascular |(stenosis, |thrombosis), |tubular |(ATN, | drugs, |ischemia), |interstitial |(infection, |drugs)
