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Pathopharmacology Intro > Module 5 > Flashcards

Module 5 Flashcards

1
Q

What percentage of water is found in the intracellular component?

A

70%

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2
Q

What percentage of water is found in the extracellular component?

A

30%

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3
Q

What are the 4 processes of fluid movement?

A

Diffusion, facilitated diffusion, active transport, osmosis

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4
Q

Define diffusion

A

movement of molecules from an area of high concentration to an area of lower concentration

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5
Q

when does diffusion stop

A

when the concentration is equal in all parts

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6
Q

define osmosis

A

movement of water down a concentration gradient - from low solute concentration to high solute concentration

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7
Q

when does osmosis stop

A

when the concentration is the same of when hydrostatic pressure builds and opposes further movement

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8
Q

What ions are primarily on the OUTSIDE of cells

A

Sodium, chloride, bicarbonate, and calcium

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9
Q

What ions are primarily on the INSIDE of cells

A

potassium, magnesium, phosphate, and sulfur

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10
Q

what are the 3 primary colloids

A

albumin, globulin, and fibrinogen

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11
Q

colloid oncotic pressure _________ with age and malnutrition

A

decreases

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12
Q

how do colloids influence oncotic pressure

A

increase it

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13
Q

what happens with hydrostatic pressure

A

pushes fluid OUT of the capillary

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14
Q

what is an example of hydrostatic pressure

A

at the capillary level - pushes water out of the vascular space into the interstitial space

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15
Q

what happens with oncotic pressure

A

pulls fluid into the capillaries

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16
Q

what primarily drives oncotic pressure

A

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

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17
Q

what primarily drives hydrostatic pressure

A

blood pressure in the capillaries

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18
Q

what are the causes of HYPOnatremia

A

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

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19
Q

What are the S/S pf HYPOnatremia

A

Confusion / altered LOC
Anorexia, muscle weakness
Can lead to seizures / coma

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20
Q

What is dilutional hyponatremia

A

low sodium as a result of taking in too much water

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21
Q

what are the S/S of dilutional hyponatremia

A

Hypervolemia
Increased BP
Weight gain
Bounding pulse
Increased urine specific gravity

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22
Q

what is depletional hyponatremia

A

low sodium as a result of absolute loss of sodium and fluid

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23
Q

what are the S/S of depletional hyponatremia

A

Hypovolemia
Decreased BP
Tachycardia
Dry skin
Weight loss
Decreased urine specific gravity

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24
Q

what is the general speed to replace sodium, why

A

SLOWLY because if you do it too quickly it causes osmotic demyelination syndrome (irreversible brain damage)

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25
Q

What routes are able to replenish sodium

A

PO and IV

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26
Q

does dilutional or depletional hyponatremia get treated with a fluid restricton

A

dilutional

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27
Q

what are the causes of HYPERnatremia

A

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

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28
Q

What are the S/S of HYPERnatremia

A

Altered LOC/confusion, seizure, coma
Extreme thirst (hyperosmolality)
Dry, sticky, mucous membranes
Muscle cramps

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29
Q

how do you treat hypernatremia

A

If water loss is the cause = add water
If sodium excess is cause = remove sodium

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30
Q

what are the causes of hypokalemia

A

Renal / GI losses (Diuresis, Diarrhea, Ileostomy drainage)
Acid / base disorders

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31
Q

what are the s/s of hypokalemia

A

Cardiac rhythm disturbances = can be lethal
Muscle weakness, leg cramps
Decreased bowel motility - constipation, nausea, ileus

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32
Q

what is the treatment of hypokalemia

A

potassium chloride

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33
Q

what are the causes of hyperkalemia

A

Decreased K+ output (renal failure, not peeing)
Burns, crush injuries, sepsis -> massive cell injury (cells burst = K+ now in the blood)
Medications

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34
Q

what are the s/s of hyperkalemia

A

Cardiac rhythm disturbances
Muscle weakness, cramps
Abdominal cramping, diarrhea, vomiting

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35
Q

how do you treat hyperkalemia

A

Kayexalate / sodium polystyrene sulfonate or D50 / insulin

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36
Q

is D50 / insulin a permanent solution for hyperkalemia

A

no it is temporary

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37
Q

what are the causes of hypomagnesemia

A

Diuresis, GI / renal losses, limited intake (starving or fasting), alcohol abuse, pancreatitis, hyperglycemia

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38
Q

what are the s/s of hypomagnesemia

A

Hyperactive reflexes, confusion, cramps, tremors, seizures
Nystagmus

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39
Q

what are the treatment routes available for hypomagnesemia

A

IV or PO

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40
Q

what are the causes of hypermagnesemia

A

Increased intake accompanied by renal failure
Chronic renal failure who takes milk of magnesium for constipation

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41
Q

what are the s/s of hypermagnesemia

A

Lethargy, floppiness, muscle weakness, decreased reflexes, flushed/warm skin, [deceased pulse/BP - mag must be REALLY high]

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42
Q

what is the treatment for hyperkalemia

A

stop replacement if chronic intake

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43
Q

what are the causes of hypocalcemia

A

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

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44
Q

what are the s/s of hypocalcemia

A

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)

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45
Q

how do you treat hypocalcemia

A

IV (only through a central line) or PO

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46
Q

what are the causes of hypercalcemia

A

Hyperparathyroidism, cancers (lung, breast, hematologic), immobility, overdose of antacids (like tums)

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47
Q

what are the s/s of hypercalcemia

A

Calcium acts like a sedative = fatigue, lethargy, confusion, weakness, leading to seizures, coma
kidney stones

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48
Q

How do you treat hypercalcemia

A

Adequate hydration
Diuretics and NaCl
Dialysis in renal failure

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49
Q

what are some of the things that calcium is responsible for

A

Enzyme reactions
Membrane potentials / nerve excitability
Hormone, NT, and chemical mediator release
Influences cardiac contractility and automaticity
Needed for blood clotting

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50
Q

what are the causes of hypophosphatemia

A

Decreased absorption
Antacids overdose
Severe diarrhea
Increased kidney elimination

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51
Q

what is refeeding syndrome

A

if someone is starving for a long time, then they get food or tube feedings -> can cause electrolyte imbalance (WANT TO INTRO SLOWLY)

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52
Q

what are the s/s of hypophosphatemia

A

severe ones: Tremor, paresthesia, confusion - coma, seizure, muscle weakness, joint stiffness, bone pain, hemolytic anemia, platelet dysfunction, impaired WBC function

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53
Q

how do you treat hypophosphatemia

A

IV or PO

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54
Q

what are the causes of hyperphosphatemia

A

Kidney failure
Laxatives / enema with phosphorus
Shift from intra to extracellular compartment (Massive trauma, Heat stroke)
Hypoparathyroidism

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55
Q

what are s/s hyperphosphatemia

A

Usually asymptomatic but can have Muscle spasms, paresthesia, tetany

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56
Q

what are the 3 modes of transmission for fungal infections

A

implantation (under the skin after injury), inhalation (airborne spores), and from taking antibiotics

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57
Q

who is more likely to get a fungal infection

A

elderly and immuno-compromised patient

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58
Q

what are dermatophytes

A

fungi that cause superficial skin infections

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59
Q

what are the characteristics of tinea pedis

A

Dry, scaling pruritic lesions
May only affect skin in the web space between the toes

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60
Q

if someone has tinea pedis - where is that located

A

on the feet (this is athletes foot)

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61
Q

what are the risk factors for tinea pedis

A

Coming into contact with infected skin or fungus in the environment (locker rooms, dirty showers)

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62
Q

how to prevent tinea pedis from starting

A

Use of shower shoes, cleaning tub/shower after each use (goal is to minimize transmission)

63
Q

how do you diagnose tinea pedis

A

cultures

64
Q

how do you treat tinea pedis

A

topical antifungal (OTC)

65
Q

what does tinea capitis affect

A

Can affects scalp, eyebrows, or eyelashes

66
Q

what are the characteristics of tinea capitis

A

Scaly erythematous lesion and hair loss
May cause permanent alopecia (baldness)

67
Q

how do you treat tinea capitis

A

PO systemic antifungals bid for 4-6 weeks
Topicals are not effective

68
Q

what does the tinea versicolor affect

A

skin of the upper chest, back, and/or arms

69
Q

what causes tinea versicolor

A

a type of yeast that lives naturally on your skin but something has caused an overgrowth of it

70
Q

what are the risk factors of tinea versicolor

A

hot climate, sweating a lot, oily skin, weakened immune system, NOT CONTAGIOUS

71
Q

what are the characteristics of tinea versicolor

A

acidic bleached spots that cause skin discoloration (can be white, pink, red, or brown

72
Q

where can you find a candidiasis infection

A

in the mouth (thrush) or the vagina (yeast infection)

73
Q

what are the risk factors of a candidiasis infection

A

Immunosuppression (iatrogenic / acquired), antibiotic use

74
Q

what dose a candidiasis infection look like

A

May appear as white lesions the in the mouth
Beefy red satellite lesions in intertriginous area (skin folds)

75
Q

how do you treat a candidiasis infection

A

with topical antifungal

76
Q

how do you treat a systemic fungal infection

A

with aggressive treatment with PO or IV antifungals

77
Q

what is characteristic for melasma

A

dark macules on the face

78
Q

who is melasma more common in

A

women

79
Q

what is the treatment for melasma

A

avoiding the sun, bleaching creams with hydroquinone, tretinoin / retin-A (vitamin A derivatives)

80
Q

what happens with vitiligo

A

pigment disappears from a patch of skin due to abnormalities in the production of melanin

81
Q

what is the treatment for vitiligo

A

there is none

82
Q

do the areas of vitiligo spread

A

yes

83
Q

what reactivates the herpes zoster virus

A

stress, illness, or immunosuppression

84
Q

what is the prodromal stage of the herpes zoster virus infection

A

burning / tingling along the dermatome

85
Q

what are the characteristics of a herpes zoster flare up

A

vesicles on red base that follow along a dermatome but are asymmetric and do not cross the midline, painful

86
Q

is herpes zoster contagious

A

yes, it can be spread to people who have never had chicken pox and who haven’t had the vaccine

87
Q

how long does it take a herpes zoster flare up to go away

A

2-3 weeks

88
Q

how do you treat herpes zoster flare up

A

with anti-virals

89
Q

what is one specific long-term complication from the herpes zoster virus

A

persistent neuralgia pain in the area where the rash was

90
Q

what are the 2 causative agents for impetigo

A

staphylococci and streptococci

91
Q

is impetigo contagious

A

yes

92
Q

what is the appearance of an impetigo bacterial infection

A

vesicles, pustules, honey-colored crust with red base around the nose

93
Q

what is the treatment for impetigo bacterial skin infections

A

topical antibacterials

94
Q

what is an abscess

A

inflamed skin with a collection of pus underneath (usually has raised and palpable borders)

95
Q

how is an abscess treated

A

incision and drainage followed by antibiotics

96
Q

what is a furuncle

A

bacterial infection of the hair follicle

97
Q

how do you treat carbuncles and furuncles

A

incision and drainage, followed by antibiotics

98
Q

what are the potential causes of cellulitis

A

insect / animal bite, an initial injury / wound that becomes infected and spreads to surrounding tissue

99
Q

is cellulitis contagious

A

no

100
Q

what is the appearance of cellulitis

A

red, painful, swollen, warm to touch - may have blisters

101
Q

how to treat cellulitis

A

PO systemic antibiotics, IV depending of severity

102
Q

how does a community acquired-MRSA infection usually begin

A

as a painful boil

103
Q

who is at risk specifically for community acquired MRSA

A

high school wrestlers, child-care workers, and people who live in crowded conditions

104
Q

what are the symptoms of a MRSA infection

A

warm to touch, purulent drainage, fever, abscess

105
Q

what is the treatment for hospital and community acquired MRSA

A

hospital = IV vancomycin
Community = bactrim

106
Q

what are actinic keratosis

A

benign lesions (rough, scaly, red plaques) that are due to damage by UV rays

107
Q

what are solar lentigos

A

benign lesions that are also known as liver / age spots

108
Q

who is more likely to get skin cancer

A

women before the age of 49 have a higher likelihood - but men have a higher likelihood after that

109
Q

the likelihood of developing basal neoplastic lesions increases with what

A

sun exposure

110
Q

what are the characteristics of basal neoplastic lesions

A

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

111
Q

what increases the likelihood of developing squamous cell neoplastic lesions

A

sun exposure

112
Q

what are the characteristics of squamous cell neoplastic lesions

A

red and scaling, slightly elevated with an irregular border

113
Q

what is the rate of metastases for melanoma

A

high

114
Q

other than on the skin where else can melanoma form

A

in the eyes and under the fingernails

115
Q

what are the risk factors of developing melanoma

A

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

116
Q

how do you assess lesions

A

ABCDEE

117
Q

is eczema contagious

A

no

118
Q

what are the characteristics of eczema

A

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

119
Q

what are the treatments for eczema

A

Lotions / creams to keep moist
Cold compress
OTC hydrocortisone cream (can use behind the counter if severe enough)
Immune modulator medications

120
Q

erythrocytes are

A

red blood cells

121
Q

what are the different types white blood cells

A

Neutrophils, Lymphocytes, Monocytes, Eosinophils, Basophils

122
Q

granulocytes release _________ _________.

A

immune mediators

123
Q

what WBC is the first to arrive at a site with inflammation

A

neutrophils

124
Q

bands vs segs (neutrophils)

A

band = immature
segs = mature

125
Q

when would you see an increase in neutrophil count

A

acute bacterial infections and trauma

126
Q

what is the “shift to the left” phenomenon with neutrophils

A

in early / acute stages of infection, there are a higher proportion of bands

127
Q

what are lymphocytes

A

B - and T - cells

128
Q

when would you see an increase in lymphocytes

A

chronic bacterial infection and acute viral infections

129
Q

when would you see an increase in monocytes

A

with bacterial infections and cancer

130
Q

when would you see an increase in eosinophils

A

allergic reactions and parasitic infections (think wheezes, worms, and weird diseases)

131
Q

when would you see an increase in basophils

A

allergic reactions

132
Q

if someone has a low Hgb, what could cause that

A

bleeding, B12 deficiency, cancers, kidney/liver disease

133
Q

if someone has a high Hgb, what could cause that

A

COPD, dehydration, shock

134
Q

what precautions can be taken to protect those with leukopenia

A

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

135
Q

what causes infectious mononucleosis

A

epstein-barr virus

136
Q

what is the primary mode of contact for infectious mononucleosis

A

saliva

137
Q

what population is more likely to get infectious mononucleosis

A

teens / young adults

138
Q

what happens in infectious mononucleosis

A

there is atypical lymphocyte proliferation

139
Q

what is the onset and incubation of infectious mononucleosis

A

onset - slow
incubation - 4 -8 weeks

140
Q

what are the clinical manifestations of infectious mononucleosis

A

swollen lymph nodes, hepatitis, splenomegaly

141
Q

if you are looking at lab values for a patient with infectious mononucleosis, what would you see

A

WBC increased (lots and lots of lymphocytes)

142
Q

what are the clinical manifestations of Myelodysplastic

A

anemia, infection, spontaneous bleeding / bruising

143
Q

what happens in the case of leukemia

A

WBC are immature and unregulated - then they proliferative rapidly in bone marrow and then go to spleen and lymph nodes

144
Q

what type of leukemia is most common in children

A

acute lymphocytic leukemia

145
Q

what type of leukemia is most common in adults

A

chronic lymphocytic leukemia

146
Q

what are s/s of acute leukemia

A

decreased (mature) WBC, decreased RBC, and decreased platelets

147
Q

what is the onset of acute leukemia

A

sudden

148
Q

what is the onset of chronic leukemia

A

insidious

149
Q

what s/s would you see with chronic lymphocytic leukemia

A

fatigue, weight loss, anorexia, infections

150
Q

what s/s would you see with chronic myelocytic leukemia

A

fatigue, weight loss, diaphoresis, bleeding, abdominal discomfort (because of enlarged spleen)

151
Q

what distinctive type of cell can be found with hodgkin’s lymphoma

A

reed-sternberg cell

152
Q

is hodgkin or non-hodgkin’s lymphoma more likely to spread

A

non-hodgkins

153
Q

what happens with plasma call cancer

A

M protein proliferates -> increases osteoclasts (which breakdown bone)

Pathopharmacology Intro (6 decks)

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