1
Q
a BMI over ___ is associated with an increase morbidity due to stroke, ischemic heart disease and diabetes that is 3 to 4 x the general population.
A
28
2
Q
Central/Android fat
A
Belly fat
Common in men
Higher incidence of metabolic complications
3
Q
Gynecoid Fat
A
Hips, buttocks, thighs
Far less metabolically active
Harder to lose weight in these regions
4
Q
STOP-BANG
A
Snoring
TIRED
Observed Apnea
Pressure (HTN)
BMI
AGE
Neck Circumference
Gender
5
Q
OSA Definition
A
cessation of airflow > 10 secs
6
Q
Hypopnea
A
Decreased flow from baseline
7
Q
of apnec/hypopneic events to diagnose OSA
A
> 5 is considered Sleep Apnea
8
Q
Utilized to reduce / eliminate OSA
Can actually increase risk of OSA in post-op period
Sedation / anesthesia for procedure itself
Edema of the airways
A
Uvulopalatopharyngoplasty (UPP)
9
Q
Pickwickian Syndrome
A
obesity hypoventilation syndrome (OHS), a disorder where obesity leads to poor breathing, resulting in low blood oxygen and high blood carbon dioxide level
10
Q
Drugs dosed on TBW
A
Thiopental
Midazolam
Sux
Atracurium
Cisatracurium
Fentanyl/ Sufentanil
11
Q
Drugs dosed on Ideal Body Weight
A
Propofol
Vecuronium
Rocuronium
Remifentanil
12
Q
Effects of pneumoperitoneum in for obese patients
A
Biphasic
At 10mmHg – actually get increased venous return with subsequent increased CO and arterial pressure
At 20mmHg see decreased venous return and decreased CO
Start to see decreased GFR from lower renal flow at this point.
13
Q
Gastric restriction surgery
A
Lap Banding
Vertical Banded Gastroplasty
14
Q
Intestinal Malabsorption surgery
A
Biliopancreatic Diversion (BPD)
Distal Gastric Bypass
15
Q
Both Restrictive and Malabsorptive surgery
A
Roux-en-Y Gastric Bypass
16
Q
Micronutrient deficiency associated with bariatric surgery
A
Iron, Vitamin B12 & Folate
Fat Malabsorption- can lead to fat-soluble vitamin deficiency
17
Q
Cardiovascular S/S of Anorexia Nervosa
A
Decreased cardiac muscle mass & myocardial contractility
Cardiomyopathy secondary to starvation & use of ipecac
Sudden Death d/t ventricular dysrhythmias (hypokalemia)
18
Q
Episodes of binge eating, purging, and dietary restriction
Often chronic with multiple relapses
Depression, anxiety disorders, and substance abuse commonly accompany this disorder
A
BUllemia Nervosa
19
Q
Metabolic derangement associated with BUllemia nervosa
A
Metabolic alkalosis
Typically hypochloremic w/ hypokalemia
20
Q
S/S of Bullemia Nervosa
A
Dry skin, dehydration, and fluctuant hypertrophy of salivary glands
Resting bradycardia
Increased serum amylase (due to parotid gland hypertrophy)
21
Q
Malnutrition S/S
A
Serum albumin < 3g/dL
Transferrin levels < 200mg/dL
Prealbumin levels depressed
22
Q
overproduction of porphyrins & their precursors
A
Porphyria
23
Q
the most important porphyrin in the human body
A
Heme
24
Q
Typically inherited as non-sex-linked autosomal dominant conditions with variable expression
No difference amongst gender with regards to inheritance…..
However, attacks are more frequent in women
Usually in the 3rd or 4th decades of life
A
Acute Porphyrias
25
Severe abdominal pain
Including diarrhea & vomiting
Autonomic nervous system instability
Electrolyte disturbances
Neuropsychiatric manifestations
Skeletal muscle weakness (can cause quadriparesis & respiratory failure)
Acute Porphyria S/S
26
Acute Porphyria Triggering mechanism
Via induction of the ALA synthetase enzyme of by interfering with the negative feedback control
27
Acute Porphyria Triggers
Barbiturates (Thiopental, methohexital)
Etomidate
(Probably)- Ketorolac, Nifedipine
28
Porphobilinogen deaminase – defective enzyme
On chromosome 11
Acute intermittent porphyria
29
Acute intermittent porphyria s/s
This is probably the most life-threatening
Systemic Hypertension, renal dysfunction
30
has actually been recommended as a treatment of acute porphyrias as it decreases heme consumption & inhibit ALA synthetase activity)
ASpiration prophylaxis
Cimetidine for aspiration prophylaxis
31
What can suppress porphyrin synthesis?
Carbohydrates
32
Treatment of Porphyric Crisis
Remove all triggering factors
Provide adequate hydration and carbohydrates
Hematin (3-4mg/kg IV over 20 minutes)
The ONLY specific therapy for acute porphyric crisis
33
The ONLY specific therapy for acute porphyric crisis
Hematin (3-4mg/kg IV over 20 minutes)
34
A Disorder of purine metabolism
Primary – inherited metabolic defect
Leads to overproduction of uric acid
Secondary - overproduction of uric acid
Possibly due to chemotherapeutic drugs
Gout
35
– inhibits the conversion of purines to uric acid
Allopurinol
36
decreases plasma concentration of uric acid
Probenecid
37
for use in acute gouty arthritis
Colchicine
38
In gout, how can we alkalinize the urine?
Sodium bicarb – alkalinize the urine
Helps facilitate further uric acid excretion
39
A genetically determined disorder of purine metabolism
Occurs exclusively in males
Often mentally retarded, characteristic spasticity and self mutilation (of the perioral region = tough intubation)
Lesch-Nyhan Syndrome
40
Deficiency or lack of enzyme glucose 6-phosphatase
Glycogen can not be hydrolyze -> leads to intracellular accumulation
Hypoglycemia can occur and patients need to feed every 2-3 hours.
Glycogen Storage Disease Type 1a
(aka von Gierke’s disease)
41
Glycogen Storage Disease Type 1a
(aka von Gierke’s disease)
Anesthetic considerations
Remember to give these patients intra-op glucose and check routine arterial pH to check for metabolic acidosis (avoid lactate containing fluids)
42
Rare autosomal recessive disease
Here glucose 6-phosphate cannot be transported to the inner surface of microsomes (transport system defect)
Hypoglycemia and lactic acidosis ensue
Glycogen Storage Disease Type 1b
43
With Glycogen Storage Disease Type 1b, if metabolic acidosis occurs,
Give sodium bicarb
44
Anesthetic considerations of Glycogen Storage Disease Type 1b
Hypoglycemia and lactic acidosis ensue
Limit pre-op fasting, provide glucose-containing infusions
Do not hyperventilate these patients
45
Mental retardation, seizures, aminoaciduria
Disorders of Amino Acid Metabolism
46
Anesthetic management of Disorders of amino acid metabolism
Maintenance of intravascular fluid volume
Acid-base homeostasis
Avoid anesthetic drugs that could evoke seizures
47
Enzymatic deficiency of phenylalanine hydroxylase
Mental retardation & seizures
Can have Vit. B12 deficiency → avoid Nitrous Oxide
Phenylketonuria
48
Defect in processing precursors of cysteine
Homocystinuria
49
Defective carboxylation of branched chain amino acids -> leads to urine that smells like maple syrup.
Maple Syrup urine disease
50
In a pt with hx of this chemotherapeutic agent,
keep FiO2 as low as humanly possible, as close to 21% as possible
Bleomycin
51
Side effects of Bleomycin
interstitial pneumonitis / pulmonary fibrosis
52
Side effects of Cisplatin
– ototoxicity, peripheral neuropathy, renal failure
53
Side effects of Cyclophosphamide
plasma cholinesterase inhibition; hemorrhagic cystitis
54
Side effect of Doxorubicin/ Adriamycin
cardiomyopathy
55
Side effects of Mitomycin
Hemolytic Uremic Syndrome (HUS
56
Paclitaxel (Taxol)
Hypersensitivity reaction, peripheral neuropathy
57
Side effects of Vincristine
Peripheral neuropathy, autonomic neuropathy
58
These are physiologic disturbances that may accompany cancer.
Paraneoplastic Syndromes
59
Hematologic abnormalities associated with cancer
Anemia
Polycythemia
Thrombocytopenia
Recurrent DVTs
60
Typically assoc. w/ lung cancer (small cell lung cancer)
May experience potentiation of both depolarizing and non-depolarizing neuromuscular blocking drugs.
Myasthenic syndrome (skeletal muscle weakness
61
Occurs following sudden destruction of tumor cells by chemotherapy
Release of uric acid, potassium, & phosphate
Tumor Lysis syndrome
62
Side effects of Tumor lysis syndrome
Uric acid – renal failure
Potassium – cardiac dysrhythmia
Hyperphosphatemia → secondary hypocalcemia
63
Most often after treatment of hematologic neoplasms
Tumor Lysis Syndrome
64
If this occurs, usually due to partial replacement of adrenal cortex by tumor or suppression of adrenal cortical function.
Most often seen in patients w/ metastatic disease
Melanoma, retroperitoneal tumors, lung cancer, or breast cancer.
Adrenal insufficiency
65
Tx for adrenal insufficiency in Cancer
Bolus intravenous administration of cortisol repeated at 6 to 8 hour intervals or given by continuous infusion.
66
Acute Cardiac Complications associated w cancer
Pericardial effusion → can lead to tamponade
67
PA Cath 5L/min, CVP 8, Wedge Pressure 10, PAP unchanged, what is the most appropriate initial management?-
Initiate Vasopressors
68
Normal CVP/ RAP
2-6 mmHg
69
Normal PCWP
3-12 mmHg
70
CPP( Coronary)
DBP- PAOP
71
(.0138x Hb x SaO2) + .003x PaO2
CaO2
71
Normal CaO2
17-20 mL/dL
72
Do2
CaO2 x CO x10
73
VO2 (Consumption)
C (a-v)O2 x CO x 10
74
Fluid overload via irrigation
Hyponatremia, Nausea, Restlessness, hypertension, wide QRS, Tachypnea, met. Acidosis-d/t deamination of glycine, CV Collapse
TURP Syndrome
75
Increase in __ will increase myocardial wall tension?
Ventricular Cavity size
76
Renin secretion from JGA is least likely to occur in response to
increased GFR
77
Not an Etiology of NAGMA
Aspirin
78
Most harmful in decompensated heart failure-
Metoprolol/Beta Blockers
79
Methanol, Uremia, DKA, Paraldehyde, Isoniazid, Lactic Acidosis, Ethanol/ Ethylene Glycol, Salicylates
HAGMA
80
Hyperalimentation/hyperaldosteronism, Acetazolamide, Renal tubular acidosis, Diarrhea, Uretero-pelvic shunt, Pancreatic fistula, Spirinolactone
NAGMA
81
Anterior MI- Which vessel is most likely to result in this acute cardiac event-
Left main Coronary artery
82
Electrolyte disturbance associated with brain death
Hypernatremia
83
Electrolyte disturbance associated with brain death
Hypernatremia
84
Intra-op MI has occurred, what is the earliest detection of myocardial ischemia?-
TEE
85
TBW Calculations
.6x Body weight
86
BMI Calculation
Weight (kg)/ Height (m)^2
87
Isolated Left Heart Failure will have what clinical features?-
Crackles on lung auscultation
88
Benign process-
Midsystolic murmur
89
In HOCM, which of the following is not an intra-op goal?- I
Increased Inotropy
Why?- HOCM’s LVOTO worsens with increased inotropy (Systolic anterior motion), highly sensitive to changes in contractility
90
CXR findings of heart failure-
Pleural Effusion
91
Interpret this ABG (pH/PaCO2/PaO2/HCO3) (7.38/52/58/30
Pickwickian syndrome
92
Least likely in patients with Significant pulmonary hypertension w normal left heart function-
Crackles
93
hich statement about the acute refractory period of a cardiac myocyte action potential is most likely true-
Encompases Phases 0-2
94
HR 120, MAP 50, which Data is most consistent with cardiogenic shock induced by Right heart failure?-
CVP 18, Wedge Pressure 12, SVR 1500
95
36 YO athlete with pHTN- what is the primary symptom seen in these patients?-
Progressive increase in shortness of breath on exertion is primary symptom
96
What is the O2 carrying capacity (arterial content) of a patient with Wt = 100kg, Hgb = 15g/dL, and SpO2 = 90% ? What is the CaO2
97
- 60% inherited disorders. Most common hemolytic anemia in Europe and US (1 in 5000). Abnormal RBC membrane proteins. Osmotic fragility-> RBC lyse easily. Pts often have splenomegaly and easy fatigue in proportion to their anemia. Hemolytic crisis can be precipitated by viral or bacterial infection
Spherocytosis
98
Usually caused by Folic Acid and Vit. B12 deficiencies. Can be caused by alcoholism- interferes w folate metabolism. Underdeveloped world- B12 malnutrition, Nitric Oxide (Prolonged exposure). Classic pathlologic findings- hypersegmented neutrophils
Macrocytic/megaloblastic anemia
99
Methemoglobinemia shift of O2 Dissoc curve
Left-Shift O2-Hgb dissociation curve
100
2 phases of tissue factor initiation
Initiation
Propagation
101
Initiation of Tissue factor
TF binds to VIIa. TF-VIIa complex converts small amounts of X to Xa, which generates small amounts of thrombin
102
Propagation of tissue factor
The small amount of thrombin leads to lots of thrombin
103
Autosomal recessive, rare deficiency. Prolonged PT, Normal PTT.
Factor VII Deificiency
104
Tx of FVII Deficiency
Severe- NovoSeven- Recombinant Factor VIIa. Proplex T- Contains Factors II, VII, IX, X
105
for 20-30% Factor level increase, how many units of FFP are required
4-6 Units of FFP
106
X, IX, VII, II (Also Protein C and S)
Vitamin-K Dependent factors
107
FVIII Deficiency
Hemophilia A
108
FIX Deficiency
Hemophilia B
109
TEG increased R Time, Give
FFP
110
TEG increased K Time, Give
Cryo
111
TEG increased Alpha angle, Give
Cryo
112
TEG increased max amplitude, Give
Platelets
113
TEG increased LY30, give
TXA/ACA
114
Tx for Syphillis
Penicillin
115
Target spot
Lyme disease
Borrelia burgdorferi
116
among top nosocomial infections
CVCs usually the predominant cause
CLABSI
117
An “umbrella” of conditions which ultimately lead back to an etiology of infection in the body.
SEPSIS
118
Inflammatory Response including 2 or more of following:
Temperature > 38C or < 36C
HR > 90/min (not the usual 100 assoc. w/ tachycardia)
RR > 20/min (or) PaCO2 < 32mmHg
WBC > 12,000, < 4000, or > 10% bands
Systemic Inflammatory Response Syndrome
119
Sepsis is
SIRS +confirmed/suspected infection
120
Severe Sepsis
Sepsis + end-organ failure
Altered Mental Status
Respiratory Failure
Renal failure (oliguria, etc.)
Anemia / thrombocytopenia
Coagulopathy (liver dysfunction)
121
Septic Shock
Sepsis + Hypotension (after appropriate resuscitation; 20ml/kg fluid bolus)
Hypotension?
Systolic < 90mmHg
MAP < 70mmHg
Hypertensive patients; SBP decrease > 40mmHg from baseline
Sepsis + Elevated Lactate
Lactate ≥ 4mmol/L
122
#1 Vasopressor choice for septic shock
Norepinephrine
123
What vasopressor is not recommended for septic shock?
Phenylephrine
124
Vasopressor choices for septic shock
-Norepinephrine (Levophed) – 1st choice
-Vasopressin (can be added to N.E.)
-Epinephrine (2nd or 3rd line agent)
-Dopamine – can be used in cases of bradycardia
125
most common bacterial cause of community-acquired pneumonia
S. pneumonia
126
often seen with alcoholic binges
K. pneumonia
127
A 55 year old male patient (probable alcoholic based on history) aspirates on induction of general anesthesia. Which of the following should be implemented?
A. Oropharnygeal suctioning
B. Stress dose steroids
C. Broad spectrum antibiotics
D. Bronchial – alveolar lavage
E. All of the above
. Oropharnygeal suctioning
128
Most common nosocomial infection in ICU
Ventilator-Associated Pneumonia (VAP)
129
ARDSNET Guide for Ventilation in the ICU
6 to 8ml/kg of ideal body weight tidal volumes
130
Persistent cough, anorexia, weight loss, chest pain, hemoptysis & night sweats
Tuberculosis
131
Obligate aerobe responsible for TB
Loves oxygen, hence it loves the apices of lungs
Mycobacterium tuberculosis
132
Gram positive anaerobe; spore producing
(don’t forget to wash you hands)
Clostridium difficile (C. diff)
133
Usually previous antibiotic therapy (Clindamycin is the usual board question answer)
C. Diff
134
Diarrhea
Pseudomembranous colitis (colonoscopy)
C. Diff
135
Tx for CDiff
Oral vancomycin
Oral metronidazole
Fecal transplantation (not a joke; real procedure
136
an accumulation of mutations in genes that regulate cellular proliferation.
Cancer
137
Etiologies of Cancer
Genetic mutations
Carcinogens (cause 80% of cancers in US)
Tobacco
Alcohol
Sunlight
138
Cancer staging
T = tumor size
N = node (lymph node involvement)
M = metastasis (distant metastasis)
Stage I – best prognosis
Stage II
Stage III
Stage IV – poorest prognosis. Usually has distant metastasis
139
interstitial pneumonitis / pulmonary fibrosis
keep FiO2 as low as humanly possible, as close to 21% as possible
Bleomycin
140
ototoxicity, peripheral neuropathy, renal failure
Cisplatin
141
plasma cholinesterase inhibition; hemorrhagic cystitis
Cyclophosphamide
142
cardiomyopathy
Side effect of what chemo drug?
Doxorubicin (Adriamycin)
143
Hemolytic Uremic Syndrome (HUS) associated w what chemo drug?
Mitomycin
144
Hypersensitivity reaction, peripheral neuropathy
associated w what chemo drug
Paclitaxel (Taxol)
145
Peripheral neuropathy, autonomic neuropathy
Associated w what chemo drug
Vincristine
146
Germ Cell cancers are typically treated w what chemo drug?
bleomycin, keep FiO2 as low as humanly possible, as close to 21% as possible
147
Includes somatic & visceral pain
Involves stimulation of nociceptors
Typically responds to opioids and nonopioids
Nocioceptive pain
148
Involves peripheral or central afferent neural pathways
Responds POORLY to opioids
Neuropathic pain
149
Tx for mild to moderate cancer pain
NSAIDs & acetaminophen
150
Moderate to severe cancer pain, use
Add in weaker opioids (ex. Tramadol, Codeine)
151
Severe cancer pain, use
Add in stronger opioids (ex. Morphine)
152
World Health Organization Pain Relief Ladder
Give meds by the clock
(i.e. every 3-6hrs)
-Not just when in
pain
153
These are physiologic disturbances that may accompany cancer.
Paraneoplastic syndromes
154
Typically assoc. w/ lung cancer (small cell lung cancer)
May experience potentiation of both depolarizing and non-depolarizing neuromuscular blocking drugs
Myasthenic syndrome (skeletal muscle weakness)
155
Ectopic hormone production
Paraneoplastic syndromes
Corticotropin
ADH
melanocyte stimulating hormone and PTH
Thyrocalcitonin
Insulin
156
Insulin Paraneoplastic
Retroperitoneal tumors
Hypoglycemia
157
Melanocyte stimulating hormone & PTH Paraneoplastic
Lung (small cell)
Hyperpigmentation
Hyperparathyroid
158
ADH Paraneoplastic
Water intoxication
159
Corticotropin paraneoplastic
Lung Cancer (small cell), thyroid, thymoma
Cushing's syndrome
160
Occurs following sudden destruction of tumor cells by chemotherapy
Release of uric acid, potassium, & phosphate
Uric acid – renal failure
Potassium – cardiac dysrhythmia
Hyperphosphatemia → secondary hypocalcemia
Tumor Lysis Syndrome
161
Tumor lysis syndrome typically occurs when?
Most often after treatment of hematologic neoplasms
162
ADrenal insufficiency in cancer
If this occurs, usually due to partial replacement of adrenal cortex by tumor or suppression of adrenal cortical function.
163
Adrenal insufficiency is typically seen in patients with
Metastatic disease
Melanoma, retroperitoneal tumors, lung cancer, or breast cancer.
164
Treatment of adrenal insufficiency from cancer
Bolus intravenous administration of cortisol repeated at 6 to 8 hour intervals or given by continuous infusion.
165
Due to spread of cancer into the mediastinum or directly into caval wall
Concerns w Resp. collapse and hemodynamic collapse/instability
Superior Vena Cava Obstruction
166
JVD, upper extremity swelling, facial swelling d/t venous congestion
Superior Vena Cava Obstruction
167
Superior Vena Cava Anesthetic considerations
Maintain spontaneous breathing,CPB, awake intubation. Avoid PPV, try to keep spontaneous, avoid muscle relaxants (causing collapse)
168
Spinal Cord compression in cancer
due to presence of metastatic lesion in the epidural space.
-Usually breast, lung, prostate, or lymphoma
-Neurological symptoms an indication for emergent decompression (ie. Laminectomy)
169
Increased ICP in cancer
due to presence of metastatic lesion in the epidural space.
-Usually breast, lung, prostate, or lymphoma
-Neurological symptoms an indication for emergent decompression (ie. Laminectomy)
170
Tx of increased ICP in Cancer
Corticosteroids, diuretics & mannitol
Radiation – can be palliative
171
A 65 year old woman has an abnormality on routine mammogram. Localized needle biopsy confirms presence of breast cancer. Cancer cells are ER+; her2 neu+, and patient has BRCA2 gene. Which of the following is next step in treatment?
a. Lumpectomy
b. Lumpectomy with sentinel lymph node dissection
c. Mastectomy with axillary lymph node dissection
d. Chemotherapy, then surgery, then radiation
e. Start patient on Tamoxifen immediately
Chemotherapy, then surgery, then radiation
172
Most important consequence of anemia is
decreased O2 carrying capacity of blood.
173
1.34 * Hb * SaO2) + (0.0031 * PaO2)
CaO2
174
CO x Cao2
D02
175
rightward shift of Oxy-Hgb dissociation curve
Decreased CaO2
176
If inadequate blood flow to tissues…kidneys ->
Release EPO -> stimulate bone marrow to make RBCs
177
Abnormal RBC membrane proteins
Osmotic fragility -> RBC lyse easily
Spherocytosis
178
Most common inherited hemolytic anemia in Europe and US (approx. 1 in 5000 individuals)
Spherocytosis
179
Symptoms of Spherocytosis
Patients often have splenomegaly and easy fatigue in proportion to their anemia
Hemolytic crisis can be precipitated by viral or bacterial infection
180
single amino acid substitution error in either the alpha or beta globin chains
Defects in Hgb structure are usually due to
181
-Defect in heme Beta-globulin
-occurs due to substitution of valine for glutamic acid
Sickle Cell Anemia
182
In deoxygenated state, the Hgb undergoes a “conformational change” such that if enough Hgb in the RBC undergoes this change, it distorts the RBC membran
Sickle Cell Anemia
183
presents early in life (hemolytic anemia)
-vaso-occlusive disease (spleen, kidney, CNS)
-episodic pain crises (aka sickle crisis)
-joint pain, chest pain
-Acute Chest Syndrome
-pneumonia-like complication
-fever, tachypnea, wheezing, etc.
-CNS can include stroke
-Infarction common in adolescents
-Hemorrhagic later in life
Sickle Cell Anemia
184
Tx for acute chest syndrome
focus on oxygenation, pain control, and transfuse as necessary to correct anemia
Inhaled nitric oxide has been shown to reduce Pulm. HTN and Improve Oxygenation (but not yet widely available)
185
Developed World = Alcoholism
-Alcoholics have poor diet & EtOH interferes with folate metabolism
Developing World = malabsorption B12 deficiency
-Tropical and nontropical sprue
Macrocytic/Megaloblastic Anemia
186
Usually caused by Folic Acid and Vit. B12 deficiencies -both are needed for DNA synthesis
-high turnover tissues are first to be affected
-Marrow becomes megaloblastic
-RBCs become macrocytic (big
Macrocytic/Megaloblastic Anemia
187
-Long / Sustained exposure to Nitrous Oxide can cause
Macrocytic/Megaloblastic Anemia
188
Symptoms of Megaloblastic/macrocytic anemia
bilateral peripheral neuropathy due to degeneration of lateral and posterior columns of spinal cord.
-memory impairment and mental depression
189
What to avoid anesthetically in Megaloblastic/macrocytic anemia?
Nitrous oxide
190
What is the classic pathological finding of megaloblastic/macrocytic anemia?
Hypersegmented neutrophils are the classic pathologic finding
191
Hgb disorders resulting in Reduced or Ineffective Erythropoiesis
Microcytic Anemia(s) (Microcytic Hypochromic)
-Iron deficiency anemia
-Inherited defects in globin chain synthesis
-thalassemias
192
-Nutritional deficiency more common in kids
-In adults, due to blood loss (GI or menstrual)
-Parturients at risk due to increased RBC mass during pregnancy and fetus need for iron
Iron deficiency anemia
193
Gold standard for iron deficiency anemia diagnosis
absence of stainable iron on bone marrow aspirates (ouch) is the gold standard
194
Factor VIII Deficiency
PT/pTT Labs
PT = normal
PTT = Prolonged
195
Tx for FVIII Deficiency
50-60 U/kg of Factor VIII (T1/2 = 12Hrs
196
Anesthetic considerations for FVIII deficiency hemophilia A
50-60 U/kg of Factor VIII (T1/2 = 12Hrs
197
Congen. Factor IX Deficiency (Hemophilia B)
PT/PTT Labs
PT = normal
PTT = prolonged
198
Tx for FIX/Hemophilia B
Recombinant / purified Factor IX available
-Typically dose 100U/kg
T1/2 = 18-24Hrs
199
Interferes w/ final step in fibrin clot formation
-usually no spontaneous bleeding, but patients have problems w/ surgery
Abnormalities in Fibrinogen
Problems when fibrinogen < 50-100mg/dL
200
more a problem with abnormal fibrinogen production.
-Often inherited defects (Autosomal dominant)
Dysfibrinogenemia
201
If pt w dysfibrinogenemia is bleeding, give
If symptomatic or bleeding with surgery…. Give cryoprecipitate
202
If pt with dysfibrinogenemia is not bleeding
give nothing
203
Tx for dysfibrinogenemia
Cryo until fibrinogen > 100mg/dL
10-12 units of cryo in an average sized adult
204
Normal PLT
Normal (150-450K platelets/μL)
205
What amount of platelets are sequestered by the spleen at any time?
approx 1/3 of all platelets sequestered by spleen at any one time (even more on CPB)
206
Platelet lifespan
Platelet life = 9-10 days
207
Platelet production requirements
(need to produce 15-45K platelets/μL each day)
208
Each “unit” of platelets likely increase patient’s platelet count by
10K
209
non-immune HIT-
can be seen in the majority of patients within first day of full dose Heparin
HIT Type I
210
immune mediated
-usually heparin > 5 days
-antibody to heparin-PF4 complex
HIT Type II
211
This type of HIT can actually lead to a thrombotic event
HIT Type II
212
Tx of HIT
stop the heparin (including LMWH)
-start a direct thrombin inhibitor
-Lepirudin or Argatroban
213
abnormal plt. function is indicative of a
Qualitative disorder
214
Qualitative disorder
-von Willebrand’s Disease****
-Bernard Soulier syndrome
-Glanzmann thrombasthenia
215
-Most common inherited bleeding disorder
-Autosomal dominant or recessive
-usually present with symptomatic
-mucocutaneous bleeding, epistaxis, easy bruising, menorrhagia, gingival bleeding
von Willebrand’s Disease
216
-bleeding time, platelet count, PT & aPTT
Screening Labs for VWD
217
Most common (80% of cases)
-Quantitative defect in vWF levels
-von Willebrand’s Disease Type 1 Disease
218
Tx for VWD Type I
DDAVP (increases release of vWF)
219
Qualitative defect in plasma vWF
-von Willebrand’s Disease Type 2 Disease
220
a virtual absence of circulating vWF &
-very low activity of vWF (&)
-very low activity of faction VII
-von Willebrand’s Disease Type 3 Disease
221
-Blood products containing vWF
-cryoprecipitate
-factor VIII-vWF concentrate
222
Acquired Abnormalities of Platelet Function
1. Myeloproliferative Disease
2. Dysproteinemia
3. Uremia
4. Liver Disease
5. Inhibition by Drugs
223
problems manufacturing platelets
Myeloproliferative Disease
224
Waldenstrom Macroglobulinemia
Dysproteinemia
225
untreated uremic patients show defect in platelet function.
URemia
226
ASA, Plavix, NSAIDs etc.
Acquired Abnormalities of Platelet Function
Inhibition by drugs
227
2 Major classes of hypercoagulable disorders
Congenital predisposition
2. Acquired / Environmental
228
heritable causes of hypercoagulability
Thrombophilia 2/2 decreased antithrombotic proteins
Hereditary Antithrombin deficiency
Hereditary Protein C & S Deficiency
-
229
Adverse affect on thrombin regulation.
Hereditary Protein C and S Deficiency
230
Autosomal Dominant Trait
20x more likely to develop VTE
Hereditary Antithrombin deficiency
231
Factor V Leiden
Prothombin G20210A Gene Mut
Heritable causes of Prothrombotic states
232
Acquired causes of hypercoagulability
1. Myeloproliferative disorders
2. Malignancies
3. Pregnancy
4. Oral Contraceptive Use
5. Nephrotic Syndrome Patients
6. Antiphospholipid Antibodies
233
Acquire Hypercoag. of the ARTERIAL vasculature
Atrial Fibrillation
2. Antiphospholipid Antibodies
234
Esophagus function
passage
235
Stomach function
Digestion
236
Small bowel function
absorption
237
Large bowel function
storage
238
reflux of gastric contents into the esophagus associated with symptoms
GERD
239
usually caused by decr. resting tone of LES
Reflux into structures of airway can cause chronic cough, pneumonia, and asthma
GERD
240
Antireflux structures
LES, crural diaphragm, GE junction locale
241
An ulcerated esophagus usually has
An open LES
242
Aspiration risk factors
emergency surgery, difficult a/w, light
anesthesia, lithotomy, IDDM, pregnancy,
obesity, decreased LOC, severe illness
243
Drugs that increase LES tone
Metoclopramide
Domperidone
Prochloroperazine
Cyclizine
Edrophonium
Neostigmine
Sux
Pancuronium
Metoprolol
Alpha-Adrenergic agonsits
Antacids
244
Drugs that decrease LES tone
Atropine
Glyco
Dopamine
Sodium nitroprusside
Ganglion blockers
Thiopental
Tricyclic antidepressants
Beta-Adrenergic stimulants
Halothane
Enflurane
Opioids
nitrous oxide
Propofol
245
Drugs w no change to LES tone
Propranolol
Oxprenolol
Cimetidine
Ranitidine
atracurium
Nitrous oxide
246
Aspiration prophylaxis (pre-op)
pepcid, bicitra, reglan
247
Aspiration prophylaxis (Intra-op)
Cricoid pressure, RSI, and
endotracheal intubation
248
Esophagectomy carries a persistent risk for
aspiration
249
highly prevalent, 10% incidence over lifetime
Peptic ulcer disease
250
bleeding: 30% hemorrhage, 15% of those die
perforation: 10% lt risk, causes peritonitis/shock
obstruction: 2/2 inflammation and scarring
Peptic ulcer dz
251
Nerve-targeting: truncal vagotomy
Vagus nerve innervates acid-producing
fundic mucosa; reduces secretion by 80%
Tx for Peptic ulcer dz
252
Tx for Peptic ulcer dz
Lesion-targeting: closure of duodenal perforation
antacids, antibiotics, anticholinergics, antihistamines,
proton pump inhibitors, coating agents
antacids, antibiotics, anticholinergics, antihistamines,
proton pump inhibitors, coating agents
253
most common chronic inflammatory dz after RA
inflammatory Bowel disease
254
usually involves entire colon
Ulcerative Colitis
255
Involves terminal ileum, plus:
Derm, Rheumatological, Hepatobilliary, Ocular, Urologic, and other body systems
Crohn's Disease
256
T/F Crohns can cause Thromboembolic disease (PE, Arterial embolism, CVA)
True
Due to thrombocytosis
Increased levels of Fibrinopeptide A, Fibrinogen, FV, FVIII
Accelerated thromboplastin Generation
ATIII Deficiency d/t increased gut losses or increased catabolism
Free protein S Deficiency
257
T/F Crohns can cause cardiac issues
True
Endocarditis
Myocarditis
Pleuropericarditis
258
T/F Crohns can cause interstitial lung disease
True
259
T/F Crohns will not cause secondary amyloidosis
False
260
Can cause Renal Calculi in 10-20% of cases, ureteral obstruction
Crohns
261
In approx 50% of cases, can cause hepatobilliary issues like hepatomegaly, fatty liver, malnutrition, cholelithiasis, Primary sclerosing cholangitis leading to biliary cirrhosis and hepatic failure
Crohns
262
Ocular complications with Crohns
1-10%
conjunctivitis
Anterior uveitis/ iritis,
Episcleritis
263
Rheumatologic complications with Crohns
Peripheral arthritis in 10-15%
264
Dermatologic complications with Crohns
Erythema nodosum in 10-15 of cases
pyoderma gangrenosum in 1-12%
265
antibiotic and anti-inflammatory MOA
used to treat IBD medically
Sulfasalazine
266
Drug used for IBD for immunosuppression
Azathioprine
267
Drug used for anti-inflammation (IL-1) with IBD
Methotrexate
268
Drug used for IBD for T cell inhibition
Cyclosporine
269
Resection of ½ SB -> Short bowel/Short gut syndrome
Need for TPN
270
usually incidental finding, but
depends on location
Carcinoid tumors
271
Carcinoid tumors in this location are usually asymptomatic
Bronchus 31%
272
Carcinoid tumors in the thymus usually present as
A mediastinal mass
273
Carcinoid tumors in the ovary or testis are typically found
on examination or via US/imaging
274
Metastasis of carcinoid tumors are typically found
In the liver
Frequently presents as hepatomegaly
275
Carcinoid tumors in the small intestine typically present with
abdominal pain, intestinal obstruction, tumor, gI bleeing
276
Carcinoid tumors in the rectum typically present with
Bleeding
Constipation
Diarrhea
277
20% of Carcinoid tumors are due to
Carcinoid Syndrome
278
20% of Carcinoid tumors, 2/2 serotonin and vasoactive subs being released by the tumor
279
Signs and symptoms of Carcinoid syndrome
sudden onset of flushing, diarrhea, wheezing
280
Associated tumors can cause ASD, VSD, PFO, TR
W/ cardiac involvement
carcinoid triad
281
intense symptoms with CV instability
May be provoked by stress of surgery
Carcinoid crisis
282
Drugs that can provoke a carcinoid crisis
Sux
Mivacurium
Atracurium
D-turbocuraraine
Epi
Norepi
Dopamine
Isproterenol
Thiopental
283
Treatment for Carcinoid syndrome
octreotide, somatostatin, GHIH
284
In Carcinoid syndrome, surgery is
curative for nonmetastatic tumors
285
Postop med for carcinoid syndrome
ondansetron
286
Intra-op pressor of choice for carcinoid syndrome
Phenylephrine/vasopressin for pressors
287
Anesthetic considerations for carcinoid syndrome
Ondansetron for PONV
Arterial line typically requred
288
Phenylephrine/vasopressin for pressors
Pancreatitis
289
Pathophysiology of Pancreatitis
autodigestion (!)
290
Protective measures in pancreatitis
packaging enzymes in protease precursors
synthesis of protease inhibitors
low intrapancreatic Ca, which decr. trypsin
loss of any of the above leads to Acute pancreatitis
291
Etiology of pancreatitis
gallstones and EtOHism cause 60-80%
292
How can gallstones cause pancreatitis?
obstruction and ductal hypertension
293
Risk of ERCP
causes Acute Pancreatitis in 1-2% of cases (!)
294
Signs and Symptoms of Acute pancreatitis
intense midepigastric pain, fever, CV instability,
mental status changes, tetany
295
Why can pancreatitis cause tetany?
Calcium issues the pancreas is responsible for. So messing w the calcium will lead to tetany
296
How is pancreatitis diagnosed?
CT, ERCP, amylase, lipase
297
Ranson criteria
age, WBC, BUN, AST, hypoxemia, fluid deficit,
glucose, LDH, Ca, anemia, metabolic acidosis
7 or more RF’s a/w 100% mortality
Risk factors for pancreatitis
298
Complications of Pancreatitis
¼ will have one
shock, renal failure, GI Bleed, DIC , Abcess formation
299
Treatment for Pancreatitis
NPO, aggressive IVF, opioids, ERCP
For chronic pancreatitis, celiac plexus block
300
Celiac Plexus Block
Celiac plexus block- sudden hypotension
Blocking the SNS- spinal dose of anesthetic, patient will tank
301
luminal obstruction, inflammation, infection
Appendicitis
302
RLQ pain, Fever
Appendicitis
303
Differential Diagnosis of Appendicitis
mesenteric lymphadenitis
Ruptured Graafian follicle
Acute pancreatitis
Perforated ulcer
Ureteral Calculus
Acute cholecystitis
Acute gastroenteritis
acute Diverticulitis
Pelvic inflammatory disease
Corpus Leuteum cyst
Strangulating intestine
Obstruction
No organic disease
304
can be deleterious without prompt treatment with octreotide
Carcinoid syndrome
305
Treatment for appendicitis
Urgent appendectomy
306
Basic Liver fxns
Digestion, metabolism, synthesis, detox
307
Prehepatic dysfxn
increased unconjugated bili
Aminotransferase enzymes-normal
Alk Phos- Normal
Causes
Hematoma, hemolysis, resorption bilirubin overload from blood transfusion
308
Intrahepatic/hepatocellular dysfunction
Increased conjugated bili
Aminotransferase enzymes- markedly incr
Alk phos normal to slightly incr
Cases
Viral infection, drugs, alcohol, sepsis,hypoxemia, cirrhosis
309
POsthepatic/cholecystatic dysfxn
increased conjugated bili
Aminotransferase- normal to slight incr
Alk phos- markedly incr
Causes
Biliary tract stones or tumors, sepsis
310
degradation product of hemo/myoglobin
Bilirubin
311
insoluble form of bilirubin, formed in periphery
unconjugated
312
soluble form of bilirubin, formed in liver
Conjugated
313
Inc production, dec hepatic uptake/conjugation
Unconjugated hyperbilirubinemia
314
Liver dysfunction, bile duct obstruction
Conjugated hyperbilirubinemia
315
hepatic gluconeogenesis enzymes
ALT and AST
316
more specific to liver than AST
ALT
317
Hepatocellular injury leads to
enzyme release
318
AST/ALT ratio can narrow the DDx
<1 nonalcoholic steatohepatitis (NAFLD)
2-4 alcoholic liver disease
>4 Wilson’s disease
319
in cholestasis, elevated bile salts damage
hepatocyte membranes, which
raises alk phos
320
alk phos T1/2 = 1 week, so
remains elevated even after
resolution of biliary obstruction
321
Liver synthesizes all clotting factors except
Everything except VIII
321
Prolongation of INR correlates strongly with
poor hepatic function and predicts survival in patients with liver failure
322
Most abundant plasma protein
Albumin
323
Synthesized exclusively by liver
Albumin
324
Major substrate transporter, so key to bioavailability and rate of most metabolic processes
Albumin
325
Protein malnutrition, protein loss (nephropathy), severe reduction of liver synthetic capacity
Hypoalbuminemia
326
Antibodies and antigens help narrow hepatitis DDx
Viral (Hepatitis A,B,C,D,E) vs. autoimmune
Other protein markers are diagnostic
a1-antitrypsin deficiency, Wilson’s disease, Hepatocellular carcinoma, genetic liver diseases
327
Bili ~3 causes
scleral icterus
328
Normal total bili
< 1
329
Bili > 4 causes
jaundice
330
Most common hereditary hyperbili (10% of pop)
Defect is mutation of glucuronosyl transferase
Bili usually < 5, but can incr quickly with stress
Gilbert’s Syndrome
331
Rare hereditary hyperbili
Defect is mutation of glucuronosyl transferase
Affected children have perinatal jaundic
Crigler-Najjar Syndrome
332
Tx of Crigler-Najjar Syndrome
photorx (why?) and liver tx
333
Anesthetic considerations for Crigler-Najjar Syndrome
photorx, minimal fasting
MS, barbs, IA, and NMB are all safe
334
Why do we do phototherapy in hyperbilirubinemia
because specific wavelengths of light convert bilirubin in the skin into water-soluble isomers, which can then be excreted by the body without needing liver conjugation, effectively lowering toxic bilirubin levels and preventing kernicterus (brain damage)
335
Occurs with long surgery, especially:
hypotension
hypoxemia
blood transfusion
Caused by incr bili production and decr clearance
Resolves spontaneously
Benign Postoperative Intrahep Cholestasis
336
Rare, presents with ESLD before adulthood
Liver transplant is the only treatment
Progressive Familial Intrahep Cholestasis
337
Progressive Familial Intrahep Cholestasis
Anesthetic considerations
malnutrition, portal HTN, coagulopathy,
hypoalbuminemia, hypoxemia
338
are formed by chemical abnormalities of
components of bile
Gallstones
339
Risk factors for diseases of the biliary tract
female, age, obesity, rapid weight loss, preg.
Also a/w cirrhosis and hemolytic anemia
340
Presentation: varies from silent to acute to chronic
Acute Cholecystitis
341
Acute Cholecystitis treatment
Treatment is medical until stable, then surgery
342
Anesthetic pharm considerations for Acute cholecystitis
: Sphincter of Odi spasm: reverse w/ naloxone,
glucagon, nitroglycerin
343
Anesthetic considerations for Acute Cholecystitis
laparoscopy pneumoperitoneum: preload, ventilation
positioning: same
344
Gallstones in common bile duct
Similar to chole, but also can cause pancreatitis
Choledocholithiasis
345
Tx for Choledocholithiasis
surgery or ERCP (endo.retro.pancreatography
346
Inflammation of liver parenchyma
Hepatitis
347
Heritable, immune-mediated, hepatotoxic
Halide metabolites acetylate liver proteins
IgG antibodies cause autoimmune reaction
halothane Hepatitis
348
Caused by halo, enfl, iso, desflurane
Sensitization causes cross reactivity to other IA
Sevo is not associated due to alternate metabolism
Halothane hepatitis
349
Postop Hepatic Dysfunction
Most common = benign cholestasis
350
Cirrhosis advanced signs
spider angiomata, gynecomastia,
testicular atrophy, ascites
JPASSAGE
351
Fibrotic degradation of liver tissue leads to:
Increased resistance to intrahepatic blood flow
Portal hypertension
352
Sx of portal hypertension
Decreased portal vein blood flow
Portal hypertension
Ascites
Hepatosplenomegaly
Varices, peripheral edema
353
Ascites medical treatment
Correct hypoalbuminemia - diet
Correct sodium and water retention - aldo antag
354
Ascites interventional treatment
Paracentesis
TIPS
355
Rapid development of severe liver damage,
synthetic function, and encephalopathy
Liver Failure
356
LF in 8 days
Fulminant liver failure
357
Often affects young, with high mortality
Outcome depends on cause and encephalopathy
Mild hepatic enceophalopathy progresses to high ICP and coma
Acute liver Failure
358
Liver Failure leads to increased ammonia and subsequent increased metabolism of ammonia to
glutamine in the CNS
359
Etiology of acute liver failure
APAP (Acetaminophen), drug rxn, viral, EtOH, fatty liver of preg
360
Tx of acute liver failure
Coag, renal failure, CV instability, metabolic dys
Supportive: ICU, vent, IVF, electrolytes
361
mortality of acute liver failure
High mortality, even w/ liver tx (65%)
362
predicts surgical mortality in cirrhosis
Child-Pugh score
363
Child pugh score uses
Encephalopathy
Ascites
Bilirubin
Albumin
INR
364
Child pugh scoring matrix
5-6 class A 100, 85
7-9 Class B 81, 57
10-15 Class C 45, 35
365
Child Pugh class A or B for anesthesia
Proceed w surgery, Monitor and treat encephalopathy, coagulopathy, metabolic, and electrolyte derangments
366
Child Pugh Class C for anesthesia
Prefer nonsurgical tx options. Defer necessary elective surgery until improvement
367
Acute hepatic dysfxn for anesthesia
Defer elective surgery until clinical improvement
368
Anesthesia pharmacokinetic considerations for liver failure
increased VD, decreased clearance
VD increase means increase loading dose, decrease maintenance doses
369
Predicts 90 day mortality without transplant
Higher score means higher priority
MELD
ICBD (I Crush beers daily)
370
Stages of liver transplant
Dissection
Anhepatic
Reperfusion
371
Dissection stage of liver transplant
CV instability 2/2 bleeding, low venous return
372
Anhepatic stage of liver transplant
Veno-veno bypass maintains venous return
No liver: acidosis, citrate. Use Ca infusion.
373
Reperfusion stage of liver transplant
Significant CV instability, metabolic changes
374
Cirrhosis causes
portal hypertension, which leads
to venous congestion and ascites
375
1 venous stasis
2 hypercoagulability
3 disruption of vascular endothelium
Virchow's triad
376
Most postop DVT’s arise from what location
in the distal leg
Originate in low-flow soleal and gastroc sinuses
But 20% originate more proximally
These can extend and become fatal PE’s...
377
Recent surgery
Trauma
Immobility
Pregnancy
Low cardiac output 2/2 CHF or MI
Stroke
Risk factors for venous stasis
378
Surgery and surgical stress
Oral contraceptives - estrogen
Cancer
Inflammatory bowel disease
Deficiencies of endogenous anticoagulants
Antithrombin III
Protein C, protein S
hypercoagulable states
379
Abnormality of the venous wall
Varicose veins
Drug-induced irritation
Morbid obesity
Advanced age
History of previous thromboembolism
Predisposing DVT Factors
380
Suspected DVt
Contrast venography
Normal-DVT Rule-out
Abnormal-A persistent intraluminal filling defect in >=2 Views- DVT Diagnosed
381
Suspected DVT
Compression ultrasonography
Normal-Repeat on days 2 and 7
normal-Critically important DVT Rule-out
Abnormal- DVT Diagnosed
Abnormal on first US- DVT Diagnosed
382
Best for proximal lesions (femoral or popliteal)
Less sensitive for distal calf lesions
Doppler ultrasound with vein compression
383
Venography
Impedance plethysmography
Doppler ultrasound with vein compression
DVT Workup
384
DVT Treatment
Anticoagulation
Heparin, LMWH, warfarin
Compression stockings and ambulation
Inferior vena cava filter
Thrombolysis
385
Failure to diagnose is a serious error because 30% of untreated patients will die vs. 8% with treatment
PE
386
Embolism
Caused by thrombosis-Clot in a vessel
387
A damaged vein with slow blood flow or blood clotting problems cause a clot to form
Thrombus
388
As the clot grows, parts may break off into the heart or lungs
Embolus
389
PE Risk Factors
Obesity, prior thromboembolism, Advanced age, malignancy,esp adenocarcinoma, Chemo, esp thalidomide, Estrogens
Venous stasis
Injury
Hypercoagulable states
indwelling lines
390
occurs when thrombi detach and are carried through great veins to the pulmonary circulation
PE
391
Anatomic DS + Alveolar DS
ToTal Deadspace
392
Portion of airway that conducts to alveoli
~30% of TV
Anatomic Dead Space
393
Portion of alveoli with no blood in pulm capillary
Think: ventilation without perfusion
Alveolar dead space
394
Perfusion without ventilation
Pneumothorax
Oxygenation difficulty
Shunt
395
Ventilation without perfusion
Pulmonary embolism- Prototypical deadspace lesion
Ventilation difficulty
Dead Space
396
PE will show sharp decrease in
ETCO2 intra-op
397
Pulmonary artery obstruction creates
Dead space
398
PE S/S
Acute dyspnea
Tachypnea
Pleuritic chest pain
Rales
Nonproductive cough
Tachycardia
Accentuation of pulmonic component of 2nd heart sound
Hemoptysis
Fever 38-39C
Homan's sign
399
a clinical test for Deep Vein Thrombosis (DVT) involving pain in the calf upon passive dorsiflexion (pointing toes up) of the foot
Homans sign
400
EKG Signs of Pulmonary Embolism
S1Q3T3
Prominent S in lead 1
Q in Lead III
Inverted T in lead III
401
What metabolic derangement is associated with a PE
Hypoxemic hypocapnic Respiratory alkalosis
402
Differential Diagnosis of PE
MI
Pericarditis
CHF
COPD
Pneumonia
Pneumothorax
Pleuritis
Thoracic herpes zoster
Anxiety/hyperventilation syndrome
Thoracic aorta dissection
RIB Fractures
403
Modified Geneva score uses
Age
Surgery
Active malignancy
Hemoptysis
Prev DVT or PE
Unilateral LL pain
HR High/higher
Pain on palpation of DVT
Unilateral edema
To Determine PE Risk
404
Best workup for PE
CTA
best method, high sensitivity and specificity
405
best method, high sensitivity and specificity
V/Q Scan
406
PE Workup imaging
CXR
CTA
VQ Scan
LE U/S
TTE/TEE
407
PE: Diagnostic Clues
ECG - right heart strain: S1, Q3, T3
ABG - Aa gradient, slight alkalosis
ETCO2 - increased dead space causes fall in ETCO2
PAC - increased RAP, RVP, PAP. Decreased QT
Cardiac markers - elevated BNP and troponins
suggest RH strain
QT= Cardiac output on PA Catheter
408
Tx of PE
Anticoagulation
Heparin is cornerstone, but not curative
Inferior vena cava filter
If recurrent or anticoagulation is contraindicated
Thrombolysis - tPA If hemodynamic compromise
409
Intra-op Presentation of PE
Sudden cardiovascular collapse
Hypoxemia or bronchospasm
Elevated CVC, PAP
TEE: right heart distention and dysfunction
410
an inflammatory process, which also reduces peripheral flow
Vasculitis
411
Focused on arterial side of circulation
Key concept is compromised flow to extremities
Chronic changes usually due to atherosclerosis
Acute changes usually due to embolism
PVD
412
Takayasu's arteritis
Thromboangitis obliterans
wegener's granulomatosis
Temporal arteritis
Polyarteritis nodosa
Acute peripheral arterial occlusive disease (embolism)
Systemic Vasculitis
413
Distal abdominal aorta or iliac arteries
Femoral arteries
Subclavian steal syndrome
Coronary subclavian steal syndrome
Chronic peripheral arterial occlusive disease (Atherosclerosis)
414
Other Vascular syndromes
Raynaud's phenomenon
Kawasaki disease
415
Chronic Arterial Insufficiency
Ankle-brachial index = PS(ankle)/PS(brachial)
Insufficiency = ABI < 0.9
Correlates well with angiogram-positive disease
416
Peripheral disease resembles atherosclerosis of
aorta, coronaries, and cerebral arteries
Chronic Arterial Insufficiency
417
systemic, with 3-5x risk of MI, CVA, death
CAI
418
If patient has claudication, 80% have fempop
stenosis, 40% tibioperoneal, 30% iliac or aortic
CAI
419
Prevalence increases with age (70% over 75 yo)
CAI
420
2x risk of PAD and claudication
Increased risk of progression from stable to limb ischemia and amputation
Smoking with PVD/CAI
421
PVD S/S
Intermittent claudication
Metabolic requirement of exercising muscle exceeds oxygen delivery
Rest pain
Arterial blood supply does not meet minimal nutritional requirements
Minor trauma can lead to ischemia
422
S/S of PVD
Most Reliable: decreased or absent arterial pulses, Bruits in abdomen, pelvis, or inguinal area indicate arterial stenosis
Chronic ischemia: atrophy, hair loss, coolness,
pallor, cyanosis, dependent redness
423
Diagnosis of PVD
Doppler ultrasound: absent pulse volume waveform
ABI
<0.9 = claudication
<0.4 = rest pain
<0.25 = ischemia or gangrene
424
Transcutaneous oximetry
60 is normal, 40 may indicate ischemia
425
PVD Tx
Medical therapy
Exercise
Risk factor modification
Smoking cessation
Lipid-lowering agents
Blood glucose-lowering agents
426
T/F Beta blockers are unsafe for PVD
False
427
is indicated for ischemic rest pain, disabling claudication, or impending limb loss
Revascularization
428
Increased incidence of periop MI in patients with PVD due to high prevalence of
CAD
429
Mortality after revascularization usually due to
MI in patients with preop evidence of IHD
430
unstable angina is
an active cardiac condition requiring prior optimization
431
In PVD, Acute withdrawal of BB and initiation of high dose BB on DOS are a/w
increased mortality
432
True/False
In PVD, Intraop heparinization is not a RA contraindication
True
433
What timeline can we place an epidural before heparinization in a pt with PVD
1 Hour
434
Occlusion of subclavian or innominate artery may result in flow reversal to distal subclavian
Diverts flow from brain to the arm
Subclavian Steal Syndrome
435
Subclavian-> Stroke-like symptoms
Subclavian steal syndrome
436
Symptoms of subclavian steal syndrome
CNS ischemia (sync, vert, ataxia, hemiplegia)
437
reduced pulse and SBP in ipsilateral arm
Symptom of subclavian steal syndrome
438
Tx of subclavian steal syndrome
subclavian endarterectomy
439
SSS Frequency
Between RSC and RCC 28%
At brachiocephalic/Inominate artery 10%
At L Subclavian 62%
440
Complication of LIMA for CABG
Proximal stenosis of left subclavian artery produces
reversal of flow through patent LIMA graft
Coronary-Subclavian Steal Syndrome
441
Symptoms: angina
Signs: reduced SBP in ipsilateral arm
Treatment: repeat CABG
Coronary-Subclavian Steal Syndrome
442
Nonatherosclerotic mechanism, usually cardiogenic
Atrial fibrillation and left atrial thrombus
Atrial myxoma
After MI, dilated cardiomyopathy
Valvular disease, endocarditis, PFO
Noncardiogenic causes
Atheroemboli from upstream plaque
Acute Arterial Occlusion
443
Acute Arterial Occlusion
Nonatherosclerotic mechanism, usually cardiogenic
Atrial fibrillation and left atrial thrombus
Atrial myxoma
After MI, dilated cardiomyopathy
Valvular disease, endocarditis, PFO
Noncardiogenic causes
Atheroemboli from upstream plaque
444
c/w limb ischemia
Intense pain, weakness, pulselessness, cool skin
Acute Arterial Occlusion
445
Tx for acute arterial occlusion
Surgical - embolectomy or amputation
Medical - anticoagulation or thrombolysis
446
episodic vasospastic ischemia of the digits
Epidemiology: affects women > men
Presentation: white fingers a/w cold or sympathetic
Rewarming leads to vasodilation with hyperemia
Raynaud’s Phenomenon
447
Classification of Raynaud's
Primary - “Raynaud’s Disease”, bilateral
Secondary - immunologic, unilateral
448
Causes of Raynauds
Scleroderma
SLE
RA
Dermatomyositis
Atherosclerosis
Thromboangiitis obliterans
Thromboembolism
Thoracic outlet syndrome
Carpal tunnel
Reflex sympathetic dystrophy
CVA
Intravertebral disc herniation
Frostbite
percussive injury
B Agonist
TCA
Antimetabolites
Ergot Alkaloids
Amphetamines
449
calcinosis, Raynaud’s phenom,
esoph. dysmotil., scleroderma, telangiectasia
CREST Syndrome
450
Large: Takayasu, temporal arteritis
Medium: Kawasaki, Buerger
Small: Wegener, PAN
Systemic lupus erythematosus, rheumatoid arth
Systemic Vasculitis
451
Rare, idiopathic, chronic, progressive, vasculitis
Can present with aortic aneurysm
Other names: “pulseless disease, occlusive thrombo-aortopathy, aortic arch syndrome”
Takayasu’s Arteritis:
452
Epidemiology of Takayasu’s Arteritis
Asian women under 40
453
Diagnosis of Takayasu’s Arteritis
angiography, CT, MRI
454
Tx of Takayasu’s Arteritis
steroids, anti-RA rx, anticoagulation, anti-HTN
455
Diagnosis of Temporal (Giant Cell) Arteritis
temporal artery biopsy - 90% specificity
456
tender, enlarged superficial temporal arteries
Temporal (Giant Cell) Arteritis
457
inflammation of head and neck arteries
Temporal (Giant Cell) Arteritis
458
S/S of Kawasaki Disease
: fever, inflammation of mucous membranes,
red hands/feet, truncal rash, cervical LAD
Course: 25% have coronary aneurysms
459
Kawasaki’s Disease (Mucocutaneous LNS) Treatment
: urgent gamma globulin and aspirin
Anesthesia: be vigilant for intraop MI
460
inflammatory vasculitis leading to occlusion of small/medium vessels of extremities
Thromboangiitis Obliterans (Buerger’s Dz)
461
smoking, men, age < 45
Pathophysiology: autoimmune response to tobacco
Thromboangiitis Obliterans (Buerger’s Dz)
462
Diagnostic criteria for Thromboangiitis Obliterans (Buerger’s Dz)
Smoking, onset < 50, distal claudication,
exclude other autoim, exclude embolic source
463
extremity claudication, ischemia, vasospasm
migratory superficial vein thrombosis
Thromboangiitis Obliterans
464
Tx of Thromboangiitis Obliterans
smoking cessation
Surgery and medical therapy are ineffective
Gene therapy with VEGF shows promise
465
presence of necrotizing granuloma in vessels of
CNS, airway, lungs, CV system, and kidneys
Wegener’s Granulomatosis
466
Presentation: sinusitis, pneumonia, renal failure
Course: progressive renal failure leads to death
Dx: +antineutrophil cytoplasmic Ab (non-specific....)
Tx: cyclophosphamide, steroids, MTX, rituxan
Wegener’s Granulomatosis
467
Tx of Wegener’s Granulomatosis
Tx: cyclophosphamide, steroids, MTX, rituxan
468
S/S of Wegener’s Granulomatosis
Cerebral aneurysms
Peripheral neuropathy
Sinusitis
Laryngeal stenosis
Epiglottic destruction
VQ mismatch
Pneumonia
hemoptysis
Bronchial destruction
Cardiac valve destruction
Disturbances of cardiac conduction
Myocardial ischemia
Hematuria
Azotemia
Renal Failure
469
Side effect of Cyclophosphamide
: low cholinesterase activit.
470
autoimmune inflammation of airway and
small vessels
Pathophysiology: cardiac, renal, neuro, GI
Churg-Strauss Syndrome
471
Patients present for ENT surgery
Be prepared for airway hyperreactivity
Churg-Strauss Syndrome
472
ANCA-negative vasculitis associated with
HepB, HepC, hairy cell leukemia
Polyarteritis Nodosa
473
If using contrast dye, check
BUN/Cr.
474
Normal Na+ Value
Serum Na = 136-145mmol/L
475
Tightly controlled by action of Vasopression (ADH)
Na+
476
Water retention > kidneys ability to excrete dilute urine.
Occurs in approx. 15% of hospitalized patients (dilution effect)
If an outpatient → likely due to chronic disease
Hyponatremia
477
How to correct acute hyponatremia
Acute
Can be corrected at the same rate at which the hyponatremia developed.
478
If Na > 160mEq/L →
mortality approaches 75%
Of those who survive → often with permanent brain damage
479
Hypernatremia w Hypervolemia and UNA>20
Sodium Gains
Hyperaldosteronism
Cushing's
Hypertonic dialysis
NaCl Tablets
Hyperalimentation
Hypertonic Saline enemas
Salt water drowning
480
Hypernatremia with euvolemia , UNA Variable
Renal water loss-DI- Central/nephrogenic/Gestational
Insensible losses-Respiratory Tract, Skin
481
Hypernatremia w Hypovolemia UNA >20
Renal salt and water loss
Osmotic diuretic
Loop diuretic
Postrenal obstruction
intrinsic renal dz
Profound glycosuria
482
Hypernatremia w hypovolemia and UNA <20
Extrarenal salt and water loss
Diarrhea
GI Fistulae
Burns
Sweating
483
Hypovolemic hypernatremic pts on induction
Can have exaggerated hemodynamic instability on induction.
484
Hypervolemic hypernatremic patients intra-op
Volume of distribution for administered medications can be significantly altered.
485
Hypokalemia Tx
Typically administer 20mEq over 30 mins
Recheck serum potassium
486
serum K > 5.5mEq/L
Hyperkalemia
Can severely alter transmembrane action potentials
In hospitalized patients, most common cause is overcorrection of hypokalemia
487
a reduction in IONIZED calcium
Hypocalcemia
488
Can occur with hyperventilation
Can occur with bicarbonate administration
Hypocalcemia
489
Hypercalcemia is usually associated with
Primary Hyperparathyroidism – usually < 11mEq/L
Malignancy – usually > 14mEq/L
Assoc w/ symptoms
490
What form of magnesium is Clinically significant
Ionized
491
Tx of Hypercalcemia
Loop diuretics to enhance Ca excretion via kidneys
Avoid thiazide diuretics (ex. HCTZ) – increase Ca absorption
492
Magnesium
60% of serum magnesium is ionized
30% bound to protein (albumin)
10% complexed to citrate, bicarbonate, or phosphorous
493
Can occur following parathyroidectomy due to
“Hungry Bone Syndrome”
hypomagnesemia
494
Tx for hypermagnesemia
Mild Cases
Consider loop diuretic and saline infusion
Promote / enhance renal excretion
Severe Cases
Temporize with intravenous calcium
May require dialysis
495
pH=6.1 + log [HCO3 / (0.03 x PaCO2)]
Henderson-Hasselbalch Equation
496
Catecholamines don’t exert their normal effect when pH
< 7.1
497
Calculating Anion Gap
Na – (Cl + HCO3)
Normal range is 8 +/- 4
Na + K – (Cl +HCO3)
Normal range 12 +/- 4
498
will lower blood pH
Stimulates respiratory centers (attempt to decrease CO2 to compensate)
Metabolic Acidosis
499
Occurs when some “other” acid is present in the ECF
The acid dissociates into H+ ion and an unknown anion
The H+ then binds HCO3- (forms carbonic acid)
HCO3- concentration decreases
HCO3- is part of the anion gap calculation
HCO3 goes down, anion gap goes up
HAGMA
500
Aka Hyperchloremic Met. Acidosis
Due to increase in Cl- ion
Loss of HCO3 ion results in retention of Cl- ion
To maintain electroneutrality
Etiologies
NAGMA
501
Tx for Metabolic Acidosis
Treat underlying cause
Ex. If due to DKA → treat with insulin and fluids
Use caution in treating patients with Sodium Bicarb
502
Impaired cerebral and coronary blood flow due to vasoconstriction
Predisposes patient to refractory ventricular dysrhythmias
Depresses ventilation
Body’s attempt to increase CO2 to compensate
Can be a problem when trying to wean from ventilator
Alkalosis
503
Occurs when there is a relative increase in plasma bicarbonate (HCO3) concentration
Body tries to compensate through increased CO2 retention
Metabolic Alkalosis
504
Due to renal or extra-renal origin
Increased loss of H+ ion (like vomiting HCl)
Increased HCO3 reabsorption by kidneys
Metabolic Alkalosis
505
– body loses excess Cl ions, kidneys maintain electroneutrality by retaining HCO3-.
This would be a case of Cl responsive Metabolic Alkalosis
Consider the case of Cystic Fibrosis (CF)
506
Hypovolemia
NG Suctioning / Vomiting
Diuretic therapy (contraction alkalosis)
Bicarbonate administration
Hyperaldosteronism
Chloride wasting diarrhea
Can look a lot like Hypocalcemia
(during alkalosis, more Ca binds with albumin)
Metabolic Alkalosis
507
pH > 7.45
Occurs when an increase in alveolar ventilation results in a decrease in PaCO2
Respiratory Alkalosis
508
34 year old female undergoes total thyroidectomy, patient develops inspiratory stridor immediately on extubation in the OR. What is the likely cause?
a. Post-op hematoma
b. Bilateral recurrent laryngeal nerve damage
c. Hypocalcemia
b. Bilateral recurrent laryngeal nerve damage
509
34 year old female undergoes total thyroidectomy, patient develops inspiratory stridor and labored breathing 2 days after surgery. What is the likely cause?
a. Post-op hematoma
b. Bilateral recurrent laryngeal nerve damage
c. Hypocalcemia
c. Hypocalcemia
510
34 year old female undergoes total thyroidectomy, patient develops inspiratory stridor and labored breathing 2 days after surgery. How do you treat it?
a. Transtracheal block
b. Immediate rocuronium administration
c. Calcium Gluconate
d. Magnesium Sulfate
c. Calcium Gluconate
511
34 year old female undergoes total thyroidectomy, patient develops inspiratory stridor and labored breathing 2 days after surgery. You treat with intravenous calcium supplementation. Which of following requires least amount (by mg) administration?
a. Calcium Gluconate
b. Calcium Chloride
b. Calcium Chloride
512
65 year old male with cancer and bone metastasis is admitted with hypercalcemia (Ca = 15mg/dL). Which of the following is primary risk of this electrolyte disturbance under anesthesia.
a. Bleeding disorder
b. Cardiac dysrhythmia
c. Hypotension
d. Larnygospasm
e. Fluid imbalance
b. Cardiac dysrhythmia
513
65 year old male with cancer and bone metastasis is admitted with hypercalcemia (Ca = 15mg/dL). How might you treat this condition.
a. Calcium Gluconate
b. Calcium Chloride
c. Normal Saline
d. Digitalis therapy
e. Fluid restrict
c. Normal Saline
514
34 y/o F w/ Cushings Disease (ACTH excess) due to pituitary adenoma. Patient undergoes trans-sphenoidal resection. Several hours following surgery, patient has really high urine output and serum Na = 156. What is the likely cause of this condition?
a. Too many diuretics given during surgery
b. Hyperglycemia
c. Nephrogenic diabetes insipidus
d. Central diabetes insipidus
d. Central diabetes insipidus
515
34 y/o F w/ Cushings Disease (ACTH excess) due to pituitary adenoma. Patient undergoes transsphenoidal resection. Several hours following surgery, patient has really high urine output and serum Na = 156. How do you treat this condition?
a. Mannitol
b. Calcium gluconate
c. DDAVP (Vasopressin / ADH)
d. 3% NaCl
c. DDAVP (Vasopressin / ADH)
516
68 year old male (Wt=100kg) undergoes TURP for BPH under general anesthesia. In recovery room patient is restless & confused. What is the most likely etiology?
a. Hyperglycemia
b. Hypocalcemia
c. Hyponatremia
d. Urinary Retention
c. Hyponatremia
517
68 year old male (Wt=100kg) undergoes TURP for BPH under general anesthesia. In recovery room patient is restless & confused. Patient is found to have serum Na = 110mEq/L. How might you treat this?
a. Fluid restriction
b. Diuretics
c. Plasmalyte infusion
d. 3% NaCl
d. 3% NaCl
518
68 year old male (Wt=100kg) undergoes TURP for BPH under general anesthesia. In recovery room patient is restless & confused. Patient is found to have serum Na = 110mEq/L. You treat with 3% NaCl until Na=120mEq/L. How many mEq of Na are needed?
a. 300mEq
b. 450mEq
c. 600mEq
d. 750mEq
c. 600mEq
519
24 year old male (otherwise healthy) presents to Pre-op for scheduled inguinal hernia repair. Day of surgery labs reveal K=3.3 What should you do?
a. Administer calcium gluconate
b. Cancel Surgery
c. Delay surgery for medicine consult
d. Proceed with surgery (remember K = 3.3 & possibly consider giving 20mEq K in OR)
d. Proceed with surgery (remember K = 3.3 & possibly consider giving 20mEq K in OR)
520
55 year old patient presents to ED following MVA. Emergently taken to OR and RSI & intubation with succinylcholine performed. On exposure of patient, an AV fistula discovered in right arm. Which of the following ECG changes might suggest hyperkalemia?
a. Narrow & peaked T-waves
b. Decrease in P wave amplitude
c. Prolonged PR interval
d. Widened QRS
55 year old patient presents to ED following MVA. Emergently taken to OR and RSI & intubation with succinylcholine performed. On exposure of patient, an AV fistula discovered in right arm. Which of the following ECG changes might suggest hyperkalemia?
a. Narrow & peaked T-waves
b. Decrease in P wave amplitude
c. Prolonged PR interval
d. Widened QRS
521
55 year old patient presents to ED following MVA. Same patient, what is the most important initial treatment.
a. Hyperventilation
b. Insulin +/- glucose
c. Calcium gluconate
d. Albuterol down ET tube
e. Dialysis
c. Calcium gluconate
522
Patient in PACU on nasal canulla 2L/min and still has A-line. ABG is obtained with following values. What is metabolic disturbance is this?
Labs = 7.42 / 38 / 104 / 24
Metabolic acidosis
Metabolic alkalosis
Normal
Respiratory acidosis
Respiratory alkalosis
523
The following ABG refers to which disturbance?
Labs = 7.48 / 31 / 70 / 23
Metabolic acidosis
Metabolic alkalosis
Normal
Respiratory acidosis
Respiratory alkalosis
Etiology?
524
The following ABG refers to which disturbance?
Labs = 7.48 / 42 / 70 / 30
Metabolic acidosis
Metabolic alkalosis
Normal
Respiratory acidosis
Respiratory alkalosis
Etiology?
525
The following ABG refers to which disturbance?
Labs = 7.24 / 31 / 70 / 19
Metabolic acidosis
Metabolic alkalosis
Normal
Respiratory acidosis
Respiratory alkalosis
Anesthesiologist Assistant
flashcards
Decks in class (25)
# Cards
-
Pharmacology (Orientation)539
-
Cardiac Physiology Yr1FA23229
-
AMDS Y1FA23101
-
Comp Exam III97
-
Pulmonary + Respiratory Physiology445
-
Drug Card Fall 2024120
-
APP 1 final185
-
Adv. Monitoring Final Review304
-
Neurophys final Review154
-
PEDS Final Review96
-
Survey of Anatomy Final Review324
-
Seminar SP 25 Final Review215
-
Pharm I Final Review484
-
Pharm I-251
-
Anatomical Imaging-SU2561
-
Pharm I Retake52
-
Pharmacology II227
-
Pharm II Final286
-
Phys III OB-Hepatlogy293
-
Pharm 3711
-
Coexisting 2527
-
Clinical Imaging39
-
APP 3- PEDS94
-
APP3- Cardiac344
-
Seminar 4197
