Module 5 Flashcards
What percentage of water is found in the intracellular component?
70%
What percentage of water is found in the extracellular component?
30%
What are the 4 processes of fluid movement?
Diffusion, facilitated diffusion, active transport, osmosis
Define diffusion
movement of molecules from an area of high concentration to an area of lower concentration
when does diffusion stop
when the concentration is equal in all parts
define osmosis
movement of water down a concentration gradient - from low solute concentration to high solute concentration
when does osmosis stop
when the concentration is the same of when hydrostatic pressure builds and opposes further movement
What ions are primarily on the OUTSIDE of cells
Sodium, chloride, bicarbonate, and calcium
What ions are primarily on the INSIDE of cells
potassium, magnesium, phosphate, and sulfur
what are the 3 primary colloids
albumin, globulin, and fibrinogen
colloid oncotic pressure _________ with age and malnutrition
decreases
how do colloids influence oncotic pressure
increase it
what happens with hydrostatic pressure
pushes fluid OUT of the capillary
what is an example of hydrostatic pressure
at the capillary level - pushes water out of the vascular space into the interstitial space
what happens with oncotic pressure
pulls fluid into the capillaries
what primarily drives oncotic pressure
the presence of colloids in the plasma, the interstitial fluid has a small amount - so it pulls fluid in from the outside to balance out the concentration
what primarily drives hydrostatic pressure
blood pressure in the capillaries
what are the causes of HYPOnatremia
GI losses = diarrhea, vomiting, fistulas, NG suctioning
Renal loses = diuretics, adrenal insufficiencies
Skin losses = burns, wound damage
Fasting diets, water intoxication (polydipsia)
Excess hypotonic fluid
What are the S/S pf HYPOnatremia
Confusion / altered LOC
Anorexia, muscle weakness
Can lead to seizures / coma
What is dilutional hyponatremia
low sodium as a result of taking in too much water
what are the S/S of dilutional hyponatremia
Hypervolemia
Increased BP
Weight gain
Bounding pulse
Increased urine specific gravity
what is depletional hyponatremia
low sodium as a result of absolute loss of sodium and fluid
what are the S/S of depletional hyponatremia
Hypovolemia
Decreased BP
Tachycardia
Dry skin
Weight loss
Decreased urine specific gravity
what is the general speed to replace sodium, why
SLOWLY because if you do it too quickly it causes osmotic demyelination syndrome (irreversible brain damage)
What routes are able to replenish sodium
PO and IV
does dilutional or depletional hyponatremia get treated with a fluid restricton
dilutional
what are the causes of HYPERnatremia
IV fluids, tube feeds, near drowning in SALT water = excess sodium intake
Not enough water intake (or too much water loss) = cognitively impaired, diarrhea, high fever, heat stroke
Profound diuresis
What are the S/S of HYPERnatremia
Altered LOC/confusion, seizure, coma
Extreme thirst (hyperosmolality)
Dry, sticky, mucous membranes
Muscle cramps
how do you treat hypernatremia
If water loss is the cause = add water
If sodium excess is cause = remove sodium
what are the causes of hypokalemia
Renal / GI losses (Diuresis, Diarrhea, Ileostomy drainage)
Acid / base disorders
what are the s/s of hypokalemia
Cardiac rhythm disturbances = can be lethal
Muscle weakness, leg cramps
Decreased bowel motility - constipation, nausea, ileus
what is the treatment of hypokalemia
potassium chloride
what are the causes of hyperkalemia
Decreased K+ output (renal failure, not peeing)
Burns, crush injuries, sepsis -> massive cell injury (cells burst = K+ now in the blood)
Medications
what are the s/s of hyperkalemia
Cardiac rhythm disturbances
Muscle weakness, cramps
Abdominal cramping, diarrhea, vomiting
how do you treat hyperkalemia
Kayexalate / sodium polystyrene sulfonate or D50 / insulin
is D50 / insulin a permanent solution for hyperkalemia
no it is temporary
what are the causes of hypomagnesemia
Diuresis, GI / renal losses, limited intake (starving or fasting), alcohol abuse, pancreatitis, hyperglycemia
what are the s/s of hypomagnesemia
Hyperactive reflexes, confusion, cramps, tremors, seizures
Nystagmus
what are the treatment routes available for hypomagnesemia
IV or PO
what are the causes of hypermagnesemia
Increased intake accompanied by renal failure
Chronic renal failure who takes milk of magnesium for constipation
what are the s/s of hypermagnesemia
Lethargy, floppiness, muscle weakness, decreased reflexes, flushed/warm skin, [deceased pulse/BP - mag must be REALLY high]
what is the treatment for hyperkalemia
stop replacement if chronic intake
what are the causes of hypocalcemia
Unable to mobilize calcium from bone (Hypoparathyroidism, Hypomagnesemia)
Increased renal loss (renal failure)
Increased binding
Decreased intake / absorption (Decreased vitamin D)
Acute pancreatitis
Thyroid / parathyroid surgery
what are the s/s of hypocalcemia
Increased neuromuscular excitability = numbness/tingling, muscle cramps, bone pain, tetany, laryngeal spasm
Hyperactive reflexes
Cardiac insufficiency
Positive Chvostek’s sign (Ipsilateral twitching of face muscle in response to a gentle tapping of the facial nerve anterior to the ear)
Positive trousseaus sign (Carpal spasm upon inflation of BP cuff to 20 mmHg above pt’s SBP for 3 minutes)
how do you treat hypocalcemia
IV (only through a central line) or PO
what are the causes of hypercalcemia
Hyperparathyroidism, cancers (lung, breast, hematologic), immobility, overdose of antacids (like tums)
what are the s/s of hypercalcemia
Calcium acts like a sedative = fatigue, lethargy, confusion, weakness, leading to seizures, coma
kidney stones
How do you treat hypercalcemia
Adequate hydration
Diuretics and NaCl
Dialysis in renal failure
what are some of the things that calcium is responsible for
Enzyme reactions
Membrane potentials / nerve excitability
Hormone, NT, and chemical mediator release
Influences cardiac contractility and automaticity
Needed for blood clotting
what are the causes of hypophosphatemia
Decreased absorption
Antacids overdose
Severe diarrhea
Increased kidney elimination
what is refeeding syndrome
if someone is starving for a long time, then they get food or tube feedings -> can cause electrolyte imbalance (WANT TO INTRO SLOWLY)
what are the s/s of hypophosphatemia
severe ones: Tremor, paresthesia, confusion - coma, seizure, muscle weakness, joint stiffness, bone pain, hemolytic anemia, platelet dysfunction, impaired WBC function
how do you treat hypophosphatemia
IV or PO
what are the causes of hyperphosphatemia
Kidney failure
Laxatives / enema with phosphorus
Shift from intra to extracellular compartment (Massive trauma, Heat stroke)
Hypoparathyroidism
what are s/s hyperphosphatemia
Usually asymptomatic but can have Muscle spasms, paresthesia, tetany
what are the 3 modes of transmission for fungal infections
implantation (under the skin after injury), inhalation (airborne spores), and from taking antibiotics
who is more likely to get a fungal infection
elderly and immuno-compromised patient
what are dermatophytes
fungi that cause superficial skin infections
what are the characteristics of tinea pedis
Dry, scaling pruritic lesions
May only affect skin in the web space between the toes
if someone has tinea pedis - where is that located
on the feet (this is athletes foot)
what are the risk factors for tinea pedis
Coming into contact with infected skin or fungus in the environment (locker rooms, dirty showers)
how to prevent tinea pedis from starting
Use of shower shoes, cleaning tub/shower after each use (goal is to minimize transmission)
how do you diagnose tinea pedis
cultures
how do you treat tinea pedis
topical antifungal (OTC)
what does tinea capitis affect
Can affects scalp, eyebrows, or eyelashes
what are the characteristics of tinea capitis
Scaly erythematous lesion and hair loss
May cause permanent alopecia (baldness)
how do you treat tinea capitis
PO systemic antifungals bid for 4-6 weeks
Topicals are not effective
what does the tinea versicolor affect
skin of the upper chest, back, and/or arms
what causes tinea versicolor
a type of yeast that lives naturally on your skin but something has caused an overgrowth of it
what are the risk factors of tinea versicolor
hot climate, sweating a lot, oily skin, weakened immune system, NOT CONTAGIOUS
what are the characteristics of tinea versicolor
acidic bleached spots that cause skin discoloration (can be white, pink, red, or brown
where can you find a candidiasis infection
in the mouth (thrush) or the vagina (yeast infection)
what are the risk factors of a candidiasis infection
Immunosuppression (iatrogenic / acquired), antibiotic use
what dose a candidiasis infection look like
May appear as white lesions the in the mouth
Beefy red satellite lesions in intertriginous area (skin folds)
how do you treat a candidiasis infection
with topical antifungal
how do you treat a systemic fungal infection
with aggressive treatment with PO or IV antifungals
what is characteristic for melasma
dark macules on the face
who is melasma more common in
women
what is the treatment for melasma
avoiding the sun, bleaching creams with hydroquinone, tretinoin / retin-A (vitamin A derivatives)
what happens with vitiligo
pigment disappears from a patch of skin due to abnormalities in the production of melanin
what is the treatment for vitiligo
there is none
do the areas of vitiligo spread
yes
what reactivates the herpes zoster virus
stress, illness, or immunosuppression
what is the prodromal stage of the herpes zoster virus infection
burning / tingling along the dermatome
what are the characteristics of a herpes zoster flare up
vesicles on red base that follow along a dermatome but are asymmetric and do not cross the midline, painful
is herpes zoster contagious
yes, it can be spread to people who have never had chicken pox and who haven’t had the vaccine
how long does it take a herpes zoster flare up to go away
2-3 weeks
how do you treat herpes zoster flare up
with anti-virals
what is one specific long-term complication from the herpes zoster virus
persistent neuralgia pain in the area where the rash was
what are the 2 causative agents for impetigo
staphylococci and streptococci
is impetigo contagious
yes
what is the appearance of an impetigo bacterial infection
vesicles, pustules, honey-colored crust with red base around the nose
what is the treatment for impetigo bacterial skin infections
topical antibacterials
what is an abscess
inflamed skin with a collection of pus underneath (usually has raised and palpable borders)
how is an abscess treated
incision and drainage followed by antibiotics
what is a furuncle
bacterial infection of the hair follicle
how do you treat carbuncles and furuncles
incision and drainage, followed by antibiotics
what are the potential causes of cellulitis
insect / animal bite, an initial injury / wound that becomes infected and spreads to surrounding tissue
is cellulitis contagious
no
what is the appearance of cellulitis
red, painful, swollen, warm to touch - may have blisters
how to treat cellulitis
PO systemic antibiotics, IV depending of severity
how does a community acquired-MRSA infection usually begin
as a painful boil
who is at risk specifically for community acquired MRSA
high school wrestlers, child-care workers, and people who live in crowded conditions
what are the symptoms of a MRSA infection
warm to touch, purulent drainage, fever, abscess
what is the treatment for hospital and community acquired MRSA
hospital = IV vancomycin
Community = bactrim
what are actinic keratosis
benign lesions (rough, scaly, red plaques) that are due to damage by UV rays
what are solar lentigos
benign lesions that are also known as liver / age spots
who is more likely to get skin cancer
women before the age of 49 have a higher likelihood - but men have a higher likelihood after that
the likelihood of developing basal neoplastic lesions increases with what
sun exposure
what are the characteristics of basal neoplastic lesions
nodular forms that begin as a small, flesh colored pink dome shaped bump that progresses into a translucent, shiny, pearly nodule, that eventually transforms into an ulcer
what increases the likelihood of developing squamous cell neoplastic lesions
sun exposure
what are the characteristics of squamous cell neoplastic lesions
red and scaling, slightly elevated with an irregular border
what is the rate of metastases for melanoma
high
other than on the skin where else can melanoma form
in the eyes and under the fingernails
what are the risk factors of developing melanoma
family hx, blonde/red hair, freckling on the upper back, 2+ blistering sunburns before the age of 20, 3+ year hx of outdoor jobs as a teen
how do you assess lesions
ABCDEE
is eczema contagious
no
what are the characteristics of eczema
Pruritus, rash on face/back of knees/wrists/hands/feet, skin very dry/thickened/scaly, lesions may appear reddish and then turn brown, lesions can ooze and crust over, can be exacerbated by heat, cold, detergents, and stress
what are the treatments for eczema
Lotions / creams to keep moist
Cold compress
OTC hydrocortisone cream (can use behind the counter if severe enough)
Immune modulator medications
erythrocytes are
red blood cells
what are the different types white blood cells
Neutrophils, Lymphocytes, Monocytes, Eosinophils, Basophils
granulocytes release _________ _________.
immune mediators
what WBC is the first to arrive at a site with inflammation
neutrophils
bands vs segs (neutrophils)
band = immature
segs = mature
when would you see an increase in neutrophil count
acute bacterial infections and trauma
what is the “shift to the left” phenomenon with neutrophils
in early / acute stages of infection, there are a higher proportion of bands
what are lymphocytes
B - and T - cells
when would you see an increase in lymphocytes
chronic bacterial infection and acute viral infections
when would you see an increase in monocytes
with bacterial infections and cancer
when would you see an increase in eosinophils
allergic reactions and parasitic infections (think wheezes, worms, and weird diseases)
when would you see an increase in basophils
allergic reactions
if someone has a low Hgb, what could cause that
bleeding, B12 deficiency, cancers, kidney/liver disease
if someone has a high Hgb, what could cause that
COPD, dehydration, shock
what precautions can be taken to protect those with leukopenia
good hand hygiene, avoid contact with people who are sick, avoid raw fruits / veggies / grains, no fresh flowers, and keep doors closed in the hospital
what causes infectious mononucleosis
epstein-barr virus
what is the primary mode of contact for infectious mononucleosis
saliva
what population is more likely to get infectious mononucleosis
teens / young adults
what happens in infectious mononucleosis
there is atypical lymphocyte proliferation
what is the onset and incubation of infectious mononucleosis
onset - slow
incubation - 4 -8 weeks
what are the clinical manifestations of infectious mononucleosis
swollen lymph nodes, hepatitis, splenomegaly
if you are looking at lab values for a patient with infectious mononucleosis, what would you see
WBC increased (lots and lots of lymphocytes)
what are the clinical manifestations of Myelodysplastic
anemia, infection, spontaneous bleeding / bruising
what happens in the case of leukemia
WBC are immature and unregulated - then they proliferative rapidly in bone marrow and then go to spleen and lymph nodes
what type of leukemia is most common in children
acute lymphocytic leukemia
what type of leukemia is most common in adults
chronic lymphocytic leukemia
what are s/s of acute leukemia
decreased (mature) WBC, decreased RBC, and decreased platelets
what is the onset of acute leukemia
sudden
what is the onset of chronic leukemia
insidious
what s/s would you see with chronic lymphocytic leukemia
fatigue, weight loss, anorexia, infections
what s/s would you see with chronic myelocytic leukemia
fatigue, weight loss, diaphoresis, bleeding, abdominal discomfort (because of enlarged spleen)
what distinctive type of cell can be found with hodgkin’s lymphoma
reed-sternberg cell
is hodgkin or non-hodgkin’s lymphoma more likely to spread
non-hodgkins
what happens with plasma call cancer
M protein proliferates -> increases osteoclasts (which breakdown bone)
