Summary NUR 631 Advanced Pathophysiology- Topics to review for mid term exams
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NUR 631
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NUR 631
NUR 631 Advanced Pathophysiology- Topics to review for mid term exams
Topics to review for Midterm
NUR 631 Advanced Pathophysiology
Action potential
Membrane Action Potential Resting Neuron = - 70 MV/ (Threshold for action potential
is -55) Action potential happens when internal cell reach...
nur 631 advanced pathophysiology topics to review for mid term exams
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Topics to review for Midterm
NUR 631 Advanced Pathophysiology
Action potential
Membrane Action Potential Resting Neuron = - 70 MV/ (Threshold for action potential
is -55) Action potential happens when internal cell reaches about -55mv/ all or nothing
phenomena/ Strength of action potential is always same what changes is the frequency and
conduction speed ( conduction speed is slower to glands, blood vessels. (Axon with large
diameter increased conduction due to less resistance, PNS myelin sheaths are formed by
Schwann cells wrapping themselves around the axon. These cell don’t touch each other and
creates a gap called NODES OF RANVIER that makes salutary (Leap) conduction making
current to run through axon faster. CNS oligodendrocytes wrap around the axons and
lacks nodes of Ranvier. )
(1) Resting neuron are in – negative charge inside the cell and + charge extracellular
(2) Sodium is in extracellular with + charge and potassium is intracellular bonded d with
negative protein with + charge
(3) Electrochemical gradient is created by Sodium Potassium pumps creating
negative charge inside the cells and positive charge in extracellular. Sodium potassium
pumps are all along the axons that exchanges 3 sodium in the cell for 2 potassium
outside the cell.
(4) Ion channels: - most are voltage-gated channels that open closes and reopens to
changes in membrane potentials. Sodium channel opens @ -55 MV
(5) Ligand-Gated Channels: - opens with neurotransmitter latched on to receptors like
hormones or serotonin
(6) Mechanical gated channels: - opens in response to the physical stretching of the
membrane and Sodium gets in the cell.
(7) Action potential depolarization: - All ions channels are closed at resting membrane
voltage - 70mv. Depolarization of neuron has to happen for those voltage channels to
open. An environmental stimulus opens mechanical channels which makes Sodium
(NA+) to get in the cell changing charge inside the cell increases from -70. Threshold for
action potential is -55mv. It is all or nothing phenomena. Stimulus that causes <-55 of
depolarization is false alarms nothing happens.
(8) @-55mv gated sodium channel opens which rushes plenty of sodium on the cell
causing depolarization which activates the sodium get next to it conducting this current in
axon. Cell massive depolarization can go all the way up to +40 mv (which stays same for
each action potential). This is action potential in action. This change in current kicks
biological change down the axon. As soon as depolarization under way the process
repolarization occurs where voltage gated potassium ions open letting K+ ( potassium )
, flow out in extracellular space. This can cause membrane to first go hyperpolarized at
about -75 before voltage channel closes and sodium potassium pumps take over.
(9) When the Ion channels are open in membrane it cannot respond to any other
stimulus. Does not matter how strong of stimulus it is. This is called Refractory Period.
(10) Refractory period: - The first phase of this period from depolarization to
repolarization is called absolute refractory period and it makes sure each action
potential is unique in its own and all or nothing event. The second phase immediately
follows the first one that spans from repolarization and back to resting potential is called
the relative refractory period
Atrophy (p. 50) – decrease or shrinkage in cellular size, can lead to the entire organ shrinking and
atrophying – can affect any organ (most common in skeletal, heart, secondary sex and brain).
Physiologic atrophy – with early development – thymus gland undergoes physiological atrophy
during childhood
Pathologic atrophy – results of decreased workload, use, pressure, blood supply, nutrition,
hormonal simulation, and nervous stimulation. Examples are individuals not moving in bed, resulting in
skeletal muscle atrophy (disuse atrophy)
Hyperplasia: (p.51) (increase in cell numbers) mechanism is increased cellular divisions,
secondary to prolonged and severe injury.
a. loss of epithelial cells and cells in the letter number and kidney triggers DNA synthesis
and mitotic division
b. 2 types of normal or physiologic hyperplasia
i. Compensatory hyperplasia- adaptive mechanism, certain organ to regenerate
(Liver- hepatocytes) (70% of liver removal can regenerate completely in 2
weeks), HGF (Hepatocyte growth factor) is mediator in vitro of liver
regeneration. Other growth factors that increases hepatic cell regeneration are
transforming growth factor- alpha (TGF—alpha), epidermal growth factor (EGF),
Interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha).
1. 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
a. For example, removal of part of the liver leads to hyperplasia of the
remaining liver cells to compensate for the loss. Even with removal of 70%
of the liver regeneration is completed in about two weeks.
ii. Hormonal Hyperplasia (p. 53): occurs in estrogen dependent organs- uterus
and breast, fertilizing ovum (Uterus enlarges as result of hyperplasia and
hypertrophy)
1. For Example: after ovulation estrogen stimulates the intermediate term to grow
in thinking for the reception of fertilized ovum. If pregnancy occurs hormonal
hypoplasia as well as height for trophy enables the uterus to enlarge.
, iii. Pathologic Hyperplasia: is the abnormal proliferation of normal cells and can
occur in response to excessive hormonal stimulations or the effects of growth
factors on target cells
1. Pathological hyperplasia- due to excessive hormonal stimulation or effect of
growth factor. (Hyperplastic cells have enlargement of the nucleus, clumping of
chromatin and presence of one or more nucleoli).
a. For Example: the most common example is pathologic hyperplasia of the
endometrium, which is caused by an imbalance between estrogen and
progesterone one secretion with the over secretion of estrogen. Pathologic
endometrial hyperplasia, which causes excessive menstrual bleeding is
under the influence of regular growth inhibition controls. If these controls
fail, hyperplastic endometrial cells can undergo malignant transformation.
b. Example- Endometrium (Caused by imbalance between progesterone and
estrogen secretion and over secretion of estrogen). If regulating growth-
inhibiting control fails endometrial cells can undergo malignant
transformation.
Anaplasia – loss of cellular differentiation, irregularities of the size and shape of the nucleus and the loss
of normal tissue structure. (p364)
Dysplasia (p. 53) – abnormal changes in the size, shape and organization of mature cells. (atypical
hyperplasia), occurs in epithelial tissue of the cervix, respiratory tract – considered mild, moderate severe
and can be reversible.
Pulmonary tuberculosis - infectious bacterial disease characterized by the growth of
nodules (tubercles) in the tissues, especially the lungs.
Capillary hydrostatic (p. 105) facilitates the outward movement of water from the capillary to the
interstitial space.
Interstitial hydrostatic (p. 105) – facilitates the inward movement of water from the interstitial space
into the capillary.
Plasma oncotic – (capilalary oncontic pressure) – osmotically attracts water from the interstitial space
back into the capillary
Interstitial oncotic – osmotically attracts water from the capillary into the interstitial space.
15. Syndrome of inappropriate antidiuretic hormone (SIADH) - SIADH p. 719
a. -na+ <130-110; high levels of ADH not by normal physiologic stimuli - ADH affect
renal collecting ducts and increase H2O reabsorption; S/S - hypotonichyponatremia
with hypervolemia; weight gain (peripheral edema absent), <130=thirst, impaired taste,
anorexia, dyspnea on exertion, fatigue; <120 = vomiting diarrhea; <115=confusion,
lethargy, muscle twitching & seizures; <110=severe neurologic damage (sometimes
, irreversible); Treatment=correct problem; give hypertonic solution, restrict fluids (800-
1000/day)
b. SIADH is associated with ectopic secretion of ADH by tumor cells – small cell
carcinoma of the lung, duodenum, stomach, and pancreases, cancers of the bladder,
prostate, endometrium, lymphomas and sarcomas
c. Pulmonary disorders – pneumonia (tuberculosis), asthma, cystic fibrosis, respiratory
failure
d. CNS – encephalitis, meningitis, intracranial hemorrhage, tumors, trauma
e. Nephrological – mutation in arginine vasopressin (AVP) gene to chronic activation of
tubular V2 receptor
f. PATHO – enhanced renal water retention, increase of renal collecting ducts cause
reabsorption of water by kidneys; causing hyponatremia, hypoosmolarity, and urine that
is inappropriately concentrated
g. S/S – hypotonic hyponatremia associated with hypervolemia and weight gain; thirst,
impaired taste, anorexia, dyspnea on exertion, fatigue, dulled sensorium (NA <140),
peripheral edema absent; vomiting and abdominal cramps (Na <130-120); confusion,
lethargy, muscle twitching and seizures (<115), below <110-115 may cause severe
neurologic damage; but usually symptoms resolve with correction
h. Eval/Treat
i. (1) serum hypoosmolality (<280) and hyponatremia (<135); (2) urine
hyperosmolarity (i.e. the osmolality of urine always higher); (3) urine sodium
excretion matches sodium intake; (4) normal renal, adrenal and thyroid function; (5)
absence of condition that can alter volume status (e.g. recent diuretic use, heart
failure, hypervolemia from any cause, renal insufficiency)
ii. TREAT – correction of underlying problem, give hypertonic saline and restriction
of fluids; resolution occurs within 3 days with a 2-3-kg weight loss; if corrected too
rapidly, severe neurologic syndrome call pontine myelinolysis can ensue, no drug
therapy to suppress ADH production, but demeclyocycline may cause renal tubules
resistance to ADH, chronic ADH may use conivaptan in hospitalized patients
Sodium and potassium imbalances
Potassium (K+) (p. 114)
a. Normal Lab Value 3.5 to 5
i. Found: major intracellular electrolyte and is found in most body fluids
ii. Function:
1. Organs Involved: Kidney
2. Know factors that influence: kidney
a. Filtered free by the renal glomerulus
b. 90% reabsorbed by the proximal tuble and loop of henle
iii. Hypokalemia (p. 115-117)
1. When K+ serum level decreased to less than 3.5mEq/L
a. Mild hypokalemia is usually asymptomatic
b. Severe Hypokalemia <2.5Meq/L
i. Neuromuscular and cardiac effects (most common)
2. Causes
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