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SNRAObPedGer > EXAM#4 Review > Flashcards

EXAM#4 Review Flashcards

1
Q

CYP 450 Isoenzymes ________= Ultra

A

CYP2D6 Rapid metabolization

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2
Q

With the CYP2D6 what happens to morphine

A

Codeine is broken down into greater quantities of morphine than normal

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3
Q

Genetic variability in _________may increase formation of active

A

UGT2B7; morphine-6- glucuronide

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4
Q

Changes at β2-adrenergic receptor →

A

alter tocolysis, require less ephedrine

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5
Q

What is responsible for the mophine-6-glucuronide formation?

A

UGT2B7

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6
Q

Activities of enzymes can be increased:• CYP450 isoenzymes

A

CYP3A4
CYP2D6
CYP2C9

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7
Q

Activities of enzymes can be increased:•UGT

A

(UGT) isoenzymes UGT1A4 and UGT2B7

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8
Q

Which enzyme can increase metabolism of drugs phenytoin?

A

CYP2C9

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9
Q

Which enzyme can increase metabolism of drug: midazolam

A

CYP3A4

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10
Q

Which enzyme can increase metabolism of drug: morphine ?

A

UGT2B7

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11
Q

Anesthetics and lactations

A

There are generally no concerns regarding anesthetic drugs and perioperative medicines in the breast milk of women who require an anesthetic

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12
Q

NSAIDS and lactation

A

No harmful effects of acetaminophen or NSAIDs have been noted except for aspirin

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13
Q

FDA has singled out ketorolac with a “black box” warning that it is

A

“contraindicated in nursing mothers because of the potential adverse effects of prostaglandin-inhibiting drugs on neonates”

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14
Q

• Normal maternal doses ,NAME 4 DRUGS that DO NOT

have obvious adverse effects on most nursing infants

A

codeine, morphine, tramadol, and meperidine

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15
Q

Neonates are particularly vulnerable because their drug

A

metabolism and elimination are poorly developed

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16
Q

Infants of breast-feeding mothers taking codeine

A

may have CNS depression

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17
Q

CYP2D6 and concentration of breastmilk?

A

ultra-rapid metabolization to morphine → high concentration in breast milk

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18
Q

Ultra-rapid metabolism has been reported as a problem for breast-feeding

A

only with codeine, although the FDA suggested that “it has the potential to affect other opioids”

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19
Q

Maternal oxycodone for postpartum analgesia has been associated with

A

neonatal depression

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20
Q

If a sedative must be used in a lactating woman, what kind of drug should be used?

A

a relatively short-acting agent with inactive metabolites,

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21
Q

Short acting benzo that can be used on pregnant women are, is recommended (MOLA)

A

midazolam
oxazepam
lorazepam
alprazolam

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22
Q

Atenolol has 10% protein binding and is 85% renally excreted =

A

bad choice!

Associated c/neonatal cyanosis and bradycardia

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23
Q

Beta-blockers and transfer

A

relatively higher transfer to breast milk

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24
Q

Which beta blocker which one more likely to accumulate in the neonate?

A

Those renally excreted more likely to accumulate in neonate

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25
Q

Amiodarone and breast milk

A

Very long half-life and still EXCRETED in breast milk weeks after d/c meds

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26
Q

ACE inhibitors and antihypertensives are considered

A

safe

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27
Q

Salbutamol, terbutaline, and salmeterol inhalers are considered

A

compatible with breast-feeding

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28
Q

Histamine type 2 (H2)-receptor antagonists theoretically

A

could suppress gastric acidity or cause CNS stimulation in the infant

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29
Q

Heparin and milk?

A

does not cross significantly into breast milk and is not active when administered orally

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30
Q

Pregnancy and vaccination in general

A

Generally appropriate to administer vaccinations during pregnancy

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31
Q

No evidence exists of risk to fetus from vaccinating pregnant women with (safe ones)

A

inactivated virus or bacterial vaccines or toxoids

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32
Q

Contraindicated vaccines for pregnancy are (VMTB)

A 
Live vaccines attenuated virus 
Varicella
Measles-mumps-rubella[MMR]) 
Tuberculosis 
Bacillus Calmette Guérin [BCG]) are contraindicated
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33
Q

For pregnant women Influenza vaccination is recommended with the

A

inactivated virus preparation

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34
Q

Best time to do surgery during pregnancy

A

2nd Trimester

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35
Q

All-or-nothing phenomenon

A

Exposure in 1st 2 weeks after conception(i.e., having either no effect or resulting in spontaneous fetal loss

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36
Q

What is the classic period of susceptibility during period of organogenesis?

A

2½ to 8 weeks after conception

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37
Q

Each organ system has __________of

sensitivity and there may significant differences in effect

A

different critical periods

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38
Q

Thalidomide @ 35-37 days’ gestation

A

ear malformations

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39
Q

Thalidomide @ 41-44 days’ gestation

A

amelia or phocomelia

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40
Q

After 8 weeks what is development or growth?

A

Growth.

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41
Q

Classic Teratogenic

A

31 days - 71 days

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42
Q

31 days two organs

A

Heart and CNS

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43
Q

71 days two organs

A

Palate ear

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44
Q

CNS development goes up to

A

16 weeks

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45
Q

Heart development goes up to

A

6 1/2 weeks for major

9 weeks total

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46
Q

________exposure during 2nd trimester results in uterine anomalies, fetal alcohol syndrome may occur with chronic exposure to alcohol during pregnancy

A

diethylstilbestrol

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47
Q

Upper limbs development

A

6-8 weeks

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48
Q

Not susceptible to teratogens

A

Week 1 and 2

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49
Q

Eyes development goes up to

A

8 1/2 weeks

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50
Q

Ear development goes up to

A

9 1/2 weeks

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51
Q

Fetal anticonvulsant syndrome

A

Orofacial
CV
Digital malformations

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52
Q

Fetal hydantoin syndrome

A

Constellation of minor anomalies, such as craniofacial abnormalities and limb anomalies

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53
Q

PH4EN Mnemonic

A

P Cleft plage, cleft lip
H Small head, hypoplastic face, hirsutism, heart defects
E Embryopathy, Antiepileptic use
N Hypoplastic nails and digits, neurologic deficits

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54
Q

Fetal carbamazepine syndrome closely resembles the malformations seen in

A

cases of fetal hydantoin syndrome

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55
Q

Fetal phenobarbital syndrome

A

Minor dysmorphic features similar to those seen with fetal hydantoin syndrome

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56
Q

Fetal valproate syndrome

DES-HFL- MUT- DTH

A 
Dysmorphic features
Epicanthal folds
Shallow orbits
\_\_\_\_\_\_\_\_\_\_\_\_
Hypertelorism
Low-set ears
Flat nasal bridge
\_\_\_\_\_\_\_\_\_\_\_\_
Upturned nasal tip
Microcephaly
Thin vermillion borders
\_\_\_\_\_\_\_\_\_\_\_\_\_
Downturned mouth
Thin overlapping fingers and toes
Hyperconvex fingernails
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57
Q

Fetal warfarin syndrome consists of (NDS-NMG)

A 
Nasal hypoplasia
Depressed nasal
Stippled epiphyses
Nail hypoplasia
Mental retardation
Growth restriction
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58
Q

Typically absent in less than 20 weeks gestation

A

Hemoconcentraton, Thrombocytopenia, Proteinuria

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59
Q

Chronic hypertension absent symptoms

Severity? when ?

A

Mild or severe
<20 weeks of gestation

Proteinuria
Uric acid RARE
Hemoconcentration
Thrombocytopenia

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60
Q

Gestational HTN absent symptoms

Severity? when ?

A

Mild
Typically in third trimester

Proteinuria
Uric acid RARE
Hemoconcentration
Thrombocytopenia

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61
Q

Pre-Eclampsia

Severity and when?

A

> 20 weeks

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62
Q

Pre-Eclampsia What is present in ALMOST ALL CASES

A

Serum uric acid > 5.5

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63
Q

Pre-Eclampsia what is present in SEVERE DISEASE

A

Hemoconcentration

Thrombocytopenia

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64
Q

Pre-eclampsia what is typically present

A

Proteinuria.

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65
Q

Diagnostic Criteria for Preeclampsia : Preeclampsia WITHOUT severe features (BPP 1E)

A 
BP ≥ 140/90mmHg after 20 weeks gestation
Proteinuria ≥ 300mg/24h
Protein-Creatinine ratio ≥0.3
1+ on urine dipstick specimen
Edema
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66
Q

Diagnostic Criteria for Preeclampsia : SEVERE Pre-eclampsia (BTSPNI)

A 
BP ≥ 160/110 mmHg
Thrombocytopenia (plt count < 100,000)
Serum Cr > 1.1mg/dl OR 2 times the baseline Cr.
Pulmonary Edema
New onset CEREBRAL+ Visual disturbances
Impaired liver function (HELLP)
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67
Q

Can you have proteinuria w/o Eclampsia?

A

Yes

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68
Q

HTN

A

the answer is NITRO

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69
Q

Nitroglycerin Pertinent information

A 
Venous > arterial relaxation
↓preload > afterload,
very rapid onset (HoTN), 
UteroPlacental Blood Flow preserved but crosses
UP/FP
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70
Q

Most common used antihypertensive

A

Hydralazine

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71
Q

Hydralazine effects (RDN)

A

Relaxes arterioles
Decrease SVR, BP and may Increase HR
NO effect on UP/FP BF

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72
Q

2nd most common use antihypertensive (LADA)

A

Labetalol
Alpha:beta 1:7
Decrease SVR with Increase HR
AVoid in asthmatic /liver dysfunction , crosses the placenta

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73
Q

Treatment goals BP

A

DBP 90-105mmHg

MAP 105-125 mmHg

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74
Q

ESMOLOL characteristics

A

IV bolus for sympathetic block during intubation.

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75
Q

Nifedipine characteristics (AC)

A

Arterial dilator with little cardiodepresion

Can exaggerate HoTN if receiving MgSO4

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76
Q

Nitroprusside characteristics (PDC)

A 
Powerful Vadodilator arterial>venous
Decrease Afterload 
Crosses Placenta (worry about cyanide toxicity)
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77
Q

HELLP stands for

A

Hemolysis, Elevated Liver Enzymes, Low Platelets

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78
Q

What is HELLP a complication of

A

Severe form of preeclampsia

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79
Q

HELLLP occurs due to

A

Occurs d/t unknown insult

→intravascular plt activation & microvascular endothelial damage

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80
Q

What is the hallmark of HELLP?

A

Hemolysis

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81
Q

All abnormal labs in HELLP

ALT

A
  • Abnormal peripheral blood smear + ↑bilirubin level (> 1.2mg/dL)
  • ↑liver enzymes AST (SGOT) > 70, LDH > 600
  • Thrombocytopenia < 100,000
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82
Q

• Nonspecific initial complaints of HELLP

A

(malaise, AB pain, N/V)

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83
Q

Maternal complications of HELLP

A

Maternal complications
• CVA, CV arrest, DIC, placental abruption,
• ALL patients show some evidence of compensated DIC
• Postpartum onset (hrs to 6 days after delivery) → ↑risk of ARF and pulmonar
edema

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84
Q

Maternal complications of HELLP

A

Maternal complications

• CVA, CV arrest, DIC, ARF placental abruption,

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85
Q

ALL patients in HELLP show some evidence of

A

compensated DIC

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86
Q

• Postpartum onset of HELLLP can occur __________And increase risk for → ↑risk of ARF and pulmonary edema

A

hrs to 6 days after delivery ;ARF and pulmonary edema

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87
Q

Postpartum onset of HELLLP can occur __________And increase risk for → ↑risk of ARF and pulmonary edema

A

hrs to 6 days after delivery ;ARF and pulmonary edema

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88
Q

HELLP check for retained products with

A

US

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89
Q

Tx meds for HELLP

A

Decadron

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90
Q

Common occurrence during C-section and vaginal delivery

A

VAE

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91
Q

Subclinical VAE occurs in both GA and

A

Spinal

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92
Q

VAE occurs less with regional

A

Because they are spontaneously breathing

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93
Q

VAE may account for common symptoms during C-section: (DASHA)

A 
Dyspnea
Angina
↓SaO2
HoTN
Arrhythmias
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94
Q

M&M of VAE is r/t volume/rate of air infusion into :

A

central circulation and site of embolization

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95
Q

VAE: Pathophysiology

A

Pressure gradient as small as -5 cmH2O between surgical field and heart allows venous air entrainment

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96
Q

What is associated with INCREASED VENOUS AIR? (SU)

A

Steep Trendelenburg position

Uterine exteriorization during C-section

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97
Q

VAE Large air volumes is fatal

A

> 3 mL/kg

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98
Q

VAE Small air volumes: VHAH

A

V/Q mismatch
Hypoxemia
Arrhythmia
HoTN

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99
Q

VAE Presentation

A

50% angina
25% Decrease SaO2
>20% drop in BP (2%)

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100
Q

Resuscitation of patient with massive venous air embolism

PDS -CEIP

A 
Prevent air entrapment (change position, flood surgical 
       field)
Discontinue Nitrous give 100% oxygen
Support ventilation and circulation
Central venous catheter to aspirate air
Expedite delivery
Imaging to rule out intercerebral air. 
Paradoxical cerebral artery gas may benefit from 
     Hyperbaric oxygen therapy
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101
Q

Risk factors of Eclampsia (FMMN-PPRST)

A 
First pregnancy 
Multiple Gestation
Molar Pregnancy
Triploidy
Preexisting HTN
Renal diseas
Non-immune hydrops fetalis
SLE
Previous hx of preeclampsia/eclampsia
102
Q

Risk Factors of Preeclampsia: Demographic factors (ABH)

A

Advanced maternal age > 35 years
Black race
Hispanic ethnicity

103
Q

Risk Factors of Preeclampsia: Demographic factors (ABH)

A

Advanced maternal age > 35 years
Black race
Hispanic ethnicity

104
Q

Risk Factors of Preeclampsia: Genetic Factors (HFHP)

A

History of Preeclampsia in previous pregnancy
Family Hx of Preeclampsia
History of Placental Abruption, Fetal growth restriction, or fetal death (PFD)
Partner who fathered a preeclamptic pregnancy pregnancy in another woman (through fetal genes)

105
Q

Risk Factors of Preeclampsia: Medical Conditions (CODCAS)

A 
Chronic HTN
Obesity
Diabetes Mellitus
Chronic Renal Disease
Antiphospholipid antibody syndrome
Systemic Lupus Erythematus
106
Q

Risk Factors of Preeclampsia:Obstetric conditions

A

Multiple Gestation

Hydatidiform mole

107
Q

Risk Factors of Preeclampsia: Behavioral factor

A

Cigarette smoking (risk reduction)

108
Q

Risk Factors of Preeclampsia: Partner related risk factors

A

Nulliparity

LIMITED PRE-CONCEPTIONAL EXPOSURE TO PATERNAL SPERM

109
Q

All risk factors for Preeclampsia together

A 
Advanced maternal age > 35 years
Black race
Hispanic ethnicity
History of Preeclampsia in previous pregnancy
Family Hx of Preeclampsia
History of Placental Abruption, Fetal growth restriction, or fetal death (PFD) 
Partner who fathered a preeclamptic pregnancy pregnancy in another woman (through fetal genes)
Chronic HTN
Obesity
Diabetes Mellitus
Chronic Renal Disease
Antiphospholipid antibody syndrome
Systemic Lupus Erythematus
Multiple Gestation
Hydatidiform mole
Cigarette smoking (risk reduction)
Nulliparity
LIMITED PRE-CONCEPTIONAL EXPOSURE TO PATERNAL SPERM
110
Q

Postparthum hemorrhage : Etiology (4) Ts

A

Tone
Tissue
Trauma
Thrombin

111
Q

Tissue cause of PPH

A

Retained products of conception

112
Q

Trauma cause of PPH

A

Genitral tract trauma

113
Q

Thrombin cause of PPH

A

Coagulation abnormalities.

114
Q

Take home message for PPH

A

Do not go over 1 MAC of anesthesia with FURTHER DECREASE UTERINE TONE

115
Q

Causes of Pregnancy Related hemorrhage

ALUCPUR

A 
Abruptio Placenta
Laceration /uterine rupture
Uterine atony
Coagulopathies
Placenta previa--> accreta, increta, percreta
Uterine bleeding
Retained placenta
116
Q

4 main causes of Antepartum hemorrhage

PPUV

A

Placenta Previa
Placenta Abruptio
Uterine Rupture
Vasa Previa

117
Q

4 types of Placenta Previa

TPML

A

Total
Partial
Marginal
Low-lying placenta

118
Q

What is a TOTAL placenta previa?

A

Internal cervical OS covered completed by placenta

119
Q

What is a PARTIAL placenta previa>?

A

Internal cervical OS partially covered by placenta

120
Q

What is a MARGINAL placenta previa?

A

Edge of placenta at margin of internal os

121
Q

What is a low lying placenta?

A

Placenta is implanted in lower uterine segment –> Placental edge does not actually reach internal os but in close proximity to it

122
Q

What are the 3 types of placenta accreta

A

Accreta vera
Placenta increta
Placenta percreta

123
Q

Placenta Accreta vera is

A

Adherence of basal plate of placenta directly to uterine myometrium without penetrating the decidua layer

124
Q

Placenta Accreta increta is

A

Chorionic villi invade myometrium

125
Q

Placenta accreta percreta is

A

Invasion through MYOMETRIUM into SEROSA and even adjacent ORGANS (bladder)

126
Q

VASA Previa is

A

rare condition where fetal vessels from placenta cross entrance of birth canal

127
Q

3 typical causes of Vasa previa

A

Bi-lobed placenta
Velamentous insertion of umbilicord
Succenturiate (accessory lobe)

128
Q

Placenta Previa symptoms Hallmark

A

Painless hemorrhage

129
Q

Placenta Previa risk Factors AMMPPS

A 
Advanced Maternal Age >35
Multiparity
Multifetal gestations
Prior C-section
Smoking
Prior Placenta previa
130
Q

Placenta abruption factors

A

External hemorrhage
Concealed (internal hemorrhage)
Total
Partial

131
Q

Hallmark of Placenta Abruption

A

Bleeding with PAIN varying from mild cramping to severe

132
Q

Placenta abruption signs and symptoms uterus

A

Firm , tender uterus with INCREASE FUNDUS HEIGH

133
Q

Placenta Abruption risk factors

PPP CCC HIUEM

A

Prior abruption
Pre-eclampsia
PROM

Chronic HTN
CIgarette smoking
Cocaine use

Hydramnios
Increage age and parity
Uterine Leiomyoma
Multiple gestation
External Trauma
134
Q

Risk factors of VASA PREVIA (LAMPP)

A 
Abnormal placenta morphology
Low lying
Multiple gestation
Pregnancies resulting from IVF 
Palpate vessel on vaginal exam
135
Q

Uterine rupture most common with

A

VBAC

136
Q

Uterine rupture classic presentation

VAPCLEP

A

Vaginal bleeding
Absence/deterioration of FHR
Pain
Cessation of contraction
Loss of station of the fetal head from birth canal
Easily palpate fetal parts
Profound Maternal TACHYCARDIA and HYPOTENSION

137
Q

Risk factors for Uterine Rupture

PPP TEMFS

A 
Prior rupture
Previous uterine sx 
Previous C section
Trauma
Excessive uterine stimulation 
Multiparity
Forceps delivery
Shoulder distocia
138
Q

Contraindications for uterotonic agents: Oxytocin

A

Hypersensitivity to drug

139
Q

Contraindications for uterotonic agents: Methergine

A

HTN, hypers.

140
Q

Contraindications for uterotonic agents: Carboprost

A

Heart, PULMONARY, RENAL, hepatic disease

141
Q

Contraindications for uterotonic agents: Vasopressin

A

CAD

142
Q

Minimize risk of aspiration

A

Small volumes (150 mL; 5.7 fluid ounces) of fluid other than milk and pulp containing juices consumed up to 2 hours before elective

143
Q

Minimizing Risk: H-2 Receptor

Antagonists

A

• Cimetidine, Ranitidine, Nizatidine, Famotidine

144
Q

H2 Receptor antagonists Reduces gastric acidity significantly approximately 30 min after IV
administration, maximal effect @ 60-90 min how?

A

• Block histamine receptors on oxyntic cell → ↓diminish gastric acid production → leading to a slight ↓ in gastric volume in fasting patient

145
Q

•Guidelines for perinatal care (American College of
Obstetrics & Gynecology, American Academy of
Pediatrics) for aspiration risk

A

“Patients in active labor should avoid
oral ingestion of anything excepts sips of clear
liquids, occasional ice chips, or moistening of
mouth/lips” Because Some clear liquids are highly acidic (e.g., cranberry juice)n

146
Q

Normal laboring patients should not receive

aspiration prophylaxis unless

A

They are high risk for C-section

147
Q

PPI minimize risk for aspiration

A

Inhibit the H+ pump on gastric surface of oxyntic cell

148
Q

Non particulate antacid:

A

30 mL Na citrate [Bicitra] can neutralize 255 mL of hydrochloric acid with a PH of 1.0

149
Q

Particulate antacids

A

(e.g.. Maalox, Mylanta)

150
Q

When aspirated causes serious pneumonitis?

A

Particulate antacids (e.g.. Maalox, Mylanta)

151
Q

When should non particulate antacid be administered?

A

Should be administered within 20 minutes of induction

of GETA

152
Q

What is short definition of action of H2 blockers

A

Keeps from making more acid

153
Q

Prior administration of what may antagonize metoclopramide action?

A

Prior administration of opioid and atropine

154
Q

How much acid is produced per day by the stomach

•

A

Up to 1500 ml highly acidic fluid

155
Q

Pyloric glands

A

Chief cells secrete pepsinogen →pepsin

156
Q

Oxyntic glands

A

Oxyntic cells secrete HCl (pH 0.8)

157
Q

This is where PPIs work

A

Oxyntic cells oxyntic glands

158
Q

Vagus stimulates

A

G cells to secrete gastrin →bind to oxyntic cells and

stimulates HCl secretion

159
Q

Ach binds

A

to muscarinic receptors and ↑Ca2+

160
Q

H-2 receptors ↑cAMP →

A

dramatic ↑ acid production (also increase calcium)

161
Q

Histamine potentiates both

A

gastrin and acetylcholine

162
Q

Acid is secreted at a low basal rate of approximately ________ even whenty

A

10% of maximal output; stomach is empty

163
Q

• Diurnal variation:

A

lowest in morning, highest in evening

164
Q

Increase dramatically with ingestion

A

• ↑ dramatically with ingestion

165
Q

No significant differences in __________________

were seen between pregnant and nonpregnant women

A

basal gastric acid secretion

166
Q

Cephalic phase:s

A

chewing, smelling, or tasting without significant

ingestion ↑ vagal stimulation

167
Q

What happens to gastric acid during the cephalic phase?

A

Gastric acid output ↑ to 55% of peak levels

168
Q

Gastric phase:

A

entry into stomach of ingested contents, acid output

peak

169
Q

When does gastric acid output peak ?

A

Gastric phase

170
Q

Intestinal phase begins

A

begins with movement of food into small intestine

171
Q

Gastrin role

A

Increase gastric acid secretion

172
Q

Pathophysiology of Aspiration Pneumonitis: Acidic Liquid

A

Acidic liquid aspiration injures alveolar epithelium
→ alveolar exudate (edema, albumin, fibrin, cellular
debris, and RBCs)

173
Q

In pathophysiology of Aspiration Pneumonitis what does Alveolar exudate/pulmonary edema leads to:

A
  • ↓ in lung compliance
  • Loss of lung volume
  • Intrapulmonary shunting of blood
  • Bronchial obstruction/ bronchospasm
174
Q

Aspirates with a ph lower than 2.5 cause

A

a granulocytic reaction

175
Q

General rule for aspiration pneumonitis

A

ph<2.5, gastric volume >25 Aspiration pneumonitis

176
Q

Pathophysiology: Particle Aspiration

• Direct airway obstruction from larger particles

A

atelectasis; Obstructing large airways

177
Q

In pathophysiology of Smaller particles: similar response as

A

with acidic liquid

178
Q

In pathophysiology of Smaller particles causes

A

exudative neutrophilic response at levels of bronchioles and alveolar ducts

179
Q

• Aspiration pneumonitits = Is is an injury from _______
What does basic aspirate do?
• Cellular debris and bronchial denuding = bronchial obstruction
• Exudative pulmonary edema, bronchial obstruction, ↓ lung
compliance, and shunting → hypoxemia, ↑ pulmonary vascular
resistance, and increased work of breathing.

A

chemical injury from sterile acid gastric contents

• Basic aspirate ↓ surfactant levels

180
Q

• MOA of Aspiration Pneumonitis:

A

↑ intraalveolar water and protein content and a loss of lung volume leading ↓ in pulmonary compliance and intrapulmonary shunting of blood

181
Q

After direct acid-mediated injury of respiratory tract,
• Amplification of these inflammatory processes may result in development of
acute lung injury or acute respiratory distress syndrome (ARDS)

A

an intense inflammatory response ensues from macrophage activation and secretion of cytokines, interleukins and tumor necrosis factor-alpha (MSIT)

182
Q

In Aspiration pneumonitis, After direct acid-mediated injury of respiratory tract, and activation of MSIT what does it lead do ? CAUA

A

Leads to :
Chemotaxis
Accumulation and activation of neutrophils in alveolar
exudate,
Up-regulation of adhesion molecules within pulmonary
vasculature and
Activation of the complement pathways

183
Q

In Aspiration Pneumonitis Neutrophils release OPLO

A

oxidants, proteases, leukotrienes, and other proinflammatory molecules

184
Q

In aspiration pneumonitis: Cellular debris and bronchial denuding.

A

bronchial obstruction

185
Q

In aspiration pneumonitis, Exudative pulmonary edema –>
BDPI
What happens to lung compliance? PVR , WOB

A

bronchial obstruction
↓ lung compliance, and shunting → hypoxemia,
↑ pulmonary vascular resistance
Increased work of breathing

186
Q

Most common site of aspiration and why?

A

RLL; d/t large size of right mainstem bronchus

187
Q

Aspiration pneumonitis: Recovery involves proliferation and differentiation of

A

surviving type II pneumocytes in alveolar epithelial cells

• Actively transport Na+ out of alveolus, water follows

188
Q

Recovery aspiration pneumonitis: Soluble proteins are removed by

A

paracellular diffusion and endocytosis

189
Q

Recovery of Insoluble proteins are removed by

A

macrophages.

190
Q

Neutrophils are removed by

A

programmed cell death and phagocytosis by

macrophages

191
Q

Aspiration pneumonitis Type II

A

Type II pneumocytes gradually restore normal composition of surfactant

192
Q

DIC Results from an

A

abnormal activation of the coagulation system

193
Q

Abnormal activation of the coagulation system DIC leads to : (FDAH)

A

Formation of large amount of thrombin
Depletion of coagulation factors
Activation of fibrinolytic system
Hemorrhage

194
Q

If severe enough DIC leads to

A

diffuse microvascular thrombosis → end-organ injury

195
Q

DIC depletion of platelet

A

Intravascular deposition of fibrin –>Thrombosis of small and midsize vessels and organ failure
Depletion of platelets and anticoagualtion factors-> Bleeding

196
Q

Obstetric triggers of DIC

A

include entry of procoagulant tissue extracts into the blood which interact with factor VII and activate the extrinsic coagulation pathway

197
Q

DIC and dead tissue

A

dead tissue and amniotic fluid contains thromboplastic substances that trigger coagulation

198
Q

What really activate the cascade?

A

Endothelial injury.

199
Q

What is the hallmark of DIC

A

Elevated D-dimer, Fibrin and Fibrin Degradation Products (FDPs)

200
Q

Other proteins Depleted in DIC

A

Antithrobin 3, Fibronectin, Plasminogen

201
Q

Decreased labs in DIC

A

Platelet count, Fibrinogen, and antithrombin III concentrates.

202
Q

DIC : There is Variable Increase in

A

PT, aPTT, and thrombin and Reptilase times

203
Q

Reptilase time is

A

Detect abnormalities in Fibrinogen

204
Q

In DIC Endothelial cells –> Plasminogen activator–>

A

Plasminogen –> Plasmin

205
Q

In DIC platelets

A

Platelets –> thrombin–> Activated platelets.

206
Q

DIC Pathophysiology: Intravascular

Fibrin Formation

A

• Formation of small strands/microclots of fibrin is the immediate result of DIC (may lead to obstruction of pulmonary vessels)

207
Q

• Fibrinolysis present in

•

A

every patient with DIC

208
Q 
• Fibrin degradation products (FDP) are Protein
fragments that (APID)
A

Act as antithrombins (↑ bleeding)
Produce defective fibrin polymer (↑ bleeding)
Impair platelet clearance
Directly damage pulmonary vasculature (ARDS!

209
Q

Tx for preeclampsia High MAG

A

Calcium gluconate and Furosemide

210
Q

33 weeks scheduled for procedure, which drug to avoid

A

Ketorolac (NSAIDS)

211
Q

33 weeks scheduled for procedure, which drug to avoid

A

Ketorolac (NSAIDS) (can close the ducturs arteriosus)

212
Q

Consistent with Preeclamspia?

A 
Proteinuria
Increased thromboxane
Decreased Prostacyclin
Vasoconstriction
Enhanced Platelet aggregation
213
Q

How does Nitroglycerin help

A

Provide uterine relaxation

214
Q

IF the patient has DIC no

A

spinal anesthesia

Alternative GA

215
Q

Late severe DIC

A

Rule out severe liver disease (elevated platelets, elevated PT)

216
Q

DIC Active bleeding or invasive procedure is required,
transfuse: FFP how much and why?
• Ventilation, multiorgan system support

A

(15 to 30 mL/kg) to maintain the PT and aPTT within

1.5 times normal values

217
Q

DIC and Cryoprecipitate or fibrinogen concentrate

A

to maintain fibrinogen concentration above 150 to 200 mg/dL

218
Q

DIC and Platelets to

A

maintain a platelet count above 50,000/mm3

219
Q

Normally, avoid neuraxial anesthesia with

A

coagulation disorders

220
Q

In selected circumstances, neuraxial anesthesia can be offered to a patient with an

A

Isolated laboratory abnormality and no clinical evidence of coagulopathy.

221
Q

With patient with coagulopathy , Frequent neurologic examinations are performed to

A

Facilitate the early detection of an “epidural hematoma” during the postpartum

222
Q

MAP 1st formula

A

MAP = (CO x SVR) + CVP

223
Q

MAP 2nd formula

A

1/3 (systolic pressure – diastolic pressure) + diastolic pressure

224
Q

Possibility of high spinal block if

A

too much LA administered

225
Q

High spinal can lead do =

A

respiratory paralysis

226
Q

Absolute Neuraxial CONTRAINDICATIONS

PUCISH

A 
• Pt refusal
• Uncorrected hypovolemia
• Clinical coagulopathy
• Infection at injection site
• Severe preeclampsia
• Hx thrombocytopenia and labs have not
resulted yet
227
Q

Can help c/maintaining hemodynamics during modest hemorrhage

A

Ketamine

228
Q

Preventing Sympathectomy

from Becoming a Problem

A
  • Phenylephrine OK but go slow

* 50 mcg until BP remains stable (SBP > 100)

229
Q

What gauge needle to Insert for Subarachnoid space:

A

25g spinal needle to subarachnoid space

230
Q

Spinal Needles: Cutting-bevel needles (Quincke) =

A

rarely used due to unacceptably ↑risk of PDPH

Still used in elderly population

231
Q

Non-cutting needles (Whitacre, Sprotte) preferred

• “Pencil-point needles” causes what?

A

Causes more trauma to dura → more intense
inflammatory response → more rapid closure of
dural defect

232
Q

• “Pencil-point needles”

A

Non-cutting needles (Whitacre, Sprotte)

233
Q

Needles that are preferred are

A

Non-cutting needles (Whitacre, Sprotte) preferred

234
Q

Bigger gauge needle advantages

A

More control, more resistant to bending/shearing from hitting bones

235
Q

Smaller spinal needles risk?

A

↓PDPH risk, harder to control

236
Q

Emergencies usually necessitate what kind of needles?

A

larger gauge needles

237
Q

Awareness during GETA
• High incidence between______and _______
• 50% N2O /O2
administered c/following agents ↓awareness to <1%
• 0.6% Isoflurane
• 1% Sevoflurane
• 3% Desflurane

A

induction of anesthesia and delivery of fetus

238
Q

What leads to maternal Awareness.?

A

Administration of only 50% N2O with O2 without other agents resulted in maternal awareness in 12-26% of cases

239
Q

What medication help prevent Awareness during GETA

A

Ketamine on induction can help

240
Q

To help prevent awareness minimize

A

Minimize time from induction to delivery

241
Q

50% N2O /O2 administered c/following agents ↓awareness to <1%

A
  • 0.6% Isoflurane
  • 1% Sevoflurane
  • 3% Desflurane
242
Q

____are now considered the preferred anesthetic

A

• SAB

243
Q

Preventing Sympathectomy from Becoming a Problem

A

• ↑SVR c/pressors - Phenylephrine

244
Q

How to Treat HoTN from Sympathectomy

• Arteriolar constrictors (pressors)

A
  • LUD
  • Proper fluid loading
  • Preload alone might not prevent hypothermia
245
Q

Treating HoTN

A

• 500mL hetastarch can be better than 1500mL

crystalloid

246
Q

For C/S If tachycardic, use

A

phenylephrine

247
Q

For Hemodynamic stability in C/S If bradycardic,

A

use ephedrine

Atropine if severe (glycopyrrolate works too slow)

248
Q

For Hemodynamic stability in C/S Bradycardia can occur with

A

generous phenylephrine boluses (HTN)

249
Q

If SBP < 110, pretreat with some

A

ephedrine (50mg IM, or 25 mg into skin local you are going to use)

250
Q

C/S meds to be available to maintain

A
  • Ketamine should be available

* Ephedrine and Phenylephrine should already be diluted

SNRAObPedGer (25 decks)

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