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NURS 5315 Advanced Patho Exam 1 Study Guide
1. Steps of the Action Potential: Depolarization
Repolarization Hyperpolarization
2. Depolarization: movement of the intracellular charge towards zero (more positive charge)
Voltage gated Na channels open and allow Na to enter the cell -> voltage inside the cell moves towards zero
3. Repolarization: Once the intracellular charge reaches zero, the negative polarity of the inside
of the cell is restored back to its baseline of -70 to -85 mV -Na channels close, K channels open
4. Hyperpolarization: when the cell's resting membrane potential is greater than
-85mV. Is less excitable, because there is a greater distance between the resting membrane potential and the threshold potential.
5. In order for the action potential to be sucessful: t has to depolarize by 15-20 mV (threshold
potential) to reach -55 to -65 mV.
6. An alteration in action potential may result from: neurologic diseases, muscle disease or
electrolyte imbalances.
7. What is the main protein responsible for maintaining the correct balance of extracellular Na and
intracellular K, which is needed for cellular excitation and membrane conductivity.: Na+-K+ ATPase
8. Resting membrane potential: when the cell is in a nonexcited state and is at -70 to -85 mV.
9. Refractory Period: is a period of time during most of the action potential which the cell
membrane resists stimulation and it cannot depolarize
10. Absolute refractory period: occurs when the membrane will not respond to ANY stimulus
no matter how strong.
11. Relative Refractory Period: occurs when the membrane is repolarizing and will only respond
to a very strong stimulus.
12. Hyperpolarized: when the cell's resting membrane potential is greater than
-85mV. Is less excitable, because there is a greater distance between the resting membrane potential and the threshold potential.
13. Hypopolarized: when the cell's resting membrane potential is closer to zero, for instance it is
-65mV. Is more excitable because the resting membrane potential is closer to the threshold potential, there is less distance between them.
14. Action potential altered by hypokalemia: (serum outside of cell is low)
-Hyperpolarized (cell becomes more negative, ex: -100) -Affects the resting membrane potential of cells -The cell is less likely to depolarize and transmit impulses Can cause a decrease in neuromuscular excitability and leads to weakness, smooth muscle atony, paresthesias, and cardiac dysrhythmias
15. Action potential altered by hyperkalemia: Hypopolarized
-Also has an effect on the resting membrane potential -If the ECF potassium increases without any change in the ICF potassium levels, the resting membrane potential of the cell becomes more positive. -The cells are more excitable and conduct impulses more easily and more quickly because the resting membrane potential is closer to the threshold potential. There- fore, the person will have peak T waves on EKG. -As potassium rises, the resting membrane potential will continue to become more positive and it will eventually become equal to the threshold potential. As this happens the EKG will show a widening QRS complex. If the resting membrane potential equals the threshold potential, an action potential will not be generated and cardiac standstill will occur. Paralysis and paresthesias may also occur.
16. Action potential altered by hypocalcemia: -Causes an increase in the cell permeability to
Na causing a progressive depolarization -Causes the RMP and the TP to be closer to one another & making it easier to initiate an action potential - the cells are more excitable. -Results in tetany, hyperreflexia, circumoral paresthesias, seizures, dysrhythmias
-Ex: most common is the change from columnar cells to squamous cells - this occurs in chronic smokers or gastroesophageal reflux (GERD)
24. Physiologic Example of Hyperplasia: -Occurs when there is an increase in tissue mass after
damage or partial resection, allowing the organ to regenerate Ex - removal of part of the liver and the cells regenerating, uterine and mammary gland enlargement occur during pregnancy to meet the demands of the increased work load, callus on foot Ex: (Hormonal) Breast and uterine enlargement during pregnancy.
25. Pathological Example of Hyperplasia: -Is an abnormal proliferation of normal cells usually
caused by increased hormonal stimulation Ex - endometrial hyperplasia (imbalnce in estrogen & progesterone with increase in estrogen - risk for cancer), Benign prostatic hyperplasia (BPH), thyroid enlargement
26. Pathological Example of Hypertrophy: left ventricular hypertrophy cardiomegaly
27. Physiological Example of Hypertrophy: Skeletal muscle, when a kidney is removed and the
other kidney steps in to function as both and increases in size
28. Physiological Example of Atrophy: Shrinking of the thymus gland during childhood,
uterus decreasing in size after childbirth Disuse - skeletal muscle atrophy that occurs from a person being immobilized or bed ridden for a period of time (arm in a cast,
29. Pathological Example of Atrophy: Decrease in workload, pressure, use, blood supply, nutrition,
hormonal stimulation, or nervous stimulation
30. Cellular Injury: -Occurs when the cell is no longer able to maintain homeostasis with the
result being disease. May or may not be reversible. This is dependent on the type of cell, level of differentiation, ability to adapt and the type, severity and duration of the injury.
31. Causes of cellular injury: hypoxia, free radicals, chemicals, radiation, direct mechanical
trauma, genetics, nutrition, infections, immunologic reactions and in- flammation.
32. Mechanisms of Cellular Injury: -ATP Depletion
-Oxygen and Oxygen derived free radicals -Intracellular Calcium and loss of calcium steady state
33. Cellular Injury (partially ischemia) triggers an increase in: Iintracellular cal- cium
-The more damage which is done, the higher the calcium concentration becomes. The elevated calcium level causes damage to the cell membrane. It also causes damage to the intracellular contents by activating enzymes which cause the damage directly.
34. ATP Depletion: results from the loss of mitochondrial production of ATP.
This contributes to cellular swelling, decreased protein synthesis, and impairs cel- lular membrane transport systems. All of these changes impair cellular membrane integrity.
35. Oxygen and Oxygen derived free radicals: decrease oxygen delivery to cells results in the
production of activated oxygen species (free radicals, H2O2, NO) which destroy the cell membranes and structures.
36. Most common cause of cellular injury: Hypoxic Injury
37. Clinical Manifestations of Hypoxic Injury: Reduced ischemia, loss of hemo- globin, diseases,
etc. Heart attack, etc
38. Pathophysiology of Hypoxic Injury: Ischemia - “ mitochondrial oxygenation, “ATP, Na-K & Na-
Ca pumps fail -> ‘ intracellular Na & Ca -> K to diffuse out of cell -> acute cellular swelling (from ‘ Na in cell), anaerobic glycolysis, ‘Lactate, necrosis
39. Reperfusion Injury: Reoxygenation, Tissue transplantation, ischemic syn- dromes of
heart, liver, GI, kidneys, and cerebrum.
40. Clinical Manifestations of Reperfusion Injury: Neutrophils especially affect- ed, causing
neutrophil adhesion to endothelium Serious complication in transplantation and ischemic diseases
41. Patho of Reperfusion Injury: -Triggers the production of highly reactive oxygen intermediates
(hydroxyl radical & hydrogen peroxide -> cell membrane damage & mitochondrial Ca overload). -WBC function is impaired as result of injury. * Xanthine dehydrogenase -> converts to xanthine oxidate -> creates massive amounts of free radicals, superoxide & hydrogen peroxide -> etc... apoptosis
be pathologic after some forms of cell injury, especially DNA damage
47. Autophagy: "eating of self" self-destructive process & survival mechanism
-When cells are starved/nutrient deprived, autophagic process institutes cannibal- izations & recycles digested contents. Maintains cellular metabolism under starvation conditions, remove damaged or- ganelles & misfolded proteins under stress conditions, improves survival of cells During times of metabolic stress, autophagy provides ATP & other macromolecules for energy and cell survival, however as the stress progresses autophagic cell death will occur. When cells lack nutrition, autophagy is triggered. If stress is excessive, autophagic programmed cell death Can suppress & facilitate tumor development Process decelerates
48. Body changes occur with aging: -Thymus atrophy, loss of ova in women, decreased
spermatogenesis, decreased gastric emptying -Muscle atrophy/sarcopenia, “height, neck, high, & arm circumference -Weight gain occurs up until age 50 in men & 70 in women -Central fat accumulation increases ‘ the risk for insulin resistance & heart disease
49. Cellular aging results in: telomere erosion, DNA damage, epigenetic stress, ROS
accumulation, and endoplasmic reticular stress.
50. Extracellular changes associated with aging: binding of collagen, ‘ free rad- ical damage,
structural changes of fascia, tendons, ligaments, bones, joints, & development of arteriosclerosis. The extracellular matrix is affected by decreased synthesis and increased degradation of collagen. These changes result in dehydra- tion and wrinkling of the skin.
51. What are the labs that are elevated as we age and are markers of increased risk for morbidity and
mortality: Interleukin 6, Interleukin 1, tumor necrosis factor -alpha and C-reactive protein
52. Frailty: is a condition of vulnerability and debility which occurs after one has experienced
a health stressor and has not recovered from it completely
53. ETOH in blood metabolizes to: Acetaldehyde in cytoplasm of cell -> Pyruvate to be changed
to LA, Oxaloacetate -> malate, this prevents gluconeogenesis -> fasting hypoglycemia. Also Glyceraldehyde-3-phosphate -> glycerol 3- phosphate combines with fatty acides to form triglycerides -> hepatosteatosis. Also “ citric acid cycle production of NADH -> utilization of
Acetyl-CoA for ketogenesis -> ketoacidosis & lipogenesis -> hepatosteatosis
54. Hepatic Changes in ETOH: (inflammation, deposition of fat, enlargement of liver, interruption
of microtubular transport of proteins & their secretions, ‘ intracellular water, “ fatty acid oxidation in mitochondria, ‘ membrane rigidity, development of liver necrosis.
55. Ketogenesis: is the formation of ketone bodies and occurs mostly in the mito- chondria of
the hepatocytes. Occurs as a result of the unavailability of glucose.
56. Role of the Hepatocytes in Ketogenesis: The major parenchymal cells in the liver:
metabolism, detoxification, and protein synthesis
57. Role of the mitochondria in ketogenesis: Membrane-bound cell organelles (mitochondrion,
singular) that generate most of the chemical energy needed to pow- er the cell's biochemical reactions. Chemical energy produced by the mitochondria is stored in a small molecule called adenosine triphosphate (ATP)
58. Triggers for ketogenesis: starvation, lack of glucose
59. Effect on oxaloacetate in ketogenesis: -Is used in gluconeogenesis. During starvation &
uncontrolled diabetes, these levels are insufficient bc it is completely used by gluconeogenesis- The depletion of increases the amount of acetyl-CoA -> acetyl-CoA is processed by hepatocytes -> undergoes transformation to 3 ketone bodies: acetoacetate, acetone, ²-hydroxybutyrate = basis for ketoacidosis
60. Tumor Markers: are substances produced by the cancer cells that are found on tumor
plasma membranes or in the blood, spinal fluid, or urine. An elevated tumor marker may suggest a specific diagnosis, but it is not used alone as a definitive diagnosis test.
61. Alpha Fetoprotein (AFP) tumor marker can be found in: liver or germ cell cancers
62. Carcinoembryonic Antigen (CEA) tumor marker can be found in: GI, Pan- creatic, Lung, and
Breast cancers
63. Beta Human Chorionic Gonadotropin (Beta HCG) tumor marker can be found in: germ cell
cancers or choriocarcinoma
64. Prostate Specific Antigen (PSA) tumor marker can be found in: prostate cancer
of the cancer cells
84. Epithelial mesenchymal transition (EMT): process by which a cancer cells changes to one
which can metastasize
85. IL-8: is a potent stimulus for cancer cells to undergo EMT
86. TNM: Tumor spread
Node Involvement Presence of Distant Metastasis
87. Autocrine stimulation: Oncogenes provide a cancer cell with the ability to secrete
growth factors that stimulate their own growth which is known as
88. Genetic Events that activate oncogenes: point mutations, translocations, gene
amplification
89. Oncogenes: -Proto-oncogenes produce proteins that regulate cellular prolifer- ation
-These are proto-oncogenes that have mutated -Cancer cells contain these
90. Tumor Suppressor Genes: -inactivation contributes to the unregulated growth and
proliferation of cancer cells -Stop cell division in damaged cells & prevent mutations
91. Known as anti-oncogenes: Tumor Suppressor Genes
*2 of these genes in each cell must be turned off by the cancer to halt their effects
92. P53 Tumor Suppressor Gene: -monitors cellular stress and activating caretak- er genes,
maintain integrity of the genome. -Produces proteins that repair damaged or mutated DNA. Controls initiation of cellular senescence (stop cell division), apoptosis, and suppresses cell division until DNA is repaired
93. BRCA gown increases the risk of: ovarian, breast, and prostate cancer
94. BRCA gene in men increases risk of: prostate, melanoma, colon, pancreatic, breast cancer
95. Paraneoplastic Syndromes: -Are a constellation of symptoms which are ignit- ed by cancer
but are not caused by direct local effects of tumor mass -Typically triggered by the release of substances from a tumor
96. These patients have an increase in apoptosis and impaired ability to regenerate cells:
Cachexia
97. Is a catabolic process and results in a wasting syndrome: Cachexia
98. S/S of Cachexia: -Loss of appetite, cardiac atrophy and dysfunction, gut barrier dysfunction,
the release of proinflammatory mediators, release of acute thermoge- nesis, weight loss and muscle wasting
99. Na is important in maintaining: -Neuromuscular Nerve Impulse Conduction
-Acid Base Balance -Cellular Chemical Processes -Cell Membrane Transport Systems
100. Sodium is regulated by: ADH, RAAS, Kidneys
101. This type of syndrome is most commonly found in the GI tract or lungs-
: paraneoplastic syndromes
102. What is responsible for shifting potassium intracellularly: Insulin
103. What shifts potassium extracellularly: -Insulin Deficiency
-Aldosterone Deficiency -Acidosis -Strenuous Exercise
104. Alpha adrenergic antagonists will cause K to shift: into the cell
105. Beta 2 antagonist (Beta Blockers) causes K to shift: extracellularly
106. Intracellular: All fluids contained inside the cells by their plasma membrane.
Consists of cytosol and fluid in cell nucleus.
107. Interstitial fluid: Extracellular space
Tissue space that surrounds cells in body Contains 20% of body water
108. Intravascular: Blood. Mixture of blood cells, colloids and solutes (glucose and ions). It's
the fluid inside blood cells and blood plasma. Contains 20% of body water
109. What happens to the BP when fluid moves out of the intravascular com- partment: BP
121. renin-angiotensin-aldosterone system (RAAS): Activated by low blood vol- ume (BV) ->
Triggers release of renin -> Renin converts angiotensinogen (plasma protein) to angiotensin I -> ACE convert angiotensin I to angiotensin II -> Angiotensin II causes arterial VC -> release of aldosterone -> stimulates renal Na reabsorption and K excretion. Water is retained with the Na -
Patient produces less urine and BV ‘.
122. Natriuretic Hormone: Hormones released from the atria or ventricles of the heart
-Work opposite of RAAS to “ BV -Promote urinary excretion of Na and water -> “ BV -Ex: ANP and BNP
123. Urea: is a solute that freely diffuses through cell membranes but has NO effect on
osmolality!
124. Isotonic: Has the same osmolality or concentration of particles as the ICF and ECF
Ex: NS, D5W
125. Hypotonic: Will cause intravascular space to become more dilute =“ solute
concentration -> “ osmolality Water will move from intravascular space to extracellular space -> dilution of extra- cellular space -> water will move to intracellular space -> cell will swell. Ex: water
126. Hypertonic: Will ‘ solute concentration in the intravascular space =‘ osmolality Water
will flow into intravascular space from extracellular space -> extracellular space will have more solutes -> water to move from intracellular space to extracel- lular space -> cell will shrink. Ex: 3% saline
127. Diffusion: Movement of solute molecule from an area of great solute concen- tration
to an area of lesser solute concentration
128. Mechanisms to maintain acid-base balance: -Physiologic (chemical) buffer systems
(plasma carbonate, phosphate, hemoglobin, and protein) - 1st line of defense -Respiratory acid-base control - 2nd line of defense -Renal acid-base control - 3rd line of defense
129. Chemical Buffer System: Bicarbonate
Phosphate Plasma Proteins Hemoglobin
130. Metabolic Acids: Carbonic Acid
Lactic Acid
143. A positive base excess represents: metabolic alkalosis or compensation for respiratory
acidosis
144. A-a Gradient: -Measures the differences between the alveolar (A) to arterial
(a) O2. -It is a calculated value which indicates the difference between alveolar and arterial O2 content.
145. An elevated A-a gradient can happen in such diseases such as: pulmonary edema,
pulmonary fibrosis, and ARDS.
146. Roles of the kidney in maintenance of acid base balance: Reabsorption of Bicarbonate
Renal Excretion of Hydrogen Excretion of Hydrogen as Ammonium
147. What inhibits HCO3 reabsorption: Acetazolamide (carbonic anhydrase in- hibitor):
blocks the action of carbonic anhydrase
148. Order of RAAS: -release of renin
-renin -> angiotensin -angiotensin -> angiotensin 1 -ACCE converts angiotensin1-> angiotensin II -> causes art VC -> release of aldosterone -> stimulates renal Na reabsorption and K excretion
149. Works opposite of RAAS to decrease blood volume: ANP and BNP Natriuretic
Hormones -promote urinary excretion of Na and water
150. may be used interchangeably with osmolality: tonicity
151. What causes an increase in hydrostatic pressure: venous obstruction or retention of
Na & water
152. what causes a decrease in oncotic pressure and osmotic pressure: de- creased plasma
protein production
153. ECF overload manifestations: HCO3 reabsorption inhibited in proximal tubule
154. ECF deficit manifestations: increase HCO3 absorption
stimulates RAAS
155. Reabsorption of bicarbonate occurs with: loop or thiazide diuretics volume
replacement with NaCl
156. Renal excretion of H+ ions occurs mostly in: distal tubule & collecting ducts
157. What assists with renal excretion of H+ ions: inorganic phosphates
158. Where does excretion of hydrogen as ammonium occur: proximal tubule, loop of henle,
and distal tubules (proximal tubule cells produce NH4+)
159. What blocks the actions of carbonic anhydrase to inhibit HCO3 reabsorp- tion:
Acetazolamide
160. High Anion Gap metabolic acidosis is likely caused by: lactic acidosis ketoacidosis
acute or chronic renal failure
161. Normal anion gap metabolic acidosis is likely caused by: GI losses from diarrhea
large volumes of saline admin medications such as NSAIDS, ace inhibitors, trimethoprim
162. Clinical Manifestations of Metabolic Acidosis: Headache and lethargy, which
progresses to confusion and coma in severe, Kussmauls respirations (form of hyperventilation that are deep and rapid), anorexia, N/V, diarrhea, abd discomfort
163. Pathological Consequences of Metabolic Acidosis: decreased myocardial contractility,
decreased CO, and catecholamine resistant hypotension, and hyper- kalemia
164. Pathological Mechanisms that cause Metabolic Acidosis: -increased acid production
-loss of bicarbonate -diminished renal excretion of hydrogen.
165. Metabolic Acidosis: Reduction of serum bicarbonate concentration and a low arterial
pH.
166. Metabolic Alkalosis: Results from an excess of HCO3 or deficiency of H ions. High pH,
high HCO
167. Causes of Metabolic Alkalosis: Gastric stomach contents (vomiting or gas- tric
suctioning), diuretic use (thiazide diuretics), diarrhea (laxative abuse), antacid ingestion, excess aldosterone
methylphenidate3, nicotine, progesterone, or mechanical ventila- tion.
177. Genotype: is a persons genetic composition
Actual genes specific to the individual
178. Phenotype: Expression of the gene is
a persons observable characteristics
179. Carrier: is a person who has a diseased gene but is phenotypically normal
180. Will a person carrying a recessive diseased allele have s/s of disease: No
181. DNA is composed of: nucleotides (adenine, thymine, guanine, cytosine)
182. What is the difference is DNA and RNA: RNA contains uracil instead of thyamine
183. Translation: process of protein synthesis
184. Transcription: process where RNA is formed from DNA and requires the RNA enzyme
polymerase
185. Autosomal Chromosomes: all chromosomes which do not have any relation to gender
186. Clastogens: harmful agents which damage chromosomes Ex:
radiation
187. Polyploidy: State of having 1/more extra sets of chromosome pairs.
E.g. 3 sets of chromosomes, incompatible with life, fetuses are often miscarried.
188. Aneuploidy: Alteration in chromosomal number
Results in a Single missing or one extra chromosome. Caused by nondisjunction, failure of chromosomes to divide properly. Uneven number of chromosomes, most are spontaneously aborted. Two main types: monosomy & trisomy
189. Monosomy: state of having one chromosome in a pair missing Ex:
Turner Syndrome
190. Trisomy: state of having more than two chromosomes to a pair Ex:
Down Syndrome (3 chromosomes)
191. Autosomal Aneuploidy: Disorders linked to the first 22 same pair of chromo- somes.
Ex: Down syndrome - 3 chromosomes on 21st pair
192. Sex Chromosome Aneuploidy: Sex linked chromosome disorder (23rd chro- mosome)
Klinefelter's syndrome - xxx/y
193. Deletion: Chromosomes broken & DNA is lost.
Ex: Cri du chat "cry of the cat" disorder of chromosomal deletion. Distinct cry of the baby, developmental delays, low birth weight, mental retardation, heart defects, & missing kidneys.
194. Inversions: 2 breaks of chromosome followed by reinsertion of missing frag- ment at
original site, but inverted. ABCDE would be ABDCE. No apparent physical effect; but off spring may have genetic issues (chromosomal deletions or duplica- tions).
195. Translocation: an exchange of genetic material btwn non- homologous chro-
mosomes. Usually no physical problems, but offspring can have genetic problems.
196. Reciprocal Translocation: When breaks take place in 2 different chromo- somes &
the material is exchanged. Carrier's gametes can be normal, carry the translocation, or have duplications & deletion.
197. Fragile Sites: When chromosomes develop microscopically observable breaks &
gaps d/t cultured in folate deficient medium. No apparent relationship to disease. Except fragile X syndrome - substantial cognitive impartment
198. Locus: position along a chromosome
199. Polymorphic: occurring in several different forms
200. Polymorphism: presence of genetic variation within a population
201. Homozygous: when the genotypes of two alleles are identical for a particular trait
Ex: two dominant or two recessive alleles (EE or ee)
202. Alleles: paired genes. one dominant/one recessive
203. Heterozygous: when a dominant and recessive allele are present Ee
204. Recessive: both alleles must be recessive, and both alleles must be affected by the
mutation (for the person to actually have the disease) if only one , then they are a carrier and will not manifest the disease
205. Homozygote: for a recessive allele to be expressed, it must be homozygote aa
206. Codominance: herozygote that are both dominate, ABO blood group
