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Hospital residence > 40 year old woman > Flashcards

40 year old woman Flashcards

1
Q

What is the number cause of hyperthyroidism?

A

Grave’s Disease

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2
Q

Grave’s disease gender

A

7-8 times more likely to affect women than men

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3
Q

Age of diagnosis of grave’s disease

A

Peak age of diagnosis is between 40-60

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4
Q

What are the causes of dyspnea and hypoxemia in the peripartum period?

A

Origins are predominantly pulmonary or cardiovascular

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5
Q

Pulmonary causes of dyspnea and hypoxemia post partum

A

Common: Pulmonary embolism, pneumonia, aspiration pneumonitis, reactive airway disease
Rare: ARDS, Amniotic-fluid embolism, vasculitis, pulmonary hypertension, pneumothorax

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6
Q

What causes pulmonary embolism in postportam?

A

Stasis, hypercoagulable blood, and vascular/endothelial damage (from vascular compression at delivery or from assisted or operative delivery)

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7
Q

How much does pregnancy affect coagulation of blood?

A
  • Pregnancy is a prothrombotic state with nearly 5x increased risk of VTE
  • The peripartum period is a hypercoagulable state, most likely an evolutionary adaptation to minimize postpartum hemorrhaging
  • Venous thromboembolism occurs in 1 or 2 in 1000 pregnancies and is
    approximately 10 times as likely post partum as during pregnancy
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8
Q

Are tachycardia and bloody sputum diagnostic of pulmonary embolism in a post partum woman?

A

Tachycardia and bloody sputum are consistent with, but not diagnostic
of, pulmonary embolism

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9
Q

Risk of pneumonia during and after pregnancy

A
  • Pregnant women have immune tolerance , which is most likely an
    evolutionary adaptation to preclude maternal rejection of the fetus
  • Immune tolerance , anatomical changes during pregnancy , and the risk
    of aspiration during cesarean delivery increase risk for pneumonia .
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10
Q

Effect of pregnancy on rheumatological diseases

A
  • Improvement in 50-75% of RA patients
  • Flare in 50% of SLE patients
  • Aggravation of APS
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11
Q

Risk of maternal complication in pregnancy in women with rheumatological diseases

A
  • No risk for RA
  • Hematological and renal complication are the most frequent in SLE
  • Thrombosis in APS patients
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12
Q

Risk for pregnancy complications in rheumatological diseases

A
  • Moderate increase in RA
  • Hypertension, pre-eclampsia, and prematurity for SLE
  • Preeclampsia, prematurity, HELLP syndrome in APS
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13
Q

Risk for fetus/neonate in rheumatological diseases

A
  • Very rare for RA
  • Fetal loss, intrauterine growth restriction, low birthweight, and neonatal lupus in SLE
  • Fetal loss, intrauterine growth restriction, low birthweight in APS
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14
Q

Vasculitis in pregnancy and in this particular patient

A
  • The immune tolerant state of pregnancy can also provide a “ holiday ” from vasculitides , which can rebound post partum
  • In this patient, the absence of inflammatory signs and negative tests for ANA and dsDNA make a diagnosis of vasculitis unlikely
  • Results of tests for antineutrophil cytoplasmic antibodies and human
    immunodeficiency virus would be helpful
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15
Q

Embolism in this particular patient

A

CT finding renders a large pulmonary embolism highly unlikely. Emboli
in the small branches of the pulmonary arteries cannot be ruled out, but
is unlikely that these would be manifested as hemodynamic collapse

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16
Q

Pneumonia in this particular patient

A

Absence of fever and of an elevated leukocyte count , in concert with findings on chest radiography and CT, makes infection unlikely

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17
Q

What is the cause and clinical feature of amniotic fluid embolism

A
  • Amniotic fluid containing fetal cells, hair, and fetal debris, as well as procoagulant and fibrinolytic activators from injured blood vessels, are released into maternal circulation during labor due to disruption of maternal fetal interface
  • If they lodge in the lung it can lead to pulmonary collapse and eventually ARDS
  • It may also create a anphylactoid reaction which would lead to vascular collapse
  • It may also cause extrinsic coagulation and fibrinolysis pathway activation, leading to DIC and prolonged postpartum bleeding
  • Symptoms include sudden onset of dyspnea and shock during labor, pulse oximetry may show sudden drop in O2 saturation, hypotension
  • cyanosis, confusion, irritability or seizures may be presenting signs
  • Blood studies may show decreased fibrinogen and elevated fibrin split products, thrombocytopenia, and prolonged PT and PTT, all suggestive of DIC
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18
Q

What are risks in this patient that can open the door for the development of amniotic fluid embolism, and what makes us think otherwise?

A
  • Advanced maternal age and delivery by C section place Mariah at risk
    for amniotic fluid embolism
  • This is a rare but catastrophic complication of pregnancy or labor
  • Patients with amniotic fluid embolism usually present with cardiorespiratory collapse , which Mariah had ; this is typically accompanied by disseminated intravascular coagulation and systemic
    inflammatory responses , which Mariah did not have
  • However , delayed manifestation of amniotic fluid embolism beyond 48
    hours after delivery is extremely rare, and thus this diagnosis is unlikely
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19
Q

Pulmonary cause as the main mechanism of disease in this patient

A
  • Very few indications of a pulmonary cause for Mariah’s presentation
  • However , the presence of orthopnea , copious pink and frothy discharge ,
    bilateral pleural effusions , leg edema, elevated serum B type natriuretic
    peptide and troponin levels , along with tachycardia , cool extremities , and
    hypotension , together suggest pulmonary venous congestion
  • Acute pulmonary edema complicates approximately 1 in 1000 pregnancies and could explain her symptoms
20
Q

Cardiovascular causes of dyspnea and hypoxemia in post partum

A

Common: Preeclampsia, iatrogenic fluid overload, edema associated with tocolysis, myocardial infarction, preexisting cardiac disease, peripartum cardiomyopathy
Rare: Septic cardiomyopathy, pericardial process, takotsubo cardiomyopathy, toxic cardiomyopathy (e.g. from alcohol or cocaine), thyrotoxicosis, aortic dissection, pericardial process, mitral valve chordal rupture (usually with mitral valve prolapse)

21
Q

Fluid overload as the diagnosis in this patient

A
  • Iatrogenic fluid overload , which compounds ongoing reabsorption of
    extracellular fluids , is the leading cause of pulmonary edema post partum
  • Women with this diagnosis usually have had a positive fluid balance of 3
    to 9 liters for the preceding 48 hours.
  • Mariah was not reported to have received excess fluid administration
22
Q

How many pregnancies does pre-eclampsia affect?

A

3-5% of all pregnancies

23
Q

What are the hallmarks of pre-eclampsia? Mechanism of action?

A

The hallmarks are hypertension and proteinuria, which are most likely elicited by the secretion of antivascular factors from the placenta in late gestation

24
Q

Pulmonary edema in preeclampsia and its relevance in this patient

A
  • Pulmonary edema is a frequent complication of preeclampsia
  • Preeclampsia pulmonary edema often becomes evident post partum
  • In this case , neither elevated blood pressure nor proteinuria was noted
    during or after pregnancy , including at the time of initial presentation
  • Post partum preeclampsia cannot be ruled out, but it is a unlikely diagnosis
25
Q

Cause of pulmonary edema in pre-eclampsia

A

Pulmonary edema is multifactorial : endothelial damage confers a predisposition to vascular leak , diastolic dysfunction and acutely elevated blood pressure confer a predisposition to pulmonary venous congestion , and
loss of serum protein lowers intravascular oncotic pressure.

26
Q

Risk of MI in pregnant woman

A
  • The risk of myocardial infarction among pregnant or recently pregnant
    women is three times as high as that among nonpregnant women
  • Absolute incidence is <1/10,000 but climbs as maternal age increases
  • Spontaneous coronary artery dissection (sCAD) causes one third of acute MI in this population , mostly peripartum
27
Q

MI as a diagnosis in this woman

A

In this patient , absence of ECG changes , normal serum creatine kinase
level , and the only slightly elevated serum troponin level , make this
diagnosis unlikely , although it cannot be ruled out. Indeed , MI could have
occurred days before the presentation

28
Q

Risks associated with Mariah being from South America

A

Mariah is from South America, which places her at risk for Chagas ’ cardiomyopathy , rheumatic heart disease , or both

29
Q

Cardiac symptoms of Chaga’s

A

Cardiac rhythm abnormalities, myocardial abnormalities, aneurysms, and thromboembolism

30
Q

Effect of pregnancy on cardiovascular system and how a preexisting’s heart condition might be the cause of Maria’s symptoms

A
  • Pregnancy generates profound hemodynamic changes , including increases in total blood volume, cardiac output , and cardiac work.
  • Underlying cardiac disease is frequently aggravated or unmasked by pregnancy
  • However , hemodynamic changes of pregnancy primarily occur during the first two trimesters , and clinical presentation with heart failure typically occurs during this time, unlike the timing in this patient
31
Q

What is peripartum cardiomyopathy and what is it characterized by?

A
  • Idiopathic form of cardiomyopathy presenting with heart failure towards the end of pregnancy, or in the months following delivery
  • Peripartum cardiomyopathy is characterized by congestive heart failure and left ventricular systolic dysfunction toward the end of pregnancy or after delivery, in the absence of other identifiable causes of cardiac disease or heart failure
  • It is a diagnosis of exclusion
32
Q

Ejection fraction in peripartum cardiomyopathy

A

The ejection fraction on echocardiography is nearly always less than 45%

33
Q

This patient’s likelihood of peripartum cardiomyopathy

A

Mariah’s hypotension and evidence of peripheral vasoconstriction suggest a
state of low cardiac output , which in the absence of a more likely explanation ,
could indicate a diagnosis of peripartum cardiomyopathy

34
Q

Causes of heart failure among female patietns

A

Most common is peripartum cardiomyopathy followed by hypertensive heart disease then rheumatoid heart disease

35
Q

Timing of peripartum cardiomyopathy

A

Over 90% of cases are manifested in the first weeks postpartum , as in this case

36
Q

Manifestations of peripartum cardiomyopathy

A

The manifestation is similar to that of other cardiomyopathies , including dyspnea , orthopnea , edema , and , in extreme cases as in this patient ), hypoxemia
* B type natriuretic peptide levels do not normally rise during pregnancy but are
typically elevated in peripartum cardiomyopathy , as are troponin levels
* Chest radiographs typically show cardiomegaly , as in this case, although
peripartum cardiomyopathy can occur without cardiac dilatation

37
Q

Top diagnosis in this patient

A
  • Because of the initial clinical presentation , peripartum cardiomyopathy is at the top of the list in differential diagnosis
  • However , should also consider ACS and coronary artery dissection
38
Q

Hemodynamic changes postpartum

A

Cardiac output is high and systemic vascular resistance low

39
Q

When is the peripartum cardiomyopathy most likely to happen?

A

In the first month following pregnancy

40
Q

Risk factors for PPCM

A
  • Remain poorly understood, most cases are idiopathic
  • Include: advanced age >30
    multiparity, African descent, multiple gestation, obesity, preeclampsia/eclampsia, hypertension ,prolonged (>4 weeks) tocolysis (medications used to suppress premature labor) with beta agonists
  • Myocarditis, autoimmune. and hemodynamic factors are invloved
41
Q

Probability score of PPCM

A

Fett and colleagues developed a scoring system, with symptoms and signs each having a possibility of 2 points including dyspnea, orthopnea, unexplained cough, pitting edema, weight gain 9th month, and palpitations
- 0-2 is low risk (monitor), 3-4 mild risk (consider blood BNP), and 5 or higher is high risk (blood BNP and echo)

42
Q

Cause of PPCM

A

Research suggests that peripartum cardiomyopathy is triggered by insults to the cardiac vasculature that occur during
late pregnancy and the postpartum period including inappropriate cleavage in the heart of circulating prolactin into a
potently antivascular fragment and the secretion of sFlt 1 from the late gestational placenta
- Prolactin and sFlt 1 begin to
circulate late in pregnancy, which may explain the timing of peripartum cardiomyopathy.
- Bromocriptine has shown to reduce serious symptoms and death

43
Q

How is diagnosis of peripartum cardiomyopathy made

A

ECG, BNP, Echo

44
Q

Medications to manage cardiomyopathy in pregnancy

A

Early pregnancy- Diuretics, hydralazine, beta blocker
Late pregnancy- Diuretics, hydralazine, beta blocker
Postpartum- Diuretics, ace inhibitors, beta blocker

45
Q

Bromocriptine dose for PCMM

A

2.5mg x2/d for 2 weeks then 2.5mg/day for 6 weeks

46
Q

Prognosis of peripartum cardiomyopathy

A
  • prognosis related to LV recovery
  • 50% recover baseline function within 6 months
47
Q

Risk in subsequent pregnancies in PPCM

A
  • 50% will show further deterioration in LV dysfunction in those with persistent LV dysfunction
  • 25% will die in those with persistent LV dysfunction
  • 50% will have premature delivery and abortion in those with persistent lv dysfunction
  • 20% will have a relapse if they completely recovered
  • Likley to have a normal susbequent pregnancy in those who fully recovered from first one
  • Better prognosis in SSP in those who completely recovered vs those with persistent LV dysfunction

Hospital residence (8 decks)

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