A variant of a class of lysosomal storage diseases known as the
Tay-Sachs disease
Pulling force created by molecules that cannot cross the cell membrane in the vascular space.
Capillary colloidal osmotic pressure
An early clinical manifestation of hemarthrosis as seen in hemophilia is:
Stiffness
Term for a type of fluid compartment; an example is between the membrane covering the lungs or heart.
Transcellular
These solutions cause fluid to move out of the vein and into the cells
Hypotonic
In which stage of carcinogenesis do normal cells undergo mutation in their genome making them susceptible to malignant transformation by a carcinogenic agent?
Initiation
Cells adapt to increased demands by changing in (3)
Size
Number
Form
Cells adapt to increased demands by changing in –Size due to (3)
atrophy and
hypertrophy;
increased workload
Cells adapt to increased demands by changing in Number due to (2)
hyperplasia;
increased workload
Cells adapt to increased demands by changing in Number due to (1)
metaplasia:
change in cell type/form due to chronic inflammatory disease/dysfunction
metaplasia:
decrease in cell size
Atrophy
increase in cell size
Hypertrophy
increase in numberof cells
Hyperplasia
replacement of adult cells
Metaplasia:
deranged cell growth of a specific tissue
Dysplasia:
Which of the following best describes the cellular adaptation seen in chronic cigarette smokers?
a.Atrophy
b.Hypertrophy
c.Hyperplasia
d.Metaplasia
e.Dysplasia
a.Metaplasia: As cells are damaged, a hardier version replaces the normal strata of cells.
Three Sources of Intracellular Accumulations (3)
Normal body substances
Abnormal endogenous products
Exogenous products
Environmental agents and pigments not broken down by the cell
Exogenous products
Lipids, proteins,carbohydrates, melanin, etc.
Normal body substances
Those resulting frominborn errors of metabolism
Abnormal endogenous products–
Abnormal tissue deposition of calcium salts, together with smaller amounts of iron, magnesium, and other minerals
Pathologic Calcifications
Pathologic Calcifications Types (2)
Dystrophic calcification
Metastatic calcification
Dystrophic calcification:
occurs in dead or dying tissue
Metastatic calcification:
occurs in normal tissue
T/F Dystrophic calcification can result from prolonged ischemia.
True: Ischemia stresses the tissue, it dies, and calcium precipitates out of solution.
Causes of Cell Injury (5)
Injury from physical agents
Radiation injury
Chemical injury
Injury from biologic agents
Injury from nutritional imbalances
Injury from physical agents (3)
–Mechanical forces
–Extremes of temperature
–Electrical forces
Radiation injury (3)
–Ionizing radiation
–Ultraviolet radiation
–Nonionizingradiation
Chemical injury (4)
–Drugs
–Carbontetrachloride
–Lead toxicity
–Mercury
Injury from biologic agents (3)
Viruses
parasites,
bacteria
Injury from nutritional imbalances (2)
–Excesses and deficiencies
Free radical and reactive oxygen species (ROS) formation
Free radicals are highly reactive chemical species with anunpaired electron, which causes them to be unstable and highly reactive.
Free radical injury (3)
–Lipidperoxidation
–Oxidative modification of proteins
–DNAeffects
Stresses Damage Cells By: (4)
Direct damage to proteins, membranes, DNA
ATP depletion
Free radical formation
Increasedintracellular calcium
Hypoxic Cell Injury
Deprives cell of oxygen and interrupts oxidative metabolism and the generation of ATP: Acute
cellular swelling (edema)
The longer tissue is hypoxic, the greater chance of ____ ____ ____.
irreversible cellular injury.
Causes of hypoxia
(5)
–Inadequate amount of oxygen in the air
–Respiratory disease
–Inability of the cells to use oxygen
–Edema
–Ischemia
Stresses Damage Cells By:(4)
Direct damage to proteins, membranes, DNA
ATP depletion
Free radical formation
Increased intracellular calcium
Cytosolic calcium levels are kept low by energetic mechanisms. (2)
–Ischemia-inducedcalcium disruption–Inappropriateactivation of enzymes
Reversible Cell Injury
Impairs cell function but does not result in cell death
Two patterns of reversible cell injury occur:
–Cellular swelling:
–Fatty change:
Cellular swelling:
impairment of the energy-dependent Na+/K+ ATPasemembrane pump, usually as the result of hypoxic cell injury.
Fatty change:
linked to intracellular accumulationof fat
Which of the following can result in membrane damage?
a. Inactivation of Na+/K+ATPase
b. Oxidation of phospholipid
c. Ischemic activation of Ca2+-regulated
protease
d. All the above
e. None of the above
d.All the above: Each of these can result in membrane damage.
Apoptosis
(fallen apart): equated with suicide
Programmed Cell Death
Apoptosis eliminates cells that are: (4)
•Worn out
•Have been produced inexcess
•Have developedimproperly
Have genetic damage
Necrosis:
(3)
–Refers to cell deathin an organ or in tissues that are still part of a living person
–Often interferes with cell replacement and tissue regeneration
–Gangrene occurs whena considerable mass of tissue undergoes necrosis
The term ____ is applied when a considerable mass of
tissue undergoes necrosis.
gangrene
The affected tissue becomes dry and shrinks, the skin wrinkles, and its color changes to dark brown or black. The spread of dry gangrene is slow
Dry gangrene
The affected area is cold, swollen, and pulseless. The skin is moist, black, and under tension. Blebs form on the surface, liquefaction occurs, and a foul odor is caused by bacterial action.
–The spread of tissue damage is rapid.
Wet gangrene
is the study of body function.
Physiology
is the study of the body’s response to dysfunction or disease.
Pathophysiology
is the interruption, cessation, or disorder of a body system or organ structure.
Disease
____;Causes of disease are _____ factors, (biologic, physical forces, chemical agents,
nutritional)
Etiology: etiological
sequenceof cellular/tissue events that take place from initial contact with etiologicalagent until disease expression
Pathogenesis:
structure or formof cells,
Morphology:
gross anatomic & microscopic changes characteristic of a disease
Morphologic changes:
the manifestations produced by a condition that make itevident that a person is sick, i.e. Fever (Structural and Functional changes are s/s)
Clinical manifestations:
a manifestation noted by an observer
Signs:
a subjectivecomplaint made by ta person with adisorder
Symptoms:
A compilation of signs and symptoms
Syndrome:
To designate thenature or cause of a health problem;
Diagnosis: a diagnostic process
The evolution of a disease
Clinical course:
Etiologic Factors (Causes of Disease) (4)
Biologic agents (e.g., bacteria, viruses)
Physical forces (e.g., trauma, burns, radiation)
Chemical agents (e.g., poisons, alcohol, nicotene)
Nutritional excesses or deficits
The study of disease occurrence in human populations
Epidemiology:
Developed to explain the spread of infectious disease during epidemics, emerged as ascience to study risk factors of multifactorial diseases i.e. heart disease
Epidemiology
look for patterns, characteristics (race, age,lifestyle, habits) in persons affected with a particular disorder
Epidemiologic Studies
are used in research studies to determine the naturalhistory of the disease, how it is spread, & how to prevent & control& eliminate it
Epidemiologic Methods
Factors Derived Using Epidemiologic Methods
How disease is spread
How to control disease
How to prevent disease
How to eliminate disease
- the extent to which an observation, when repeated, gives the same result
Reliability
the extent to which a measurement tool measures what it is intended to measure
Validity
how well the test or observation identifies people with orwithout a disease,
Sensitivity and specificity-
the proportion of people with a disease who testpositive on the test for that disease, “true positive” test,
Sensitivity:
if a sensitive test is _____, means the disease has been excluded, or “ruled out”
negative
proportion of people without a disease who test negative on the test for that disease, “true negative”
Specificity
extent, a value, to which an observation or test result is able to predict the presence (positive)or absence (negative)of a given disease or condition in a population
Predictive value
studies use the simultaneous collection of information necessary for classification of exposure and outcome status
Cross-sectional
compare case subjects to control subjects
Case-control studies
involve groups of people born at the time or who sharesome factor
Cohort studies
an existing case or the number of new episodes of a particular illness
Disease case
the number of new cases arising in a population at risk duringa specified time
Incidence:
a measure of existing disease in a population at a given pointin time
Prevalence:
describes the effects of an illness on a person’s life, the effects on human functioning
Concerned with the incidence, persistence, and long-term consequences of disease
Morbidity:
death producing characteristics of a disease; providesinformation about trends in the health of a population
Mortality:
Used as a predictor of outcome for diseases for which there is no effective treatment (disease progression & projected outcome without medical intervention)
Natural History of a Disease
Information about the____ ____ _ _ ____ and the potential of effective treatment methods, services, provides direction for preventive measures.
natural history of a disease
Primary Prevention
(e.g., immunizations): removing risk factors so diseasedoes not occur
SecondaryPrevention
(e.g., Pap smears): detecting disease while it is stillcurable
Tertiary Prevention
(e.g., antibiotic use): preventing further deteriorationor reducing complications of disease once it has been diagnosed
the conscientious, explicit, and judicious use of current best evidence in making decisions about the care of individual patients
Evidence-based practice:
Characteristics of the Cell Membrane (5)
a)Lipid bilayer
b)Transmembrane proteins
c)Peripheral proteins
d)Aquaporins
e)Receptors
Cell Communication (5)
Gap junctions
Autocrine signaling
Paracrine signaling
Endocrine signaling
Synaptic signaling
Types of Cell Receptors (4)
–Cell surface
–G-Protein linked
–Enzyme –linked
–Ion-channel- linked
ATP and ADP
Catabolism
Anabolism
Metabolism
–Citric acid cycle
–Electron transportchain
Aerobic metabolism
Glycolysis
Anaerobic metabolism
The Basics of Cell Firing (9)
1. Cells begin with a negative charge: resting membrane potential
2.Stimulus causes some Na+ channels to open
3.Na+ diffuses in, making the cell more positive
4. At threshold potential, more Na+ channels open
5. Na+ rushes in, making the cell very positive: depolarization
6. Action potential: the cell responds (e.g., by contracting)
7. K+ channels open
8. K+ diffuses out, making the cell negative again: repolarization
9. Na+/K+ ATPase removes the Na+ from the cell and pumps the K+ back in
process whereby proliferating cells become progressively more specialized with each cell division, adult cell is fully differentiates, specific set of structure & function characteristics
Cell differentiation:
loss of cell differentiation
anaplasia
Process of increasing cell numbers by mitotic cell division, normally regulated : cells
dividing and forming =cells dying
Cell Proliferation:
proliferation increases, but differentiation remains normal
Benign neoplasms:
both proliferationand differentiation increases (solid tumors & hematologic cancers)
Malignant neoplasms
malinant, pervasive tumor,has remained in site of origin, not crossed the basement membrane
Carcinoma in situ:
malignant cancercells break loose from primary site, travel to another location, form another neoplasm
Metastases:
Cyclins (proteins), activate cyclin-dependent kinases (CDK’s) to ...
they also ....., and are regulated by... which ... to allow for ...
control the entry & progression of cells through the cell cycle;
synthesize degrade cyclin;
CDK inhibitors,
regulate the cell cycle
DNA replication repair
an inherent mutation phenotype/genic instability in cancer cells (cc)
Genetic Instability:
____ ____ ____ proliferate in absence GF
Growth factor independence
Loss of celldensity-dependent (contact) inhibition:
do not stop growing when touch neighboring cells
Loss of cohesiveness & adhesion
lack of cohesiveness & adhesiveness, shed surface cells easily
Loss of anchorage dependence
independent, do not die when not attached to basement membrane/neighboring cells
Faulty cell-to-cellcommunication
changes in intercellular connections (gap Junctions) responsiveness to membrane signals
Infinite cell lifespan
immortality,unlimited lifespan
Cancer cell characteristics (10)
Genetic Instability
Growth factor independence
Loss of cell density-dependent (contact) inhibition
Loss of cohesiveness & adhesion
Loss of anchorage dependence
Faulty cell-to-cell communication
Infinite cell lifespan
Abnormal spread of degradative enzymes
Antigen Expression
Abnormal cytoskeletal characteristics
metastatic spread & or ectopic hormone production
Abnormal spread of degradative enzymes=
synthesize& secrete enzymesto break down proteins, Seeding due to cell shedding, use of blood & lymphto travel, Rapid/Unlimited Growth Grow larger, own blood supply, faster celldivision, (growth fraction higher, faster doubling time)
Ability to Invade and Metastasize:
Genetic Basis of Cancer (9)
•Proto-Oncogenes
•Tumor Suppressive Genes
•Genetic mutations, translocations
•Epigenetic mechanisms
•DNA repair defects
•Defects in growth factor signaling pathways
•Evasion of or Faulty Apoptosis
•Evasion of cellular senescence
•Invasion & metastasis properties
Other factors that contribute to Cancer (3)
Microenvironment
Carcinogenesis:
Host & Environmental factors:
Other factors that contribute to Cancer Microenvironment
Multiple cells inbody contribute: macrophages, fibroblasts, endothelia cell, immune &inflammatory cells, extracellular matrix, & substances that signal andregulate body function i.e. hormones, cytokines, *chemokines-(*regulate growthhormone) – Reversal in research
Other factors that contribute to Cancer: Carcinogenesis:
•Process by which carcinogenic agents cause normal cells to become cancer, believed to bemultistep: Initiation, Promotion, Progression
Other factors that contribute to Cancer Host & Environmental factors:
secondary prevention for EARLY RECOGNITION i.e. oral & skin exams, Pap smears,
Mammography, Prostate exams, Colonoscopy
Cancer Diagnosis:
CT scan, MRI, PETScan, Tumor markers, (antigens on surface of tumor cells, elevatedhormone/enzyme levels, oncofetal proteins in bloodused to screen/Dx, monitor TX effectiveness, establish prognosis i.e. hCG, CA-125, CEA, AFP, PSA, CD
Cancer Cytology:
Pap smear, Tissue biobsies, Immunohistochemistry (antibodies used for identification of cellproducts/surface markers) Microarray technology (gene chips for miniature assay)
Bone Marrow suppression and reduced blood cellcounts,
anorexia,
N/V,
Alopecia,
chemo is mutagenic,
teratogenic,
carcinogenic to cells
Hormone Therapy Drugs
used to disrupt hormone environment of cancer cells, suppress hormone levels in blood, alter hormone receptor function
Biotherapy: Biologic response modifiers 3 types:
Cytokines:
Hematopoetic growth factors
Monoclonal antibodies:
Cytokines:
interferons & interleukins,endogenous polypeptides that inhibitreplication, protein synthesis, & cellularcommunication
Hematopoetic growth factors
stimulate blood cell production
Monoclonal antibodies:
IGG antibodies cloned in lab highly specific {targeted} to antigens on cancer cell
Immunotherapy
(using cultured bacteria tostimulate immune system to kill cancer cells, Also, using cultured immune cells i.e. culturednatural killer cellsto kill cancer cells)
Other Targeted Therapies
proteins that block enzymes, cancer cells only
Radiation therapy:
Most common treatment, high energy radiation particles & waves, damage kill cells, Types: beam, seed, implants
Nursing Intervention- Cancer
Patient & Family Education:
•Administration of medications & Chemooordination of treatment and follow up
•Assess , Monitor & Report all adverse effects, CM lab & other testing results
•Documentation all care & education
Patient & Family Education Cancer:
Cancer &clinical manifestations, treatment and adverse effects (chemo precautions, neutropenia precautions),
–Cutaneous & Subcutaneous lesions that project from skin
–a few to many hundred, can form large, painful (subcut.) benign tumors causing skeletal deformities
–Tumors may become malignant neoplasms
–Usually manifests near adolecense
–Children may have neurologic complications, learning disability, ADD, seizures
–Also: Café Au Lait spots on skin,pigmented nodules of iris, (Lisch nodules), aid in diagnosis
Phenylketonuria (PKU)
A rare metabolic disorder caused by a deficiency of the liver enzyme phenylalanine hydroxylase
Tay-Sachs disease
–A variant of a class of lysosomal storage diseases, known asthe gangliosidoses
–Ganglioside in the membranes of nervous tissue is deposited in neurons of the central nervous system and retina because of a failure of lysosomal degradation
Tay-Sachs disease: Clinical manifestations
–Infants appear normalat birth
–Progrssive weakness, muscle flaccidity
–Decreased attentiveness at 6-10 months
–Then rapid deterioration of motor & mental function, seizures
–Retinal : visual impairment, eventual blindness
Tay-Sachs disease: Treatment
•No cure, death before age 4-5
•Serum (blood) analysis for hexosaminidase deficiency
Types of Hemophilia
Hemophilia A (classic)- Accounts for 75% of cases
Hemophilia
B (Christmas disease)- less severe
Hemophilia Prevalence and inheritance pattern
X – linked recessiveor new mutation
Hemophilia: Expression
Severity depends on level of factor present
Hemophilia Clinical Manifestations
•Hemorrhage/bleeding:
–May occur anywhere; subcutaneous and intramuscular common
–S/S depends on location
•Hemarthrosis
–Knees,elbows and ankles most common
–Early s/s – stiffness, tingling, aches
–Later s/s – warmth, redness, swelling, severe pain
Hemophilia Diagnosis:
–Analysis of directgene mutation
– DNA Linkage studies
–Amniocentesis or Chorionic villus sampling (these are to predict complications in fetus/newbornand determine therapy, one day for gene addition)
Examples of Multifactorial Inheritance Disorders
Cleft lip or palate
Clubfoot
Congenital dislocation of the hip
Congenital heart disease
Pyloric stenosis
Urinary tract malformation
Chromosomal Disorders
A major category of genetic diseasse
Alterations in the number of chromosomes
Stuctural changes due to breakage, and then rearrangement & possible deletion of chromosomes caused by many factors
If small amount of genetic material lost/translocated, often goes unnoticed, Difficulty arises during meiosis, results in gametes with unbalanced number of chromosomes
is the net movement of water from an area of LOW solute concentration to an area of HIGHER solute concentration across a semi-permeable membrane.
Osmosis
is the net movement of solutes from an area of HIGH solute concentration to an area of LOWER solute concentration.
Diffusion
Osmolality (4)
The number of solutes per kg of water (by weight)
Used to describe the concentration of body fluids
Normal osmolality of ICF & ECF ranges between 275/280-295mOsm/kg
Estimate the serum osmolality by doubling the serum sodium concentration
Tonicity
Effect that the osmotic pressure of a solution with impermeable solutes exerts on cell size because of water movement across cell membrane
Osmolarity (outside body)
Osmolar concentration in 1 L of solution (mOsm/L)
Isotonic Solutions
*Same solute concentration as RBC/Plasma
Isotonic Solutions Example Fluids:
*0.9% NaCl (aka Normal Saline)
*Lactated Ringers solution (LR)
Hypertonic Solutions
*Higher solute concentration than RBC / Plasma
Isotonic Solutions *If injected into vein:
no net movement of fluid; Body cells placed in isotonic solution neither shrink nor swell
Hypertonic Solutions *If injected into vein:
fluid has greater concentration of solutes than plasma so,
Fluid moves INTO veins: Water in cells moves to outside to equalize concentrations:
fluid has lower concentrationof solutes than plasma Fluid moves OUT of veins: Water outside cells moves to inside of cells; cells will swell and eventually burst(hemolyze) Example: 0.45% NaCl
Hypotonic Solutions Example:
0.45% NaCl
Hypothalamic Regulation
Thirst center in brain is the primary regulator of water intake
Antidiuretic hormone: responds to osmolality & blood volume
Pituitary Regulation
Works under control of hypothalamus to release ADH
Renal Regulation
Regulator of volume & osmolality by controlling excretion of water & electrolytes
Adrenal Cortical Regulation
Renin-angiotension-aldosterone mechanism: response to a drop in bloodpressure;
results from vasoconstriction and sodium regulation by aldosterone
Cardiac Regulation
Atrial natriuretic factor (hormone released by cardiac atria in response to increased atrial pressure);
causes vasodilation & increased urinary excretion of sodium & water (which decreases blood volume);
inhibits renin secretion& blocks effects of aldosterone
Capillary filtration pressure,
b/c vascular fluid moves intointerstitial spaces
Capillary colloidal osmotic pressure,
b/c of in adequate production or loss of plasma proteins, *albumin, which exert force to pull fluid back in capillary space (kidney / liver disease, burns)
Capillary permeability
capillary pores enlarged/walls damaged protein and other osmotic particles leak out into interstitial space
Obstruction to lymph flow
lymphedema when particles/proteins cannot be reabsorbed through cap membrane pores
Venous obstructionLiver disease with portal vein obstruction
Acute pulmonary edema
Venous thrombosis (thrombophlebitis)
Decreased arteriolar resistance
Calcium channel–blocking drug responses
Decreased Colloidal Osmotic Pressure (6)
Increased loss of plasma proteinsProtein-losing kidney diseases
Extensive burns
Decreased production of plasma proteins
Liver disease
Starvation, malnutrition
CAUSES OF EDEMA:Increased Capillary Permeability (4)
Infammation
Allergic reactions (e.g., hives)
Malignancy (e.g., ascites, pleural effusion)
Tissue injury and burns
CAUSES OF EDEMA:Obstruction of Lymphatic Flow (2)
Malignant obstruction of lymphatic structures
Surgical removal of lymph nodes
Edema Assessment:
visual inspection ,
palpation,
daily weight(1 liter=2.2 lbs or 1 Kg),
measurement
Edema Treatment
depends on type of edema,
correcting life altering types,
controlling the cause,
Diuretic Therapy,
elastic stockings,
massage for lymph edema,
elevating extremities,
pt/family education
Concentrations of Extracellular Sodium
135-145 mEq/L
Concentrations of Extracellular Potassium
3.5-5.0 mEq/L
Concentrations of Extracellular Chloride
98-106 mEq/L
Concentrations of Extracellular Bicarbonate
24-31 mEq/L
Concentrations of Extracellular Calcium
8.5-10.5 mg/dl
Concentrations of Extracellular Phosphorus
2.5-4.5 mg/dL
Concentrations of Extracellular Magnesium
1.8-3.0 mg/dL
Regulation of Na+/water balance:
Maintenance of effective circulating volume (arterial BV), vascular & Kidney baroreceptors, ADH & Renin/Angiot./Aldost. system
Regulation of sodium (Na+ most abundant cation in body, (3)
Gains and Losses (In GI, out *Kidney & GI, skin)
Sources of sodium (diet, need 500 mg/day, most take in 6000-15,000/day
Causes of loss *Kidney (disease), GI (vomiting/diarrhea), skin/sweat
Electrolyte Disorders: Sodium: Overview (2)
Normal level is 135–145 mEq/L
Regulates ECF fluid volume and osmolarity
Hyponatremia
<135 mEq/L
Common, Plasma loss,
Hyponatremia Hypertonic translocational:
shift H2O out of ICF,
Diabetes
Hyponatremia: *Hypotonic (dilutional) water retention,
classified by volemia/ECFvolume
Hyponatremia: Hypovolemic hypotonic:
H2O & Na= loss, but more Na+ loss: excessive sweating
Hyponatremia: Euvolemic Hypotonic:
retain H2O, dilute Na+, ECF WNL= SIADH
Hyponatremia: Hypervolemic hypotonic (edema):
Heart Failure, Kidney & liver disease
Hyponatremia Clinical Manifestations (11)
(sudden or slow):
Muscle cramps,
weakness,
fatigue,
Finger print edema,
n/v/d,
abd cramps,
Neuro:
lethargy,
apathy,
headache,
disorientation &
confusion
Hyponatremia Diagnosis & TX:
Labs, exam, SIADH (syndrome of inappropriate antidiuretic hormone secretion):
limit water intake,
removing medications,
correct underlying cause,
Oral or IV saline solutions,
occasionally a diuretic,
CNS: requires slow correction
Hypernatremia
(>145 mEq/L)
Hypernatremia Causes:
Net loss of H2O (unable to drink, increasedloss in urine )
or Na+ gain (rapid ingestion, IVinfusion)
Follows a loss of body fluids that have low concentration of Na+, so more fluid than sodium loss(loss in respiratory tract/fever, strenuous exercise,watery diarrhea, tube feedings)
Syndrome of Inappropriate Secretion of ADH (SIADH)
Diabetes Insipidus: (Neurogenic & Central/Nephrogenic) ADHdeficiency or decreased response, inability to concentrateurine in periods of water restriction, excrete large volumes ofurine, 3-30L/day, excessive thirst, little alteration in body fluidlevels if thirst is nl & fluids available, danger if these are impactedor cannot communicate need for water.
Neurogenic & Central/Nephrogenic) ADH deficiency or decreased response, inability to concentrate urine in periods of water restriction, excrete large volumes of urine, 3-30L/day, excessive thirst, little alteration in body fluid levels if thirst is nl & fluids available, danger if these are impacted or cannot communicate need for water.
Diabetes Insipidus:DX:
24 Hour UOP measurement,
r/o kidney & glucose disease,
ADH levels,
urine osmolality before & after fluid deprivation,
correct underlying cause
Diabetes Insipidus:TX:
pharmacologic replacement of synthetic ADH with response monitoring,
MRI pituitary & hypothalamus,
drugs: Desmopressin for chronic DI, thiazide diuretics, other…
Syndrome of Inappropriate ADH (SIADH): CM:
Same as dilutional hyponatremia,
high urine osmolality,
LOW serum osmolality,
decreased UOP, (despite fluid intake),
serum Hematocrit,
sodium, & BUN all decreased,
Syndrome of Inappropriate ADH (SIADH): 5 cardinal features for DX:
hypotonic hyponatremia
natriuresis
Urine osmolality in excess or serum osmolality
Absence of edema & volume depletion
Normal renal& Adrenal function
Syndrome of Inappropriate ADH (SIADH): TX:
Depends on severity,
fluid restriction,
Drugs: Diuretics, Lithium, otherdrugs, hypertonic 3% saline for severe cases only
Extracellular: blocks Na+gates in nerve and musclecells
Clotting
Leaks into cardiac muscle,causing it to fire
Intracellular: needed for all muscle contraction
Acts as second messenger in many hormone and neurotransmitter pathways
Hypocalcemia
(< 8.5mg/dL)
Hypercalcemia
(>10.5mg/dL)
Magnesium
Normal level is 1.8–2.7 mg/dL
Magnesium Cofactor in enzymatic reactions
Involving ATP
DNA replication
mRNA production
Normal value: pH
= 7.35–7.45
Acid (H+) Hydrogen Ion
Blocks Na+ gates
Controls respiratory rate
Individual acids have different functions
Byproducts of energy metabolism (carbonic acid, lacticacid)
Digestion (hydrochloric acid)
“Food” for brain (ketoacids)
An increase in CO2 will cause (3)
Increases in CO2 (increased PCO2)
Increases in H+ (lower pH)
Increases in bicarbonate ion
Normal Hydrogen Ion Concentration
7.35 - 7.45
Acidic Solution
Higher H+, lower pH
pH <7.4
Basic Solution
Lower H+, higher pH
pH >7.4
3 Major Mechanisms for Regulating pH
ICF and ECF buffering systems
Lungs (control elimination of CO2)
Kidneys (reabsorb HCO3 [bicarbonate] and eliminate H+)
Respiratory Acidosis
Increased PCO2
Increased Carbonic Acid
Increased H+ = low pH
Increased Bicarbonate
Respiratory Alkalosis
Decreased PCO2
Decreased Carbonic Acid
Decreased H+ = low pH
Decreased Bicarbonate
Decrease in pH,
Increase in CO2.
Caused by slow respirations, over-sedation, chest wall trauma, pulmonary edema, emphysema, asthma, and bronchitis. Tx: Adjust ventilation.
Respiratory Acidosis
Decrease in pH, Decrease in HCO3. Caused by lactic acidosis, poor perfusion, renal failure, DKA. Tx: Adjust ventilation, administration of HCO3.
Metabolic Acidosis
Increase in pH.
Decrease in CO2.
Caused by hypermetabolic states (fever), lung disease, liver failure. Tx: Decreasing ventilation, breathing through bag, decreasing hypermetabolic states.
Respiratory Alkalosis
Increase in pH.
Increase in HCO3.
Caused by vomiting, GI suctioning, diruretics, and excessive HCO3 intake.
Tx: Respiratory compensation through hypoventilation (increases CO2 which increases H+, lowering pH), renal compensation by decreasing acid excretion through urine and bicarbonate regeneration.
Metabolic Alkalosis
PCO2
Partial Carbon dioxide
H2CO3
Carbonic Acid
HCO3
Bicarbonate
Metabolic Acidosis
Increased H+ = low pH(<7.35)
Decreased bicarbonate
Heavier breathing causes
decreased PCO2
Metabolic alkalosis
Decreased H+ = high pH(>7.45)
Increased bicarbonate
Lighter breathing causes increased PCO2
Normal Arterial PCO2 level
35-45 mEq/L
Normal HCO3
22-28 mEq/L
The condition of respiratory alkalosis is present if the PCO2 number is below 35 mmHg. This means there is too little carbon dioxide in the blood
the PCO2 number is below 35 mmHg. This means there is too little carbon dioxide in the blood
The condition of respiratory acidosis is present if
the PCO2 number is above 45 mmHg. There is too much carbon dioxide in the blood
An HCO3 level is below 24 mEq/L
indicates metabolic acidosis. The body cannot produce enough bicarbonates to keep up with the carbonic acid in the blood.
An HCO3 level above 26 mEq/L indicates
metabolic alkalosis. There are too many bicarbonates in the blood.
