EXAM#4 Review Flashcards
1
Q
CYP 450 Isoenzymes ________= Ultra
A
CYP2D6 Rapid metabolization
2
Q
With the CYP2D6 what happens to morphine
A
Codeine is broken down into greater quantities of morphine than normal
3
Q
Genetic variability in _________may increase formation of active
A
UGT2B7; morphine-6- glucuronide
4
Q
Changes at β2-adrenergic receptor →
A
alter tocolysis, require less ephedrine
5
Q
What is responsible for the mophine-6-glucuronide formation?
A
UGT2B7
6
Q
Activities of enzymes can be increased:• CYP450 isoenzymes
A
CYP3A4
CYP2D6
CYP2C9
7
Q
Activities of enzymes can be increased:•UGT
A
(UGT) isoenzymes UGT1A4 and UGT2B7
8
Q
Which enzyme can increase metabolism of drugs phenytoin?
A
CYP2C9
9
Q
Which enzyme can increase metabolism of drug: midazolam
A
CYP3A4
10
Q
Which enzyme can increase metabolism of drug: morphine ?
A
UGT2B7
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
12
Q
NSAIDS and lactation
A
No harmful effects of acetaminophen or NSAIDs have been noted except for aspirin
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”
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
15
Q
Neonates are particularly vulnerable because their drug
A
metabolism and elimination are poorly developed
16
Q
Infants of breast-feeding mothers taking codeine
A
may have CNS depression
17
Q
CYP2D6 and concentration of breastmilk?
A
ultra-rapid metabolization to morphine → high concentration in breast milk
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”
19
Q
Maternal oxycodone for postpartum analgesia has been associated with
A
neonatal depression
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,
21
Q
Short acting benzo that can be used on pregnant women are, is recommended (MOLA)
A
midazolam
oxazepam
lorazepam
alprazolam
22
Q
Atenolol has 10% protein binding and is 85% renally excreted =
A
bad choice!
Associated c/neonatal cyanosis and bradycardia
23
Q
Beta-blockers and transfer
A
relatively higher transfer to breast milk
24
Q
Which beta blocker which one more likely to accumulate in the neonate?
A
Those renally excreted more likely to accumulate in neonate
25
Amiodarone and breast milk
Very long half-life and still EXCRETED in breast milk weeks after d/c meds
26
ACE inhibitors and antihypertensives are considered
safe
27
Salbutamol, terbutaline, and salmeterol inhalers are considered
compatible with breast-feeding
28
Histamine type 2 (H2)-receptor antagonists theoretically
could suppress gastric acidity or cause CNS stimulation in the infant
29
Heparin and milk?
does not cross significantly into breast milk and is not active when administered orally
30
Pregnancy and vaccination in general
Generally appropriate to administer vaccinations during pregnancy
31
No evidence exists of risk to fetus from vaccinating pregnant women with (safe ones)
inactivated virus or bacterial vaccines or toxoids
32
Contraindicated vaccines for pregnancy are (VMTB)
```
Live vaccines attenuated virus
Varicella
Measles-mumps-rubella[MMR])
Tuberculosis
Bacillus Calmette Guérin [BCG]) are contraindicated
```
33
For pregnant women Influenza vaccination is recommended with the
inactivated virus preparation
34
Best time to do surgery during pregnancy
2nd Trimester
35
All-or-nothing phenomenon
Exposure in 1st 2 weeks after conception(i.e., having either no effect or resulting in spontaneous fetal loss
36
What is the classic period of *susceptibility* during period of organogenesis?
2½ to 8 weeks after conception
37
Each organ system has __________of
| sensitivity and there may significant differences in effect
different critical periods
38
Thalidomide @ 35-37 days’ gestation
ear malformations
39
Thalidomide @ 41-44 days’ gestation
amelia or phocomelia
40
After 8 weeks what is development or growth?
Growth.
41
Classic Teratogenic
31 days - 71 days
42
31 days two organs
Heart and CNS
43
71 days two organs
Palate ear
44
CNS development goes up to
16 weeks
45
Heart development goes up to
6 1/2 weeks for major
| 9 weeks total
46
________exposure during 2nd trimester results in uterine anomalies, fetal alcohol syndrome may occur with chronic exposure to alcohol during pregnancy
diethylstilbestrol
47
Upper limbs development
6-8 weeks
48
Not susceptible to teratogens
Week 1 and 2
49
Eyes development goes up to
8 1/2 weeks
50
Ear development goes up to
9 1/2 weeks
51
Fetal anticonvulsant syndrome
Orofacial
CV
Digital malformations
52
Fetal hydantoin syndrome
Constellation of minor anomalies, such as craniofacial abnormalities and limb anomalies
53
PH4EN Mnemonic
P Cleft plage, cleft lip
H Small head, hypoplastic face, hirsutism, heart defects
E Embryopathy, Antiepileptic use
N Hypoplastic nails and digits, neurologic deficits
54
Fetal carbamazepine syndrome closely resembles the malformations seen in
cases of fetal hydantoin syndrome
55
Fetal phenobarbital syndrome
Minor dysmorphic features similar to those seen with fetal hydantoin syndrome
56
Fetal valproate syndrome
| DES-HFL- MUT- DTH
```
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
```
57
Fetal warfarin syndrome consists of (NDS-NMG)
```
Nasal hypoplasia
Depressed nasal
Stippled epiphyses
Nail hypoplasia
Mental retardation
Growth restriction
```
58
Typically absent in less than 20 weeks gestation
Hemoconcentraton, Thrombocytopenia, Proteinuria
59
Chronic hypertension absent symptoms
| Severity? when ?
Mild or severe
<20 weeks of gestation
Proteinuria
Uric acid RARE
Hemoconcentration
Thrombocytopenia
60
Gestational HTN absent symptoms
| Severity? when ?
Mild
Typically in third trimester
Proteinuria
Uric acid RARE
Hemoconcentration
Thrombocytopenia
61
Pre-Eclampsia
| Severity and when?
>20 weeks
62
Pre-Eclampsia What is present in ALMOST ALL CASES
Serum uric acid > 5.5
63
Pre-Eclampsia what is present in SEVERE DISEASE
Hemoconcentration
| Thrombocytopenia
64
Pre-eclampsia what is typically present
Proteinuria.
65
Diagnostic Criteria for Preeclampsia : Preeclampsia WITHOUT severe features (BPP 1E)
```
BP ≥ 140/90mmHg after 20 weeks gestation
Proteinuria ≥ 300mg/24h
Protein-Creatinine ratio ≥0.3
1+ on urine dipstick specimen
Edema
```
66
Diagnostic Criteria for Preeclampsia : SEVERE Pre-eclampsia (BTSPNI)
```
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)
```
67
Can you have proteinuria w/o Eclampsia?
Yes
68
HTN
the answer is NITRO
69
Nitroglycerin Pertinent information
```
Venous > arterial relaxation
↓preload > afterload,
very rapid onset (HoTN),
UteroPlacental Blood Flow preserved but crosses
UP/FP
```
70
Most common used antihypertensive
Hydralazine
71
Hydralazine effects (RDN)
Relaxes arterioles
Decrease SVR, BP and may Increase HR
NO effect on UP/FP BF
72
2nd most common use antihypertensive (LADA)
Labetalol
Alpha:beta 1:7
Decrease SVR with Increase HR
AVoid in asthmatic /liver dysfunction , crosses the placenta
73
Treatment goals BP
DBP 90-105mmHg
| MAP 105-125 mmHg
74
ESMOLOL characteristics
IV bolus for sympathetic block during intubation.
75
Nifedipine characteristics (AC)
Arterial dilator with little cardiodepresion
| Can exaggerate HoTN if receiving MgSO4
76
Nitroprusside characteristics (PDC)
```
Powerful Vadodilator arterial>venous
Decrease Afterload
Crosses Placenta (worry about cyanide toxicity)
```
77
HELLP stands for
Hemolysis, Elevated Liver Enzymes, Low Platelets
78
What is HELLP a complication of
Severe form of preeclampsia
79
HELLLP occurs due to
Occurs d/t unknown insult
| →intravascular plt activation & microvascular endothelial damage
80
What is the hallmark of HELLP?
Hemolysis
81
All abnormal labs in HELLP
| ALT
* Abnormal peripheral blood smear + ↑bilirubin level (> 1.2mg/dL)
* ↑liver enzymes AST (SGOT) > 70, LDH > 600
* Thrombocytopenia < 100,000
82
• Nonspecific initial complaints of HELLP
(malaise, AB pain, N/V)
83
Maternal complications of HELLP
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
84
Maternal complications of HELLP
Maternal complications
| • CVA, CV arrest, DIC, ARF placental abruption,
85
ALL patients in HELLP show some evidence of
compensated DIC
86
• Postpartum onset of HELLLP can occur __________And increase risk for → ↑risk of ARF and pulmonary edema
hrs to 6 days after delivery ;ARF and pulmonary edema
87
Postpartum onset of HELLLP can occur __________And increase risk for → ↑risk of ARF and pulmonary edema
hrs to 6 days after delivery ;ARF and pulmonary edema
88
HELLP check for retained products with
US
89
Tx meds for HELLP
Decadron
90
Common occurrence during C-section and vaginal delivery
VAE
91
Subclinical VAE occurs in both GA and
Spinal
92
VAE occurs less with regional
Because they are spontaneously breathing
93
VAE may account for common symptoms during C-section: (DASHA)
```
Dyspnea
Angina
↓SaO2
HoTN
Arrhythmias
```
94
M&M of VAE is r/t volume/rate of air infusion into :
central circulation and site of embolization
95
VAE: Pathophysiology
Pressure gradient as small as -5 cmH2O between surgical field and heart allows venous air entrainment
96
What is associated with INCREASED VENOUS AIR? (SU)
Steep Trendelenburg position
| Uterine exteriorization during C-section
97
VAE Large air volumes is fatal
> 3 mL/kg
98
VAE Small air volumes: VHAH
V/Q mismatch
Hypoxemia
Arrhythmia
HoTN
99
VAE Presentation
50% angina
25% Decrease SaO2
>20% drop in BP (2%)
100
Resuscitation of patient with massive venous air embolism
| PDS -CEIP
```
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
```
101
Risk factors of Eclampsia (FMMN-PPRST)
```
First pregnancy
Multiple Gestation
Molar Pregnancy
Triploidy
Preexisting HTN
Renal diseas
Non-immune hydrops fetalis
SLE
Previous hx of preeclampsia/eclampsia
```
102
Risk Factors of Preeclampsia: Demographic factors (ABH)
Advanced maternal age > 35 years
Black race
Hispanic ethnicity
103
Risk Factors of Preeclampsia: Demographic factors (ABH)
Advanced maternal age > 35 years
Black race
Hispanic ethnicity
104
Risk Factors of Preeclampsia: Genetic Factors (HFHP)
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
Risk Factors of Preeclampsia: Medical Conditions (CODCAS)
```
Chronic HTN
Obesity
Diabetes Mellitus
Chronic Renal Disease
Antiphospholipid antibody syndrome
Systemic Lupus Erythematus
```
106
Risk Factors of Preeclampsia:Obstetric conditions
Multiple Gestation
| Hydatidiform mole
107
Risk Factors of Preeclampsia: Behavioral factor
Cigarette smoking (risk reduction)
108
Risk Factors of Preeclampsia: Partner related risk factors
Nulliparity
| LIMITED PRE-CONCEPTIONAL EXPOSURE TO PATERNAL SPERM
109
All risk factors for Preeclampsia together
```
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
Postparthum hemorrhage : Etiology (4) Ts
Tone
Tissue
Trauma
Thrombin
111
Tissue cause of PPH
Retained products of conception
112
Trauma cause of PPH
Genitral tract trauma
113
Thrombin cause of PPH
Coagulation abnormalities.
114
Take home message for PPH
Do not go over 1 MAC of anesthesia with FURTHER DECREASE UTERINE TONE
115
Causes of Pregnancy Related hemorrhage
| ALUCPUR
```
Abruptio Placenta
Laceration /uterine rupture
Uterine atony
Coagulopathies
Placenta previa--> accreta, increta, percreta
Uterine bleeding
Retained placenta
```
116
4 main causes of Antepartum hemorrhage
| PPUV
Placenta Previa
Placenta Abruptio
Uterine Rupture
Vasa Previa
117
4 types of Placenta Previa
| TPML
Total
Partial
Marginal
Low-lying placenta
118
What is a TOTAL placenta previa?
Internal cervical OS covered completed by placenta
119
What is a PARTIAL placenta previa>?
Internal cervical OS partially covered by placenta
120
What is a MARGINAL placenta previa?
Edge of placenta at margin of internal os
121
What is a low lying placenta?
Placenta is implanted in lower uterine segment --> Placental edge does not actually reach internal os but in close proximity to it
122
What are the 3 types of placenta accreta
Accreta vera
Placenta increta
Placenta percreta
123
Placenta Accreta vera is
Adherence of basal plate of placenta directly to uterine myometrium without penetrating the decidua layer
124
Placenta Accreta increta is
Chorionic villi invade myometrium
125
Placenta accreta percreta is
Invasion through MYOMETRIUM into SEROSA and even adjacent ORGANS (bladder)
126
VASA Previa is
rare condition where fetal vessels from placenta cross entrance of birth canal
127
3 typical causes of Vasa previa
Bi-lobed placenta
Velamentous insertion of umbilicord
Succenturiate (accessory lobe)
128
Placenta Previa symptoms Hallmark
Painless hemorrhage
129
Placenta Previa risk Factors AMMPPS
```
Advanced Maternal Age >35
Multiparity
Multifetal gestations
Prior C-section
Smoking
Prior Placenta previa
```
130
Placenta abruption factors
External hemorrhage
Concealed (internal hemorrhage)
Total
Partial
131
Hallmark of Placenta Abruption
Bleeding with PAIN varying from mild cramping to severe
132
Placenta abruption signs and symptoms uterus
Firm , tender uterus with INCREASE FUNDUS HEIGH
133
Placenta Abruption risk factors
| PPP CCC HIUEM
Prior abruption
Pre-eclampsia
PROM
Chronic HTN
CIgarette smoking
Cocaine use
```
Hydramnios
Increage age and parity
Uterine Leiomyoma
Multiple gestation
External Trauma
```
134
Risk factors of VASA PREVIA (LAMPP)
```
Abnormal placenta morphology
Low lying
Multiple gestation
Pregnancies resulting from IVF
Palpate vessel on vaginal exam
```
135
Uterine rupture most common with
VBAC
136
Uterine rupture classic presentation
| VAPCLEP
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
Risk factors for Uterine Rupture
| PPP TEMFS
```
Prior rupture
Previous uterine sx
Previous C section
Trauma
Excessive uterine stimulation
Multiparity
Forceps delivery
Shoulder distocia
```
138
Contraindications for uterotonic agents: Oxytocin
Hypersensitivity to drug
139
Contraindications for uterotonic agents: Methergine
HTN, hypers.
140
Contraindications for uterotonic agents: Carboprost
Heart, PULMONARY, RENAL, hepatic disease
141
Contraindications for uterotonic agents: Vasopressin
CAD
142
Minimize risk of aspiration
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
Minimizing Risk: H-2 Receptor
| Antagonists
• Cimetidine, Ranitidine, Nizatidine, Famotidine
144
H2 Receptor antagonists Reduces gastric acidity significantly approximately 30 min after IV
administration, maximal effect @ 60-90 min how?
• Block histamine receptors on oxyntic cell → ↓diminish gastric acid production → leading to a slight ↓ in gastric volume in fasting patient
145
•Guidelines for perinatal care (American College of
Obstetrics & Gynecology, American Academy of
Pediatrics) for aspiration risk
“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
Normal laboring patients should not receive
| aspiration prophylaxis unless
They are high risk for C-section
147
PPI minimize risk for aspiration
Inhibit the H+ pump on gastric surface of oxyntic cell
148
Non particulate antacid:
30 mL Na citrate [Bicitra] can neutralize 255 mL of hydrochloric acid with a PH of 1.0
149
Particulate antacids
(e.g.. Maalox, Mylanta)
150
When aspirated causes serious pneumonitis?
Particulate antacids (e.g.. Maalox, Mylanta)
151
When should non particulate antacid be administered?
Should be administered within 20 minutes of induction
| of GETA
152
What is short definition of action of H2 blockers
Keeps from making more acid
153
Prior administration of what may antagonize metoclopramide action?
Prior administration of opioid and atropine
154
How much acid is produced per day by the stomach
| •
Up to 1500 ml highly acidic fluid
155
Pyloric glands
Chief cells secrete pepsinogen →pepsin
156
Oxyntic glands
Oxyntic cells secrete HCl (pH 0.8)
157
This is where PPIs work
Oxyntic cells oxyntic glands
158
Vagus stimulates
G cells to secrete gastrin →bind to oxyntic cells and
| stimulates HCl secretion
159
Ach binds
to muscarinic receptors and ↑Ca2+
160
H-2 receptors ↑cAMP →
dramatic ↑ acid production (also increase calcium)
161
Histamine potentiates both
gastrin and acetylcholine
162
Acid is secreted at a low basal rate of approximately ________ even whenty
10% of maximal output; stomach is empty
163
• Diurnal variation:
lowest in morning, highest in evening
164
Increase dramatically with ingestion
• ↑ dramatically with ingestion
165
No significant differences in __________________
| were seen between pregnant and nonpregnant women
basal gastric acid secretion
166
Cephalic phase:s
chewing, smelling, or tasting without significant
| ingestion ↑ vagal stimulation
167
What happens to gastric acid during the cephalic phase?
Gastric acid output ↑ to 55% of peak levels
168
Gastric phase:
entry into stomach of ingested contents, acid output
| peak
169
When does gastric acid output peak ?
Gastric phase
170
Intestinal phase begins
begins with movement of food into small intestine
171
Gastrin role
Increase gastric acid secretion
172
Pathophysiology of Aspiration Pneumonitis: Acidic Liquid
Acidic liquid aspiration injures alveolar epithelium
→ alveolar exudate (edema, albumin, fibrin, cellular
debris, and RBCs)
173
In pathophysiology of Aspiration Pneumonitis what does Alveolar exudate/pulmonary edema leads to:
* ↓ in lung compliance
* Loss of lung volume
* Intrapulmonary shunting of blood
* Bronchial obstruction/ bronchospasm
174
Aspirates with a ph lower than 2.5 cause
a granulocytic reaction
175
General rule for aspiration pneumonitis
ph<2.5, gastric volume >25 Aspiration pneumonitis
176
Pathophysiology: Particle Aspiration
| • Direct airway obstruction from larger particles
atelectasis; Obstructing large airways
177
In pathophysiology of Smaller particles: similar response as
with acidic liquid
178
In pathophysiology of Smaller particles causes
exudative neutrophilic response at levels of bronchioles and alveolar ducts
179
• 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.
chemical injury from sterile acid gastric contents
| • Basic aspirate ↓ surfactant levels
180
• MOA of Aspiration Pneumonitis:
↑ intraalveolar water and protein content and a loss of lung volume leading ↓ in pulmonary compliance and intrapulmonary shunting of blood
181
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)
an intense inflammatory response ensues from macrophage activation and secretion of cytokines, interleukins and tumor necrosis factor-alpha (MSIT)
182
In Aspiration pneumonitis, After direct acid-mediated injury of respiratory tract, and activation of MSIT what does it lead do ? CAUA
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
In Aspiration Pneumonitis Neutrophils release OPLO
oxidants, proteases, leukotrienes, and other proinflammatory molecules
184
In aspiration pneumonitis: Cellular debris and bronchial denuding.
bronchial obstruction
185
In aspiration pneumonitis, Exudative pulmonary edema -->
BDPI
What happens to lung compliance? PVR , WOB
bronchial obstruction
↓ lung compliance, and shunting → hypoxemia,
****↑ pulmonary vascular resistance****
Increased work of breathing
186
Most common site of aspiration and why?
RLL; d/t large size of right mainstem bronchus
187
Aspiration pneumonitis: Recovery involves proliferation and differentiation of
surviving type II pneumocytes in alveolar epithelial cells
| • Actively transport Na+ out of alveolus, water follows
188
Recovery aspiration pneumonitis: Soluble proteins are removed by
paracellular diffusion and endocytosis
189
Recovery of Insoluble proteins are removed by
macrophages.
190
Neutrophils are removed by
programmed cell death and phagocytosis by
| macrophages
191
Aspiration pneumonitis Type II
Type II pneumocytes gradually restore normal composition of surfactant
192
DIC Results from an
abnormal activation of the coagulation system
193
Abnormal activation of the coagulation system DIC leads to : (FDAH)
Formation of large amount of thrombin
Depletion of coagulation factors
Activation of fibrinolytic system
Hemorrhage
194
If severe enough DIC leads to
diffuse microvascular thrombosis → end-organ injury
195
DIC depletion of platelet
Intravascular deposition of fibrin -->Thrombosis of small and midsize vessels and organ failure
Depletion of platelets and anticoagualtion factors-> Bleeding
196
Obstetric triggers of DIC
include entry of procoagulant tissue extracts into the blood which interact with factor VII and activate the extrinsic coagulation pathway
197
DIC and dead tissue
dead tissue and amniotic fluid contains thromboplastic substances that trigger coagulation
198
What really activate the cascade?
Endothelial injury.
199
What is the hallmark of DIC
Elevated D-dimer, Fibrin and Fibrin Degradation Products (FDPs)
200
Other proteins Depleted in DIC
Antithrobin 3, Fibronectin, Plasminogen
201
Decreased labs in DIC
Platelet count, Fibrinogen, and antithrombin III concentrates.
202
DIC : There is Variable Increase in
PT, aPTT, and thrombin and Reptilase times
203
Reptilase time is
Detect abnormalities in Fibrinogen
204
In DIC Endothelial cells --> Plasminogen activator-->
Plasminogen --> Plasmin
205
In DIC platelets
Platelets --> thrombin--> Activated platelets.
206
DIC Pathophysiology: Intravascular
| Fibrin Formation
• Formation of small strands/microclots of fibrin is the immediate result of DIC (may lead to obstruction of pulmonary vessels)
207
• Fibrinolysis present in
| •
every patient with DIC
208
```
• Fibrin degradation products (FDP) are Protein
fragments that (APID)
```
Act as antithrombins (↑ bleeding)
Produce defective fibrin polymer (↑ bleeding)
Impair platelet clearance
Directly damage pulmonary vasculature (ARDS!
209
Tx for preeclampsia High MAG
Calcium gluconate and Furosemide
210
33 weeks scheduled for procedure, which drug to avoid
Ketorolac (NSAIDS)
211
33 weeks scheduled for procedure, which drug to avoid
Ketorolac (NSAIDS) (can close the ducturs arteriosus)
212
Consistent with Preeclamspia?
```
Proteinuria
Increased thromboxane
Decreased Prostacyclin
Vasoconstriction
Enhanced Platelet aggregation
```
213
How does Nitroglycerin help
Provide uterine relaxation
214
IF the patient has DIC no
spinal anesthesia
| Alternative GA
215
Late severe DIC
Rule out severe liver disease (elevated platelets, elevated PT)
216
DIC Active bleeding or invasive procedure is required,
transfuse: FFP how much and why?
• Ventilation, multiorgan system support
(15 to 30 mL/kg) to maintain the PT and aPTT within
| 1.5 times normal values
217
DIC and Cryoprecipitate or fibrinogen concentrate
to maintain fibrinogen concentration above 150 to 200 mg/dL
218
DIC and Platelets to
maintain a platelet count above 50,000/mm3
219
Normally, avoid neuraxial anesthesia with
coagulation disorders
220
In selected circumstances, neuraxial anesthesia can be offered to a patient with an
Isolated laboratory abnormality and no clinical evidence of coagulopathy.
221
With patient with coagulopathy , Frequent neurologic examinations are performed to
Facilitate the early detection of an "epidural hematoma" during the postpartum
222
MAP 1st formula
MAP = (CO x SVR) + CVP
223
MAP 2nd formula
1/3 (systolic pressure – diastolic pressure) + diastolic pressure
224
Possibility of high spinal block if
too much LA administered
225
High spinal can lead do =
respiratory paralysis
226
Absolute Neuraxial CONTRAINDICATIONS
| PUCISH
```
• Pt refusal
• Uncorrected hypovolemia
• Clinical coagulopathy
• Infection at injection site
• Severe preeclampsia
• Hx thrombocytopenia and labs have not
resulted yet
```
227
Can help c/maintaining hemodynamics during modest hemorrhage
Ketamine
228
Preventing Sympathectomy
| from Becoming a Problem
* Phenylephrine OK but go slow
| * 50 mcg until BP remains stable (SBP > 100)
229
What gauge needle to Insert for Subarachnoid space:
25g spinal needle to subarachnoid space
230
Spinal Needles: Cutting-bevel needles (Quincke) =
rarely used due to unacceptably ↑risk of PDPH
| Still used in elderly population
231
Non-cutting needles (Whitacre, Sprotte) preferred
| • “Pencil-point needles” causes what?
Causes more trauma to dura → more intense
inflammatory response → more rapid closure of
dural defect
232
• “Pencil-point needles”
Non-cutting needles (Whitacre, Sprotte)
233
Needles that are preferred are
Non-cutting needles (Whitacre, Sprotte) preferred
234
Bigger gauge needle advantages
More control, more resistant to bending/shearing from hitting bones
235
Smaller spinal needles risk?
↓PDPH risk, harder to control
236
Emergencies usually necessitate what kind of needles?
larger gauge needles
237
Awareness during GETA
• High incidence between______and _______
• 50% N2O /O2
administered c/following agents ↓awareness to <1%
• 0.6% Isoflurane
• 1% Sevoflurane
• 3% Desflurane
induction of anesthesia and delivery of fetus
238
What leads to maternal Awareness.?
Administration of only 50% N2O with O2 without other agents resulted in maternal awareness in 12-26% of cases
239
What medication help prevent Awareness during GETA
Ketamine on induction can help
240
To help prevent awareness minimize
Minimize time from induction to delivery
241
50% N2O /O2 administered c/following agents ↓awareness to <1%
* 0.6% Isoflurane
* 1% Sevoflurane
* 3% Desflurane
242
____are now considered the preferred anesthetic
• SAB
243
Preventing Sympathectomy from Becoming a Problem
• ↑SVR c/pressors - Phenylephrine
244
How to Treat HoTN from Sympathectomy
| • Arteriolar constrictors (pressors)
* LUD
* Proper fluid loading
* Preload alone might not prevent hypothermia
245
Treating HoTN
• 500mL hetastarch can be better than 1500mL
| crystalloid
246
For C/S If tachycardic, use
phenylephrine
247
For Hemodynamic stability in C/S If bradycardic,
use ephedrine
| Atropine if severe (glycopyrrolate works too slow)
248
For Hemodynamic stability in C/S Bradycardia can occur with
generous phenylephrine boluses (HTN)
249
If SBP < 110, pretreat with some
ephedrine (50mg IM, or 25 mg into skin local you are going to use)
250
C/S meds to be available to maintain
* Ketamine should be available
| * Ephedrine and Phenylephrine should already be diluted
