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NCC Board Prep > VUSN Notes > Flashcards

VUSN Notes Flashcards

1
Q

Describes a chronic, inflammatory, debilitating, skin follicular disease involving the apocrine gland-bearing areas of the body, most commonly the axillary, inframammary, and anogenital areas. This condition manifests as deep painful cystic nodules, sinuses, and scarring. It is an acute and chronic follicular occlusive process, just like acne vulgaris, and is analogous to acne mechanica.

A

hidradenitis suppurativa

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2
Q

Most common areas of the body to be affected by hidradenitis suppurativa (3)

A
  • axillary folds
  • inframammary folds
  • anogenital areas
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3
Q

Gestational diabetes refers to onset of diabetes in pregnancy after ____ weeks EGA

A

> 20 weeks

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4
Q

GDMA1

A

controlled with diet and exercise

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5
Q

GDMA2

A

controlled with medication

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6
Q

Exponential increase in insulin resistance occurs when in pregnancy

A

2-3rd trimesters

aka, beyond 14 weeks

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7
Q

Screen all folks for GDM at ____ weeks EGA

A

24-28 weeks

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8
Q

High risk folks who should be screened for DM at the first prenatal visit

A

overweight + any of the following:

  • h/o GDM, macrosomia, stillbirth, or congenital anomalies affecting a prior pregnancy
  • A1c >5.7% (prediabetes)
  • HLD
  • CVD
  • PCOS
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9
Q

Positive 1-hr 50g OGTT screening results

A

> 130-140

if >200, that is diagnostic

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10
Q

Positive 3-hr 100g OGTT diagnostic results

A

need 2 or more abnormal values

  • fasting >95
  • 1hr >180
  • 2hr >155
  • 3hr >140
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11
Q

Are the OGTTs for GDM in pregnancy fasting or non-fasting?

A

1hr 50-g OGTT for screening is not fasting.

3-hr 100g OGTT is fasting

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12
Q

Definition of macrosomia

A

> 4000g

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13
Q

Who should be counseled on c-section with GDM and macrosomia

A

> 4500g

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14
Q

Who should be counseled on c-section with macrosomia but no GDM

A

> 5000g

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15
Q

Recommended home blood sugars for pregnant person with GDM

A

fasting <95
1-hr post prandial <140
2-hr post prandial <120

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16
Q

First line medication for GDM

A

insulin

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17
Q

When to start insulin in someone with GDM

A

> 25-50% of home blood sugars are elevated

OR

if fasting blood sugars are regularly elevated, as these are unlikely to improve with diet alone

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18
Q

Changes to pregnancy monitoring in GDM

A
  • monitor urine for ketones
  • growth US Q3-4 weeks after dx
  • weekly NSTs/BPPs after 32 weeks
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19
Q

Delivery timing in GDM

A
  • GDMA1 = await full term
  • GDMA2 = deliver in 39th week (before 40 weeks)
  • GDM poorly controlled = deliver in 37th or 38th weeks (before 39 weeks)
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20
Q

Changes to postpartum monitoring in GDM

A
  • screen for diabetes or impaired glucose metabolism 4-12 weeks postpartum with a 2-hr 75 OGTT
  • A1c DM screening Q1-3 years for the rest of life
  • screen early for GDM in all future pregnancies
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21
Q

Results on 75-g 2-hr OGTT post partum that diagnose DM

A

fasting >125

2-hr >199

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22
Q

% of folks with pre-gestational diabetes (pre-existing) who will have SAB

A

25%

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23
Q

Changes to pregnancy monitoring if pre-gestational diabetes (pre-existing)

A
  • addtl baseline labs (A1c, TSH, MSAFP, CBC/CMP, 24hr urine PCR, UA with culture)
  • ophthalmology referral at first prenatal visit and 3rd trimester
  • home blood sugar checks 6-8x daily
  • early fetal anatomy US (18-20 weeks)
  • fetal echocardiogram (20-22weeks)
  • monthly growth US starting at 24 weeks
  • twice weekly NST/BPPs starting between 28-32 weeks
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24
Q

Delivery timing in pre-gestational diabetes (pre-existing)

A

Well-controlled: 39th week (before 40 weeks)

Poorly-controlled: deliver in 36th - 38th weeks (before 39 weeks)

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25
Q

How to diagnose hyperemesis gravidarum

A
  • > 3 episodes vomiting/day
  • 5% pre-pregnancy weight loss
  • electrolyte imbalance
  • ketonuria
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26
Q

prevalence of hyperemesis gravidarum

A

1% of all pregnancies

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27
Q

anticipatory guidance regarding hyperemesis gravidarum

A

80% will resolve by 20 weeks

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28
Q

Add’l baseline lab testing to do with hyperemesis gravidarum to assess possible contributory factors

A
  • TSH (thyroid dz)

- h. pylori

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29
Q

Severe HTN

A

> or = 160 SBP

> or = 110 DBP

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30
Q

Gold standard medication for CHTN in pregnancy

A

labetalol

alternative options: nifedipine, methyldopa

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31
Q

Changes to pregnancy monitoring & delivery timing in CHTN

A
  • twice weekly NSTs/BPPs after 32 weeks
  • deliver in 38th or 39th week (before 40w) if no complications
  • if develops superimposed pre-ex, deliver in 34-37th weeks depending on severity
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32
Q

3 methods of defining proteinuria for a pre-eclampsia diagnosis

A
  • 24-hr urine >300mg
  • urine protein/creatinine ratio >0.3 mg/dL
  • 2+ protein on dipstick
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33
Q

Urine dipstick is the least reliable method for determining proteinuria, compared to a spot urine protein/creatinine ratio. What is the likelihood of false positive on dipstick 2+?

A

17% are false positives

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34
Q

Define thrombocytopenia in pre-eclampsia

A

platelet count <100,000/mL

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35
Q

Define impaired liver function in pre-eclampsia

A

AST/ALT elevated to 2x normal (>70)

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36
Q

Define renal insufficiency in pre-eclampsia

A

serum creatinine >1.1mg/dL

or a doubling of the serum creatinine in the absence of other renal disease

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37
Q

What is the pathophysiology behind low platelets in hypertensive disorders of pregnancy?

A

platelets are used to repair endothelial damage

endothelial damage from hypertension&raquo_space; using up all your platelets

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38
Q

What is the pathophysiology behind elevated liver enzymes in hypertensive disorders of pregnancy?

A
  • liver is working overtime to process all of the platelets

- poor blood flow to the liver from vasoconstriction and vascular damage

39
Q

What is the pathophysiology behind pulmonary edema in hypertensive disorders of pregnancy?

A

leaky endothelium s/t endothelial damage from HTN

40
Q

Complications with which you would lean towards delivery at 34 weeks in someone with pre-eclampsia (4)

A
  • ROM
  • IUGR
  • oligohydramnios
  • non-reactive fetal strip
41
Q

All folks at high risk for preeclampsia should be starting on aspirin when during pregnancy

A

after 12 weeks EGA

42
Q

When should you plan for delivery in someone with pre-eclampsia without severe features or fetal complications

A

37 weeks

43
Q

Diagnosis of pre-eclampsia

A

elevated BP > or = 140 / > or = 90 after 20 weeks

PLUS

proteinuria (>300mg in 24 hrs, >0.3 protein/cre ratio, 2+ on dipstick)

OR

end organ damage

  • low platelets (<100,000)
  • renal insufficiency (>1.1 creatine, serum)
  • elevated liver enzymes (>70)
  • new onset headache, unrelieved by OTC measures
  • focal neuro symptoms
  • pulmonary edema
44
Q

Mortality rate with eclamptic seizures

A

15-20%

45
Q

Only cure for eclampsia

A

delivery of the placenta

46
Q

Diagnose gestational HTN

A

new onset HTN (> or = 140/ > or = 90) after 20 weeks EGA with no proteinuria or severe features

47
Q

Anticipatory guidance with gestational HTN

A

BP can be labile, often transient, rarely severe

No medications unless becomes severe

Can usually await full term spontaneous labor if no complications

48
Q

Pre-eclampsia WITH severe features typically onsets when….

A

before 34 weeks

49
Q

Blood type of Rh- or Rh+ is derived from the status of the blood having….

A

antigens against RhD

50
Q

When is RhoGAM routinely given

A

Rh- or unknown status pregnant folks and any of the following:

  • 26-28 weeks for all
  • 2nd dose is given postpartum if infant is determined to be Rh+
  • anytime there is abdominal trauma, bleeding, invasive procedures (e.g., CVS, amnio), or abortion
51
Q

standard RhoGAM dose

A

300mcg IM to deltoid muscle

52
Q

what does the Kleinhauer-Betke test tell you

A

estimates the volume of RBCs transfused; quantifies the amount of fetal RBCs in maternal circulation

this can be useful for knowing the amount RhoGAM dose needed

53
Q

Rh negative inheritance is autosomal….

A

recessive

54
Q

RhoGAM must be given within ______ of a possible exposure in order to be effective

A

<72 hours (3 days)

55
Q

Anticipated fetal outcomes for maternal antibodies to

  • Kell antigen
  • Lewis antigen
  • Duffy antigen

Mnemonic

A

Kell kills
Lewis lives
Duffy dies

Kell and Duffy = severe hemolytic disease

56
Q

Presence of Rh antibodies in pregnancy should always warrant this from the WHNP

A

referral to physician

57
Q

(3) sequelae for the fetus from maternal isoimmunization in a prior pregnancy

A
  • recurrent early spontaneous miscarriage
  • abnormal fetal growth
  • fetal immune hydrops
58
Q

What is fetal hydrops

A

accumulation of fluid within the fetal body compartments stemming from fetal anemia

typically occurs when fetal RBCs are attacked by maternal antibodies (isoimmunization), causing the fetal RBCs to be lysed, causing massive accumulation of fluid in the fetal tissues.

59
Q

Hgb definition of anemia, non-pregnant female

A

<12 g/dL

60
Q

Hgb definition in pregnancy, by semester

A 
1st = <11 g/dL
2nd = <10.5 g/dL
3rd = <11 g/dL
61
Q

Hgb >15 or Hct >45% in 2nd trimester of pregnancy

A

think poor blood volume expansion, as normally hgb/hct would be hemodiluted in 2nd trim

may be associated with HTN, dehydration, smoking, high altitudes

62
Q

% of anemias in pregnancy that are from iron deficiency

A

75%

63
Q

General overview of what is G6PD anemia

A

a drug-induced hemolytic anemia that results from genetic susceptibility (X-linked) to hemolysis of RBCs

Symptoms r/t to this condition are episodic, as a result to periodic exposures to drugs, surgery, infections

Common drugs to provoke exacerbation:

  • sulfonamides
  • nitrofurantoins
  • antipyretics/analgesics

there is no universal screening for this in pregnancy

64
Q

Folks with G6PD anemia in pregnancy need this additional screening every trimester

A

UA with culture and sensitivity, given increased risk for UTI

65
Q

General overview of what is hereditary spherocytosis

A

an inherited hemolytic anemia with autosomal dominant inheritance pattern with variable penetrance. Results from a structural defect in the erythrocyte membrane. The RBCs lose their shape and volume, become spherical in appearance, and these morphological changes reduce the oxygen-carrying capacity of the RBC.

there is no universal screening for this in pregnancy

66
Q

General overview of what is hereditary elliptocytosis

A

An inherited hemolytic anemia with autosomal dominant inheritance pattern and usually mild disease. Results from a defect in the polarization of hemoglobin molecules, causing the RBC to contract along its long-axis becoming rod-shaped, elongated. These morphological changes reduce the hemoglobin-binding affinity of the RBC

67
Q

Thalassemias refer to ______ changes in Hgb production

A

quantitative

Normal hemoglobin is being synthesized at an abnormally slow rate, in contrast to structural hemoglobinopathies which are being produced at a normal rate but the Hgb is not normal in structure

68
Q

Hemoglobin is made up of ____ subchains.

A

4 subchains, 2 alpha and 2 beta

69
Q

[alpha vs. beta] subchains produce most of the adult hemoglobin

A

alpha

70
Q

Racial/ethnic groups with highest proportion of hemoglobinopathies

A
  • mediterranean
  • african
  • middle eastern
  • south east asian
71
Q

most abundant form of fetal hemoglobin

A

hemoglobin F, which has a higher affinity for oxygen than adult hemoglobin

72
Q

Inheritance pattern of the thalassemias

A

autosomal recessive

73
Q

General overview of alpha thalassemia

A

a diagnosis of exclusion, based on the exclusion of iron-deficiency anemia and beta thalassemia

1 alpha chain affected = silent carrier, asymptomatic

2 alpha chains affected = alpha thalassemia minor, mild hypochromic microcytic anemia that is difficult to tell from IDA

3 alpha chains affected = severe

4 alpha chains affected = incompatible with life, stillbirth

there is no universal screening in prenatal care

74
Q

Most common thalassemia encountered in WHNP practice

A

beta thalassemia minor (heterozygous)

75
Q

General overview of beta thalassemia

A

A diagnosis of exclusion, based on the exclusion of IDA (not responding to iron supplementation), low MCV (<80) is the key feature, diagnosed on hemoglobin electropheresis.

Beta thalassemia minor (heterozygous) tends to be minor

Beta thalassemia major (homozygous) typically dies in the first few decades of life, severe disease

there is no universal screening in prenatal care

76
Q

Key feature of thalassemias = MCV that is….

A

low (<80)

77
Q

Normal results on hemoglobin electrophoresis

A 
HgbA1 = 95-98%
HgbA2 = 2-3%
HgbF = 0.8-2%
HgbS = 0%
HgbC = 0%
78
Q

elevated HgbA2 (>3.5%) on hemoglobin electrophoresis, think…..

A

beta thalassemia

79
Q

Prevalence of sickle cell TRAIT (Ss) in African Americans

A

1 in 12

80
Q

Sickle cell disease is autosomal….

A

recessive

81
Q

% of pregnancies ending in miscarriage, stillbirth, or neonatal death if mother has sickle cell disease SS genotype (homozygous)

A

33%

82
Q

Pregnant folks with sickle cell TRAIT require this additional screening every trimester

A

UA with culture (higher risk of asymptomatic bacteruria and UTI)

83
Q

Risks of sickle cell TRAIT for pregnancy

A
  • increased risk of UTI
  • increased risk of asymptomatic bacteruria
  • increased risk of pre-eclampsia suggested in some studies
  • NO increase in risk of miscarriage, perinatal mortality, low birth weight, or GHTN has been found
84
Q

Symptoms in sickle cell DISEASE are related to (3)

A
  • hemolysis
  • vasooclusive disease
  • increased risk for infection
85
Q

WHNP management of pregnant patient presenting in sickle cell crisis

A

hospitalization

86
Q

General overview of hemoglobinopathies C and E in pregnancy

A

Heterozygous for these (trait) is usually asymptomatic and no pregnancy consequences

Homozygous for these (disease) is usually only mild and stable

87
Q

Abnormal antibody production in Antiphospholipid Antibody Syndrome (APLS) leads to increased risk for….

A

blood clots

88
Q

Clinical presentations suggestive of antiphospholipid antibody syndrome (APLS) (4)

A
  • recurrent pregnancy loss
  • severe early-onset pre-Ex
  • abnormal fetal growth
  • unexplained blood clots
89
Q

There is no routine anticoagulation recommended for inherited thrombophilias except in cases of….. (3)

A
  • compound heterozygotes
  • family history of a VTE
  • personal history of a VTE
90
Q

Common types of inherited thrombophilias

A
  • Factor V Leiden (heterozygous, homozygous)
  • Protein C deficiency
  • Protein S deficiency
  • Prothrombin mutation
  • Antithrombin deficiency
  • Homocystein mutation (MTHFR)
91
Q

Who requires endocarditis prophylaxis before birth or any medical procedures (e.g., dental procedure)

A
  • prosthetic (mechanical) heart valve
  • prosthetic (mechanical) material used for a valve repair
  • h/o infective endocarditis
92
Q

Do you require endocarditis prophylaxis in patient with mitral valve prolapse?

A

NO! not anymore

93
Q

Do you require endocarditis prophylaxis in patient with prosthetic heart valve?

A

yes

94
Q

Endocarditis prophylaxis is done with a single dose of ______ 30 min before procedure

A

penicillin

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