Module 1 Flashcards

1
Q

most common skin condition in USA

A

acne vulgaris

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2
Q

Acne vulgaris has the highest incidence among individuals aged

A

12 to 25 years, with incidence peaking at 15 years of age.

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3
Q

closed comedones

A

(“whiteheads”

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4
Q

open comedones

A

blackheads

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5
Q

Although androgen excess may lead to acne formation

A

, most individuals with acne do not overproduce androgens. However, their pilosebaceous glands are likely hypersensitive to these hormones and more prone to retention hyperkeratosis

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6
Q

mild acne

A

, lesions are primarily noninflammatory comedones with occasional small papules.
face, chest, neck

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7
Q

moderate acne

A

, lesions are mainly inflammatory lesions such as papules and pustules. The papules range in size from a few millimeters to one-half centimeter. The color of the acne papules in light-skinned patients ranges from light pink to bright red.

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8
Q

Scarring is more likely with

A

larger and deeper pustules

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9
Q

severe acne

A

severe acne, or nodulocystic acne, lesions are mainly nodules and cysts. This form of acne always results in scar formation
more common in males

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10
Q

acne conglobat

A

a is severe cystic acne in which nodules, cysts, and abscesses develop; lesions are predominantly located on the trunk area instead of the face. Females with acne conglobata should be evaluated for polycystic ovary syndrome (PCOS)

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11
Q

acne fulminan

A

s is rare and is seen in young adolescent males. This condition is characterized by acute onset of multiple painful, ulcerated acne lesions, along with systemic symptoms such as fever, chills, malaise, and generalized joint and muscle aches.

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12
Q

rosacea

A

Rosacea, previously termed “acne rosacea,” should be ruled out. Rosacea is more common in adults and older patients and is located more centrally on the face, cheeks, chin, and nose. Comedones are never found in rosacea. There is a tendency for easy flushing in response to alcohol or heat. Telangiectasias (dilations of small groups of superficial blood vessels) may be present at the skin surface. Rosacea can be accompanied by eye complaints such as excessive dryness and irritation, and it is more common in patients of Irish, Scottish, or English descent.

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13
Q

hot tub folliculitis

A

“hot tub folliculitis” (folliculitis lesions caused by Staphylococci), which appears within 1 to 4 days after hot tub use, due to insufficient temperature and inadequate chlorination of the water. Patients will complain of small red pustules that are occasionally pruritic. Folliculitis is located on the areas of the body that were immersed in the water, such as the lower torso, buttocks, and legs.

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14
Q

primary goal of acne treatment

A

is to prevent and/or minimize scarring and permanent pigmentation changes

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15
Q

topical tx for comedonal acne

A

topical retinoids (Retin-A)
dryness, erythema, scaling

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16
Q

topical tx inflammatory acne

A

topical abx
applied once-twice daily, refrigerate when stored

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17
Q

Systemic Antibiotic and Hormonal Treatment of Moderate to Severe Acne

A

if have not responded to topical meds x2-3 months
moderate-severe
doxycycline, minocycline

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18
Q

doxycycline

A

take with full glass of water
se: photosensitive, GI upset
do not take with antacids, dairy product, iron vitamins

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19
Q

severe acne tx

A

derm referral

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20
Q

tretinoin tx

A

0.5mg/kg daily in two divided doses, increase gradually
SE: dry skin, hypertriglyceridemia

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21
Q

acne f/u

A

every 4-6 weeks to evalaute response

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22
Q

Rosacea is characterized by flare-ups that include three cutaneous components

A

the first component is vascular in nature, with persistent erythema that primarily involves the central face
he second component is cutaneous and involves the development of recurrent acneiform, erythematous papules and pustules around the central face. The third component consists of connective tissue hyperplasia around the central face with discrete sebaceous gland hyperplasia, consisting of persistent yellow papules particularly around the nose

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23
Q

rosacea tx

A

metronidazole cream, may take 6-8 weeks to work
ABX if flare (tetracycline, minocycline, doxycycline)

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24
Q

Seborrheic keratosis

A

is one of the most common noncancerous skin growths seen in older adults. It is characterized by benign, warty-appearing growths that are usually found on the trunk, but they may also be seen on the hands and face. They develop in both sun-exposed and sun-protected areas

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25
Q

Seborrheic keratosis tx

A

does not require tx
removal if symptomatic

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26
Q

ABCDEs of malignant melanoma.

A

A = asymmetry

B = border irregularity

C = color change

D = diameter larger than a pencil eraser (greater than 6 mm)

E = an evolving lesion (changing over time); may also be used for elevated, as in a raised lesion

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27
Q

Actinic keratosis (AK

A

), also called solar keratosis and senile keratosis, is the most common precancerous skin lesion found in lighter-skinned (white) patients. They are found on sun-exposed areas of skin that have been damaged by cumulative sun exposure
rough or scaly rash
removal indicated

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28
Q

All melanomas should be tested for mutations in

A

BRAF, a gene involved in cell growth signaling,

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29
Q

Basal cell carcinoma

A

(BCC) is a malignant tumor of the skin that originates in the basal cells of the epidermis. It is a slow-growing and locally invasive tumor that rarely metastasizes. It represents the beginning of a continuum of skin cancers in both severity and mortality.

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30
Q

Squamous cell carcinoma

A

(SCC), a malignant tumor originating from keratinocytes, can invade the dermis and occasionally metastasize to distant sites.

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31
Q

more common of the two nonmelanomatous skin cancers and the most common type of skin cancer overall

A

basal cell

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32
Q

The most important risk factor for both BCC and SCC is

A

chronic accumulated sun exposure

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33
Q

A typical patient with nonmelanomatous skin carcinoma is an adult or elderly patient who presents with

A

complaints of a spot or a bump that is getting larger or a sore that is not healing. Often the lesion appears as a thick, rough patch that may bleed if scratched or scraped.

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34
Q

surgery has the highest cure rate for both BCC and SCC.

A

Mohs microsurgery

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35
Q

Refractory errors include

A

myopia, hyperopia, astigmatism, and presbyopia

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36
Q

what is responsible for central visual acuity

A

macula of retina, most important portion of retina for distinguishing visual details

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37
Q

Light ray convergence in front of the retina causes

A

myopia, or near-sightedness

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38
Q

If light rays converge posterior to the retina, the patient is

A

hyperopic, or farsighted.

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39
Q

if light rays focus on two separate lines rather than a single point, the patient has .

A

astigmatism

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40
Q

refractive error presentation

A

change in vision, headache
gradual onset
not typically accompanied by pain
worsened visual acuity

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41
Q

the lens of eye cannot

A

shed unviable cells

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42
Q

3 types of cataracts

A

nuclear- significant near sightedness
cortical- no significant impairment to vision
posterior- haze, severe glare in bright light, associated with steroid use, faster progression

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43
Q

Age-related cataracts tend to be

A

bilateral in nature and may manifest as blurred or distorted vision, with complaints of a glare when driving at night or in bright light

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44
Q

Glaucoma is defined as

A

a group of diseases characterized by progressive damage to the optic nerve, resulting in optic nerve atrophy and blindness, most typically associated with elevated intraocular pressure

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45
Q

most common glaucoma

A

open angle, is characterized as a chronic form of the disorder that, before loss of peripheral visual fields, is asymptomatic. It has an excellent prognosis if treated early and appropriately

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46
Q

angle closure glaucoma

A

most often associated with acute episodes of significant eye pain, redness, and acute visual loss, which, if untreated, may rapidly lead to permanent blindness.

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47
Q

most common cause blindness in African Americans

A

glaucoma

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48
Q

open angle glaucoma presentation

A

asymptomatic until optic nerve damage advanced
gradual onset, slow painless bilat periph vision loss, poor night vision

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49
Q

angle-closure glaucoma

A

a rapid onset, with unilateral pain and pressure, blurred vision, seeing halos around lights, and photophobia, followed by loss of peripheral vision, subsequently followed by central vision loss
unreactive pupil

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50
Q

Normal intraocular pressure is

A

12 to 22 mm Hg.

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51
Q

tx goal glaucoma

A

prevent progression of damage
decrease intraocular pressure

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52
Q

1st line therapy glaucoma

A

beta blocker or prostaglandin

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53
Q

meds given during acute glaucoma attak

A

diamox or IV mannitol

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54
Q

Diabetic retinopathy

A

is a noninflammatory disorder of the retina that develops in patients with diabetes mellitus.

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55
Q

3 stages diabetic retinopathy

A
  1. background diabetic retinopathy, (2) preproliferative diabetic retinopathy, and (3) proliferative diabetic retinopathy.
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56
Q

leading cause of new cases of legal blindness among Americans aged 20 to 64

A

diabetic retinopathy

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57
Q

Almost all patients with diabetes will develop background diabetic retinopathy after they have had diabetes for at least .

A

20 years

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58
Q

background diabetic retinopathy fundoscopic exam

A

, microaneurysms, intraretinal hemorrhage, macular edema, and lipid deposits may be apparent.

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59
Q

The only pharmacologic agent that has been found to slow the progression of diabetic retinopathy is

A

lisinopril, an angiotensin-converting enzyme inhibitor.

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60
Q

the leading cause of blindness in patients older than 60 years

A

macular degeneration

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61
Q

dry macular degeneration

A

characterized by slow, progressive atrophy and degeneration of the retina

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62
Q

wet macular degeneration

A

new blood vessels develop under the retina in the macula, causing a sudden distortion or loss of central vision

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63
Q

Vision that corrects with the pinhole test implies an

A

uncorrected refractive error.

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64
Q

hyperthyroidism

A

includes a heterogeneous group of conditions characterized by the excessive secretion and synthesis of one or both of the thyroid hormones thyroxine (T4) and triiodothyronine (T3).

65
Q

hyperthyroidism more common in

A

women than men (8:1)
20-40 yr olds

66
Q

Graves’ dx

A

by far the most common cause of spontaneous hyperthyroidism in the United States. An autoimmune disorder characterized by autoreactive, agonistic antibodies to the thyroid-stimulating hormone (TSH) receptor,
most common hyperthyroid during pregnancy

67
Q

Subacute thyroiditis

A

most common cause of thyrotoxicosis
Characterized by glandular inflammation and follicular cell destruction, it is thought to be of viral etiology, frequently occurring following an acute viral infection.

68
Q

hyperthyroid clinical presentation

A

anxiety, nervousness, diaphoresis, fatigue, heat intolerance, palpitations, weight loss, and insomnia. In situations in which the thyroid tissue has become enlarged, the patient may complain of fullness or pressure in the neck. Additional symptoms include weakness, exercise intolerance, tremors, lower extremity edema, weight loss in the presence of an increased appetite, menstrual irregularities, frequent bowel movements or diarrhea, and exertional dyspnea.

69
Q

thyroid acropachy

A

Patients with long-standing hyperthyroidism may also have clubbing of the digits and signs of new bone growth in the hands, termed

70
Q

thyroid storm

A

fever
n/v, abdominal pain
agitation, severe
elevated ft4
TX: PTU

71
Q

hyperthyroid labs

A

TSH less than 0.35
FT4 >12.5

72
Q

tx of choice for hyperthyroidism

A

radioactive iodine

73
Q

tx of subacute thyroiditis

A

beta adrenergic blocking meds, NSAIDs
if unresponsive to above, steroids

74
Q

most common worldwide cause of thyroid disorders is

A

iodine deficiency,

75
Q

most common cause hypothyroidism USA

A

Hashimotos thyroiditis

76
Q

hypothyroidism clinical presentation

A

fatigue, dry skin, slight weight gain, cold intolerance, constipation, and heavy menses. Myalgia, muscle cramps, headaches, and weakness

77
Q

diagnostic test for Hashimotos thyroiditis

A

high (1;400) anti TPO antibody titer

78
Q

hypothyroidism tx

A

levothyroxine, 1.6 mcg/kg per day for full replacement
take in morning on empty stomach, avoid nighttime insomnia

79
Q

lab for hypothyroidism after starting tx

A

TSH in 4-8 weeks

80
Q

myxedema coma

A

—a life-threatening state of multiorgan failure, characterized by progressive respiratory depression, decreased cardiac output, and fluid and electrolyte abnormalities (including hyponatremia)—or even death, result from untreated hypothyroidism x10-15 yrs

81
Q

target TSH level

A

0.3-2.4

82
Q

major risk factor for thyroid cancer

A

exposure to ionizing radiation

83
Q

major symptom of thyroid cancer

A

lump/nodule in neck, typically painless

84
Q

Cushing’s syndrome

A

persistent inappropriate hypercortisolemia.
pituitary adenomas secrete excessive amounts of ACTH. The hypersecretion is random, episodic, and does not follow the usual circadian rhythm of ACTH secretion in terms of amplitude and duration

85
Q

most frequent cause of Cushing’s syndrome,

A

however, is prolonged administration of exogenous glucocorticoid hormones—an iatrogenic etiology that is ACTH-independent

86
Q

cushing dx clinical presentation

A

weight gain, back pain, headaches, skin changes, and muscle weakness. Women may complain of menstrual irregularities and hirsutism, and men often report decreased libido and impotence.
“moon face”

87
Q

cushing dx diagnostic tests

A

urine free cortisol (at least two measurements), late-night salivary cortisol (two measurements), 1-mg overnight dexamethasone suppression test (DST), or a longer low-dose DST (2 mg/day for 48 hours).

88
Q

Addison’s dx

A

primary adrenal insufficiency, failure of adrenale glands to produce hormones b/c of problem in bland
autoimmune destruction of adrenal cortex

89
Q

addison dx clinical presentation

A

fatigue, weakness, anorexia, weight loss, nausea, abdominal pain, diarrhea, hypoglycemia, and hypotension (particularly orthostatic hypotension

90
Q

most common endocrine disorder

A

diabetes

91
Q

DM type I

A

a metabolic disorder characterized by severe insulin deficiency resulting from beta cell destruction, which produces hyperglycemia due to the altered metabolism of lipids, carbohydrates, and proteins.

92
Q

immune mediated DM (type 1A)

A

caused by autoimmune destruction of insulin-producing pancreatic beta islet cells. The triggering factor in the development of type 1 DM is thought to be an infection or toxic insult in persons with a genetic predisposition. The most commonly identified infectious agents are congenital rubella
90% of cases

93
Q

The classic symptoms of type 1 DM are

A

polyuria (increased urination), polydipsia (increased fluid intake due to excessive thirst), nocturnal enuresis, polyphagia with paradoxical weight loss (due to reduced glucose metabolism, despite increased consumption), visual changes (especially blurred vision), and eventual fatigue, weakness, and anorexia
repeated or complicated infections

94
Q

diagnosis of DM

A
  • Glycosylated hemoglobin (A1C) of 6.5% or higher
  • Symptoms of diabetes (e.g., polyuria, polydipsia, weight loss) plus a random plasma glucose level of 200 mg/dL or higher
  • Fasting plasma glucose level of 126 mg/dL or higher (following 8 hours of no caloric intake)
  • Two-hour plasma glucose level of 200 mg/dL or higher during an oral glucose tolerance test (OGTT) with a 75-g glucose load

first 3- confirm with repeat testing

95
Q

glucose level goal for DM before meals

A

80-130

96
Q

glucose level goal for DM 2h after meal

A

180 or less

97
Q

Optimal SMBG for patients with type 1 DM is

A

three to four times a day—before each meal and before bedtime

98
Q

hypoglycemia symptoms

A

diaphoresis, tachycardia, hunger, shakiness, altered mentation (ranging from an inability to concentrate to frank coma), slurred speech, and seizure
<70 BS

99
Q

appropriate foods for hypoglycemia tx

A

1/2 cup of fruit juice
6 oz regular soda
1 cup milk
glucose tabs
check blood sugar 15m after tx

100
Q

Somogyi effect

A

, for example, is a unique combination in which a diabetic patient develops hypoglycemia during the night with rebound hyperglycemia in the morning

101
Q

type 1 DM exercise guidelines

A
  • Check blood glucose before, every 30 to 60 minutes during, and after exercise.
  • Avoid exercise if fasting glucose is more than 250 mg/dL and ketosis is present or if the glucose level is more than 300 mg/dL, regardless of whether ketosis is present.
  • Consume additional carbohydrate if the glucose level is less than 100 mg/dL and as needed to avoid hypoglycemia.
  • Identify when changes in insulin dose or food intake are necessary.
102
Q

type 2 DM

A

abnormal secretion of insulin, resistance to the action of insulin in the target tissues, and/or an inadequate response at the level of the insulin receptor. Type 2 DM reduces life expectancy because of complications that are affected by the duration of DM, the degree of blood glucose control, and other cardiovascular risk factors such as smoking and hypertension.

103
Q

Type 2 DM is associated with two physiological abnormalities:

A

insulin resistance and impaired insulin secretion by the beta islet cells of the pancrea

104
Q

If weight loss is indicated for type II DM

A

, a moderate caloric restriction of 500 to 750 calories less than the patient’s average daily intake, as calculated from a detailed food history (which can be tracked with a food diary), can be instituted.

105
Q

DM exercise recommendations

A

150 min/week of moderate-intense physical exercise
at least 3 days/week

106
Q

biguanide

A

metformin
works by suppressing excessive hepatic glucose production and by increasing glucose utilization in peripheral tissues
contra: kidney dx
500mg/day with meal x1 week, then bid

107
Q

Sulfonylureas

A

glucotrol
work by stimulating pancreatic insulin secretion; thus, pancreatic beta cells must still be producing insulin in order for sulfonylureas to be effective, as they do not reduce insulin resistance
higher risk of hypoglycemia
lowest possible dose with once daily at breakfast

108
Q

thiazolidinediones

A

actos
work by sensitizing peripheral tissues to insulin by activating the nuclear glitazone receptor (also known as peroxisome proliferator-activated receptor-γ), which lowers serum glucose levels without increasing pancreatic insulin secretion
caution if risk for fracture

109
Q

DPP4-I

A

Januvia
prolong and enhance the activity of incretins, which suppresses glucagon secretion and modestly reduces A1C by 0.5% to 0.8
nasopharyngitis, abdominal pain

110
Q

GLP1 analogues

A

Victoza
enhance insulin secretion in a glucose-dependent manner in response to food intake. GLP1 analogues also improve insulin sensitivity, increase beta cell mass, and decrease glucagon secretion.

111
Q

SGLT2

A

Invokana
block the activity of SGLT proteins in the renal proximal tubule, thereby reducing glucose reuptake and increasing the secretion of glucose in the urine. The medication is given once daily. Patients often lose weight due to the loss of sugar through the kidney
increase risk of UTI

112
Q

adult hypoglycemia

A

<55

113
Q

Anemia

A
  • can mean any of several problems that involve suboptimal red blood cell (RBC) number or function
  • World Health Organization (WHO) identifies anemia as a hemoglobin of less than 13.0 g/dL (less than 42% Hct) in men and less than 12.0 g/dL (less than 36% Hct) in women
114
Q

microcytic anemia

A
  • Linked to nutritional deficiencies
  • MCV value of less than 80 fL
  • incidence is high among women of childbearing age, with up to one-third of pregnant women developing anemia in the third trimester
115
Q

microcytic anemia causes

A

inadequate oral intake or GI uptake of dietary iron
anemia of chronic disease
thalassemia
sideroblastic anemia

116
Q

o Inadequate oral intake or GI uptake of dietary iron

A

microcytic anemia
 Most common cause
 Monitor especially with vegans/vegetarians
 Dx- Iron deficiency- ferritin
 Tx- increase dietary iron (animal protein, legumes, dark green leafy veggies) , supplement if needed
 If supplement, 325mg iron tid
 Recheck level 2-4 weeks later
 Parental iron only if failed oral iron supplements
 F/u- CBC

117
Q

anemia of chronic disease

A

microcytic anemia
 Caution for malignancy
 Tx- underlying disease. Recommend parental iron
 Monitor hgb twice weekly for 2-6 weeks after increase in dose
 Consider epogen or Procrit if needed
 Chronic use of NSAIDs

118
Q

thalassemia

A

microcytic anemia
 Depletion or mutation in genes that code for subunits of the protein component in hgb
 DX- CBC, Hgb electrophoresis
 “vigilance” concerning hematological markers

119
Q

sideroblastic anemia

A

microcytic anemia
 Host of molecular defects that affect biosynthesis of heme moiety of hgb. Iron delivered appropriately, but not incorporated into uptake
 DX- Prussian blue stain of a bone marrow aspirate
 RBC transfusion may be required

120
Q

subjective anemia presentation

A

o Tachycardia, fatigue, SOB, palpitations, poor concentrations, dizziness

121
Q

objective anemia presentation

A

o Hgb below 10- fatigue, sallow colored skin, pale mucous membranes, tachycardia, tachypnea

122
Q

anemia screening recommendations

A

if pregnant
children at 1 yr
if fatigue, generalized weakness, SOB with exertion, pallor, dizziness, fainting, chest pain, HA, evidence of GI bleed

123
Q

Hct is __x value of Hgb

A

3

124
Q

Norocytic Anemia

A
  • MCV = 81–99 fL
  • presumed mechanism for this is through increased phagocytosis by macrophages, which results in increased clearance of erythrocytes from the circulation
  • increase in plasma volume
  • increased blood volume loss
  • recent history of trauma
  • DX: CBC, absolute retic count, periph smear
  • Retic count higher in proliferative normocytic anemia
  • TX: focus on cause of disorder
  • Symptomatic first
  • Correct, stabilize, prevent underlying cause (ACD, AIHA, heart valve abnormalities, vasculitis, HTN, HELLP syndrome, DIC)
125
Q

AIHA tx

A

oral or IV steroid tx- 1-2 mg/kg in divided dose, then decreased. Supplement with vitamin D, calcium, folic acid, bisphosphonates for prophylaxis against osteoporosis
o Possible splenectomy if steroids ineffective
o DX- Coombs test positive

126
Q

Vasculitis tx

A

o Tx- high dose prednisone
o Additional immunosuppressive therapy (Cytoxan) may be needed

127
Q

DIC tx

A

o Tx- heparin and plt transfusion- admission to hospital

128
Q

Macrocytic Anemia

A
  • anemia with an MCV equal to or greater than 100 fL
  • greatest among people of northern European and Caucasian descent. Incidence increases past 60 years of age
129
Q

causes of macrocytic anemia

A

b12 def
folate def
antimetabolite meds
misc drugs- etoh, liver disease

130
Q

vitamin b12 def anemia

A

macrocytic anemia
Pernicious anemia is a macrocytic anemia caused by a hereditary autoimmune disorder in which destructive antibodies are directed against intrinsic factor
 Caution with vegan/vegetarian
 Tx- oral supplementation- 1,000mcg/day until b12 levels achieved
 If needed, parenteral B12 IM daily x7 days, then weekly x1 month

131
Q

folate def anemia

A

macrocytic anemia
 presents with a low serum folate level and a normal level of vitamin B12. It is almost always related to inadequate dietary intake
 Adequate dietary intake is 50 to 100 mcg/day, except in pregnant women who need 800 mcg/day to prevent neural tube defects during fetal development.
 tx- 1mg/day of supplemental folic acid

132
Q

macrocytic anemia subjective presentation

A

o stomatitis, glossitis, nausea, anorexia, diarrhea, peripheral neuropathies, and malaise

133
Q

macrocytic anemia objective presentation

A

o pale or icteric mucosa, a dry and cracked oropharynx, a thickened and smooth-surfaced tongue, tachycardia, a systolic ejection murmur, tachypnea, and diffuse abdominal tenderness

134
Q

Sickle cell anemia

A
  • Autosomal recessive disorder
  • Dx with sickled cells on peripheral blood smear, positive family hx, recurrent painful episode of vaso occlusive pain, pattern of mutated hgb S on electrophoresis
  • inherited conditions that occur most commonly in people of West African descent
  • initial symptoms typically occur within 1 year of life
135
Q

sickle cell anemia patho

A

o Sickled cells become lodged in microvasculature as small thrombi
o If against vascular membrane, they create occlusion to blood flow
o Ischemic injuries/infarcts cause pain as ischemia continues
o Rate of sickling increases as tissues become hypoxic and acidotic
o Body attempts to compensate with expansion and upregulation of bone marrow
o Microthrombi occurs in many parts of bodies- chest, vertebrae, long bones of legs, leg ulcers
o Organs affected- heart, liver, penis, kidneys, retinopathy, spleen

136
Q

watch if sickle cell anemia

A

splenic sequestration
acute chest syndrome
CVA

137
Q

sickle cell anemia subjective presentation

A

o Severity of anemia, pain. Pain is sudden, characterized as excruciating, lasts several hours- day, unrelieved by rest
o nausea, anorexia, light-headedness, significant anxiety or panic, heart palpitations, and shortness of breath, depression, anxiety

138
Q

sickle cell anemia objective presentation

A

o Low grade fever, point tenderness, guarding, pinpoint pupils, inability to follow command

139
Q

sickle cell anemia DX

A

o CBC with periph blood smear
o Sickle cells will constitutee 5-10% of peripheral blood smear
o Presence of Howell-Jolly bodies
o Indirect bili level

140
Q

sickle cell anemia tx

A

o Folic acid supplementation- 1mg/day, diet rich in vitamin b and C
o Rehydration
o Prophylactic PCN from children 2month- 5years
o UTD on all vaccines
o Packed RBC transfusion in children

141
Q
  • If sickle cell crisis-
A

hospitalization, symptom control of pain, rehydration, O2 supplementation
* Only cure- transplant of stem cells

142
Q

sickle cell anemia f/u

A

every 3 m if stable, seen twice annually by hematologist

143
Q

polycythemia

A
  • Hct greater than 51% in women and 54% in men is characteristic of the condition
  • More prevalent in men older than 70 years of age
  • Causes of relative polycythemia include decreased fluid intake, increased fluid loss from the body, and extravasation (redistribution) of vascular fluid into the tissues
144
Q

Relative polycythemia

A
  • is a condition in which there is a decrease in plasma volume while the total number of circulating erythrocytes remains constant.
    o Almost always dehydration (vomiting, burns, fevers)
145
Q

absolute polycythemia

A

is a condition in which the actual numbers of circulating erythrocytes are increased with a corresponding increase in measured RBC mass
o Primary- polycythemia vera, which is a chronic myeloproliferative disorder caused by an abnormally dividing pluripotential stem cell that leads to a clonal erythrocytosis that is erythropoietin independent, as well as a variable leukocytosis (increased myelocytes) and thrombocytosis
o Secondary- chronic hypoxia, carboxyhemoglobinemia, Cushing’s syndrome, chronic corticosteroid use, erythropoietin-secreting tumors, and cardiopulmonary diseases

146
Q

subjective polycythemia presentation

A

o Chronic cough, cyanosis, hypersomnolence, SOB, headache, blurred vision, weakness, fatigue, irritability, dizziness, and, on occasion, tinnitus

147
Q

objective polycythemia presentation

A

o Erythromelalgia, tendency for thrombosis, hemmorhage
o Dark flushed face

148
Q

tx polycythemia

A

o Relative- rehydrate
o Absolute- progressive phlebotomies

149
Q

leukemia

A
  • neoplastic disease of malignant hematopoietic stem cells that differentiate and proliferate according to specific lineage trajectories that distinguish the types of leukemia as either acute or chronic
150
Q

AML

A

more prominent over age 40

151
Q

ALL

A

o 2-15 years
o B-cell lymphoblasts increase
o Philadelphia chromosome poor prognostic indicator

152
Q

CML

A

o More prominent over 60, median age: 42
o Philadelphia chromosome

153
Q

CLL

A

o > 60 years
o most common leukemia in Western (developed) countries
o increased number of small B lymphocytes

154
Q

acute leukemia subjective presentation

A

o bone and joint pain, as well as fevers, chills, palpitations, shortness of breath, and signs of infection
o skin eruptions, easy bruising, or prolonged bleeding from simple wounds form a significant part of the subjective history.

155
Q

objective presentation acute leukemia

A

o High fever, tachycardia, tachypnea, pale, confusion

156
Q

subjective presentation chronic leukemia

A

o fatigue, night sweats, and low-grade fevers.

157
Q

objective presentation chronic leukemia

A

splenomegaly

158
Q

tx for acute leukemia

A

chemo

159
Q

tx for chronic leukemia

A

“watchful vigilance”