Hematology, GI, Renal and Peds Flashcards
1
Q
What are the two components of blood volume?
A
Plasma 55%
Cellular components 45%
2
Q
What are the components of the Plasma?
A
91% water
7% blood proteins
2% Nutrients, Hormones and Electrolytes
3
Q
What are the cellular components in blood volume?
A
Buffy coat & RBCs
4
Q
What are the two components that make up the buffy coat of the blood?
A
WBC and Platelets
5
Q
What causes erythropoietin to be released from the kidneys?
A
Hypoxia, reduced O2 levels in blood
6
Q
What is the function of erythropoietin once released by the kidneys?
A
Stimulates red bone marrow to produce more RBCs
7
Q
What is the name for immature erythrocytes in the blood stream?
A
Reticulocytes
8
Q
What is the lifespan for a RBC?
A
120 days
9
Q
What cellular structures does a erythrocyte lack?
A
Nuclei, mitochondria and ER
10
Q
How do erythrocytes create ATP?
A
Cytoplasmic enzymes (anaerobic glucose metabolism)
11
Q
What is the normal range of Hgb in adult males?
A
13.5-17.5g/dL
12
Q
What is the normal range of Hgb for adult females?
A
12-16g/dL
13
Q
What can indicate if enough red blood cells are being produced in the bone marrow?
A
Reticulocyte count
14
Q
How would the provider calculate the reticulocyte index?
A
(Ret% x Hct)/(0.45)
15
Q
What vitamins are required for Hgb synthesis?
A
B12, B6, B2, E, C, folic acid, pantothenic acid and niacin
B12 DNA synthesis, maturation
Folate DNA/RNA synthesis, maturation
16
Q
How is Hgb formed?
A
Fe released into erythroblast mitochondria
17
Q
What removes RBS from circulation?
A
Macrophages (spleen), broken down
18
Q
What conditions shift the oxyhemoglobin dissociation curve to the left?
A
Decrease temperature, PaCO2, 2,3 DPG and increased pH
More likely to hang on to O2
19
Q
What conditions shift the oxyhemoglobin dissociation curve to the right?
A
Increased temperature, PaCO2, 2,3 DPG and decreased pH
More likely to release O2 at the site
20
Q
What is anemia?
A
It is a decrease in O2 carrying capacity that can lead to tissue hypoxia
21
Q
What are common symptoms of anemia?
A
Fatigue, weakness, dyspnea and pallor
22
Q
What are the causes of anemia?
A
Impaired erythrocyte production
Actue/chronic blood loss
Increased erythrocyte destruction
23
Q
When does WHO suggest the diagnosis of anemia?
A
Non pregnant females Hgb less than 11
Males less than 13
24
Q
Why might a patients spleen be enlarged from anemia?
A
Trying to make more RBCs
25
What can bone marrow function test tell us about RBCs?
Can tell us the gross cellular structure and if there are abnormal cells present
DOES NOT indicate efficiency of activity
26
What tests can indicate the structural and functional characteristics of erythrocytes?
Mean corpuscular volume (MCV)
Mean corpuscular Hb (MCH)
Mean corpuscular HB concentration (MCHC)
27
What are normal hematocrit levels for males and females?
M: 42-52%
F: 36-48%
28
What are normal RBC count for males and females?
M: 4.2-5.4
F: 3.6-5
29
What are considered causes for microcytic anemia?
Iron deficiency
Thalassemia
Sideroblastic anemia
30
What are considered causes for macrocytic anemia?
Megaloblastic
Cobalamin deficiency
Folic acid deficiency
31
What are causes of normocytic anemia?
```
Primary bone marrow failure
Aplasia
Myelophthisis
Secondary Anemia
Inflammation
Uremia
Liver disease
Decreased endocrine function
```
32
What are characteristics of underproduction RBCs leading to anemia?
Reticulocyte count is inappropriately low (normal is 0.5-1.5%) and the onset is usually insidious
33
What are typically the causes of anemia due to RBC destruction?
Environmental factors
Membrane defects
Defects of cell interior
34
What is polycythemia?
An abnormally high number of RBCs
35
What might a patients Hct be if diagnosed with polycythemia?
55-60%
36
Why are patients with polycythemia at risk for having a stroke?
Due to increased viscosity of the blood, patients are at a higher rate of developing VTEs
37
What conditions are thought to cause relative polycythemia?
Dehydration, diarrhea, vomiting, diuretics-fluid loss results in and increased RBC count and Hgb/Hct value
38
What are causes of absolute polycythemia?
Abnormality of BM stem cells --> polycythemia vera
Increased in EPO in response to chronic hypoxia/tumors
Abnormal Hgb
39
What is the most common cause of polycythemia?
Tumor secreting
40
What is polycythemia vera?
An increase in all blood cells and spenomegaly
41
What are treatment options for polycythemia vera?
Meylosuppressive therapy
| Phlebotomy to draw off
42
What is pernicious anemia?
Occurs when there is a lack of intrinsic factor from gastric parietal cells, B12 deficiency
43
What are causes of pernicious anemia?
Congenital
Adult onset gastric mucosal atrophy (alcoholism)
Autoimmune
44
What are characteristics of pernicious anemia?
Unsteady gait, problems with reflex cognition, peripheral neuropathies and nerve demyelination
45
What might a patients labs look like with pernicious anemia?
Low Hgb 8-10
| Normal reticulocyte count (problem with absorption)
46
How should pernicious anemia be treated?
Vitamin B12 replacement
47
What is the most common type of anemia?
Iron deficiency anemia
48
What are the causes of iron deficiency anemia?
Nutritional iron deficiency
Inadequate intake/blood loss
Metabolic or functional deficiencies
Insufficient iron delivery
49
What are clinical manifestation of iron deficiency anemia?
Hgb levels 7-8g/dL
Red, sore and painful tongue
Brittle, thin, coarsely ridged and spoon shaped nails
50
What is the most sensitive indicator for iron deficiency anemia?
Serum ferritin
| 1ug/L --> 8-10mg of storage iron/kg
51
What is given for iron replacement therapy?
Ferrous
52
What are normal serum ferritin levels?
Male: 12-300 ng/mL (nanograms per millilter)
Female: 12-150 ng/mL
53
What conditions is anemia of chronic disease typically seen in?
AIDS, RA, Lupus, Erythematosus, hepatitis, renal failure and malignancies
54
What is the pathophysiology of anemia of chronic disease?
Decreased erythrocyte life span, ineffective bone marrow response to erythropoietin and altered iron metabolism
55
What is unique about all anemias?
They all lead to the same end results --> tissue hypoxia
56
What compensatory mechanisms are seen when anemia leads to tissue hypoxia?
```
Ischemia
Claudication
Weakens, increased fatigue
Pallor
Increased RR
Liver and CNS changes
```
57
How does anemia affect the oxyhemoglobin dissociation curve?
Shifts it to the right
58
What is sickle cell anemia?
Genetically determined defect of Hgb synthesis resulting in instability and insolubility
59
What is the abnormality of in the Hgb structure of a patient with sickle cell anemia?
Beta S chain
60
What occurs during a sickle cell crisis?
Red blood cells sickle and are unable to pass through small arteries causing vascular occlusion
61
What is the life span of a sickle cell?
12-17 days there is a constant need to produce more
62
How does sickle cell trait and disease affect preoperative morbidity and mortality?
Sickle cell trait doe not increase preoperative morbidity and mortality however sickle cell disease does
63
What surgeries are high triggers for a sickle cell crisis?
Intracranial
Intrathoracic
Orthopedic
64
What conditions should be avoided in order to prevent a sickle cell crisis?
```
Stress
Cold
Dehydration
Hypoxia
Acidosis
```
65
What structures are affected by vasoocclusive crisis from a sickle cell crisis?
Joint/bone pain
Spleen engagement
Painless hematuria
66
What is acute chest syndrome?
Complication of a sickle cell crisis that looks like pneumonia due to pulmonary infiltrates on chest x-ray
67
When does acute chest syndrome typically develop?
2-3 days into the post operative period
68
How is acute chest syndrome treated?
O2 blood transfusion, pain medications and fluids
69
What preventative measures can be taken to lessen the extent of acute chest syndrome?
Pre operative blood transfusions and post op incentive spirometer
70
How does the use of a tourniquet intraoperatively affect patients in sickle cell crisis?
Cuts off blood flow and increases incidence of preoperative complications
Use for the least amount of time
71
What is the physiological process that occurs when decreased red cell mass or oxygen saturation is sensed by the kidneys?
Stimulates the release of erythropoietin
72
What are the three main components of hemostasis?
Vasculature
Platelets
Clotting factors
73
What causes blood coagulation?
Transformation of soluble fibrinogen to insoluble fibrin
74
What term is used to describe an inactive clotting factor precursor?
Zymogen
75
What is considered primary hemostasis?
After an injury, vasoconstriction of the vessel is followed by platelet plug which seals the injured endothelium
76
What is considered secondary hemostasis?
The coagulation cascade promotes the formation of a blood clot via protein meshwork
77
What is considered tertiary hemostasis?
Clot dissolution via fibrinolysis
78
How is a platelet plug formed during primary hemostasis?
Exposure to collagen causes platelets to adhere and activate additional platelets, aggregation resulting in the formation of a platelet plug
79
What are the three A's of primary hemostasis?
Adhesion
Activation
Aggregation
80
What initiates the intrinsic pathway of the coagulation cascade?
Factor XII --> XIIa when sub endothelial substances are exposed
81
What initiates the extrinsic pathway of the coagulation cascade?
Tissue factor released by damaged endothelial cells
82
What has to be present in order for clot formation to occur?
Fibrin and Activated platelet
83
What prostaglandin derivatives are involved in the clotting cascade?
Thromboxane TXA2
| Prostacyclin (PGI2)
84
What is the function of TXA2?
Produced by activated platelets, stimulates activation of new platelets, increases fibrinogen receptors, causes degranulation and vasoconstriction
85
What is the function of prostacyclin?
Synthesized by endothelial cells lining the walls of arteries and veins; it is a potent vasodilator and a potent inhibitor of platelet aggregation
86
What is considered tertiary hemostasis?
Dissolving the clot
87
What are the three main components of the fibrinolytic system?
t-PA
Plasminogen --> plasmin
Fibrin degradation products
88
What vasoconstrictors are released when platelet activation and clot formation occur?
Serotonin and Thromboxane A2 from platelet activation
| Endothelin-1 from clotting protein thrombin
89
What is the end result of primary homeostasis?
Platelet plug formation at site of injury
90
What is the end result of secondary homeostasis?
Clot formation from fibrin mesh
91
What is the goal of the intrinsic pathway of the coagulation cascade?
Amplification of thrombin production, create prothrombinase activity on platelet surface
92
What does a bleeding time measure?
Platelet function and vascular integrety
93
What does a prothrombin time measure?
Factors I, II, V, VII, X (extrinsic and common pathway)
94
What does a partial thromboplastin time and activated clotting time measure?
Factors I, II, V, VII, IX, X, XI, XII
95
What does a thrombin time measure?
Factors I, II
96
What is a normal platelet count?
150-400
97
What is a normal prothrombin time?
10-12 seconds
98
What is a normal partial thromboplastin time?
25-35 seconds
99
What is a normal activated clotting time?
9-120 seconds
100
What is a normal fibrinogen level?
160-350mg/dL
101
What is a normal fibrin degradation products?
Less than hug/mL
102
What coagulation tests does low dose heparin affect?
Normal PT, prolonged PTT
| Inhibits factor IX
103
What coagulation tests does high dose heparin affect?
Prolonged PT and PTT
| Inhibits factors II, IX, X
104
What coagulation tests does low dose warfarin affect?
Prolonged PT and normal PTT
| Inhibits factor VII
105
What coagulation tests does high dose warfarin affect?
Prolonged PT and PTT
| Inhibits factors II, VII, IX, X
106
Activation of what factor is the beginning of the common final pathway?
X
107
How is thrombin activated?
Prothrombin is cleaved by factor Xa to produce thrombin
108
How is fibrin activated?
Thrombin cleaves fibrinogen by removing the N-terminal tails out of the proteins forming fibrin
109
What is considered thrombocytopenia?
Platelet count of less than 100
110
At what platelet level does spontaneous bleeding being to occur?
10-15k/mm
111
What is immune thrombocytopenia purpura (ITP)?
An autoimmune disorder characterized by decreased platelet count and normal bone marrow
112
What is thrombotic thrombocytopenia purpura?
Extensive microscopic clots form in the small blood vessels throughout the body
113
How does TTP cause organ damage?
Platelets aggregate and occlude arterioles and capillaries
114
What are causes of thrombocytopenia?
```
Inadequate produtos
Sequestration in the spleen
Consumption from tissue injury or platelet activation
Dilution due to massive transfusion
Destruction by immune mechanisms
```
115
What is HIT?
Development of thrombocytopenia (a low platelet count), due to the administration of various forms of heparin
116
What is the difference between HIT1 and HIT2?
HIT1: platelets 100,000 develops in 1-4days and d/c of heparin resolves the issue
HIT2: platelets 60,000 develops 5-14 days after therapy and often develop thrombus formation
117
What are the most common inherited coagulation disorders?
```
Hemophilia A (VIII)
Hemophilia B (IX)
Von Willebrand Disease (XI)- Von willebrand factor deficiency
```
118
What coagulation pathway is generally affected in inherited bleeding disorders?
Intrinsic pathway
119
What population is predominately diagnosed with Hemophilia A?
Males, x-linked
120
What labs are abnormal in Hemophilia A?
Prolonged PTT but normal bleeding time
121
What labs are abnormal in Von Willebrands disease?
Prolonged PTT and Prolonged bleeding time
122
What bleeding pattern is typically seen in Hemophilia A?
Hemarthrosis and Hematomas
123
What type of bleeding is seen in Von Willebrands disease?
Mucosal bleeding
124
What clotting factors are vitamin K dependent?
II, VII, IX, X
125
What is the purpose of vitamin K?
Without vitamin K we can't bind on top of platelets
126
What is the CHADs assessment?
```
Risk assessment for stroke
Congestive heart failure
HTN
Age
DM
Stroke
```
127
What is disseminated intravascular coagulation?
Occurs secondary to an initial assault that causes widespread activation of thrombin within the microvasculature leading to diffuse circulatory insufficiency
128
What is the treatment for DIC?
Treating the underlying disorder, anticoagulants and FFP
129
What lab values indicate DIC?
Fibrin degradation product and D-dimer levels will increase
130
What is the end result of DIC?
Consumption of platelets and clotting factors resulting in bleeding
131
What causes a venous thrombosis?
Blood stasis, extend in direction of growth, prone to embolus
132
Where are venous thrombi typically found?
Superficial or deep veins of the legs
133
What are symptoms of a venous thrombi?
Local congestion, pain, swelling, tenderness, rarely embolize
134
What is an embolus?
A detached intravascular solid, liquid or gaseous mass
135
What can occur if greater than 60% of pulmonary circulation is obstructed by thromboembolism?
Sudden death, for pulmonale or CV collapse
136
What systemic effects do medium sized pulmonary thromboembolism have on the body?
Collateral flow, not usually infarct but problem with LV failure
137
What systemic effects do small sized pulmonary thromboembolism have on the body?
Associated with infarct, multiple can lead to pulmonary HTN with right heart failure
138
What is considered a massive transfusion?
Acute replacement of more than 1 blood volume
139
What are the most common causes of massive transfusion?
Trauma and OR blood loss
140
What are the components of coagulopathy in massive transfusion?
Dilution of factors
Hypothermia
Tissue perfusion/acidosis
141
What are the components of whole blood?
RBC
Granulocytes
Plasma
Platelets
142
What are the components that make up plasma?
FFP and Fractionated products
143
What are the components that make up FFP?
Cryoprecipitate and cryosupernatant plasma
144
What clotting factors are part of fractionated products?
VIIa, VIII, IX, Albumin and Immune globulin
145
What blood type can be given to patients with O blood type?
Only group O whole blood and red cells
146
What blood type an be given to patients with A blood type?
Group A whole blood and red cells AND Group O red cells if A not available
147
What blood type can be given to patients with B blood type?
Group B whole blood and red cells AND Group O red cells if group B blood not available
148
What blood type can be given to patients with AB blood type?
Group AB whole blood and red cells, Group A or B red cells if group AB blood not available AND Group O red cells as a last alternative
149
What are the components of coagulopathy in massive transfusion?
Dilution of factors
Hypothermia
Tissue perfusion/acidosis
150
What are the components of whole blood?
RBC
Granulocytes
Plasma
Platelets
151
What are the components that make up plasma?
FFP and Fractionated products
152
What are the components that make up FFP?
Cryoprecipitate and cryosupernatant plasma
153
What clotting factors are part of fractionated products?
VIIa, VIII, IX, Albumin and Immune globulin
154
What blood type can be given to patients with O blood type?
Only group O whole blood and red cells
155
What blood type an be given to patients with A blood type?
Group A whole blood and red cells AND Group O red cells if A not available
156
What blood type can be given to patients with B blood type?
Group B whole blood and red cells AND Group O red cells if group B blood not available
157
What blood type can be given to patients with AB blood type?
Group AB whole blood and red cells, Group A or B red cells if group AB blood not available AND Group O red cells as a last alternative
158
What is considered the GI tract?
The pharynx to the anus
159
What three layers make up the muscular tube of the GI tract?
Intralumenal
Transmural
Extraluminal
160
What are the names of the two interconnected plexuses from the esophagus to the anus?
Myenteric (Auerbach's)
| Submucosal (Meissner's)
161
What is the function of the Myenteric Plexus?
Motor control of GI system
162
Where is the Myenteric plexus located?
Outer longitudinal and middle circular muscle layers
163
What is the function of the Submucosal plexus?
Innervates the glandular epithelial cells, intestinal endocrine cells and submucosal blood vessels
GI secretions and local blood flow
164
What three systems control the function of the GI tract?
ANS
Paracrine secretion
Endocrine activity
165
What are the most common paracrine secretions in the GI tract?
Histamine & Somatostatin
166
What is known to cause muscle contraction in the GI tract?
Ach and tachykinin (Substance P)
167
What factors are known to cause GI muscle relaxation?
VIP, Nitric oxide and ATP
168
What initiates peristalsis?
When the gut wall is stretched
169
What system generates and which system modulates peristalsis?
Generated by the enteric nervous system
| Modulated by the autonomic nervous system (PSNS increases)
170
Where does the esophagus originate?
C6, extends from cricopharygyngeal sphincter to gastroesophogeal sphincter
171
What are the three functional zones of the esophagus?
Upper esophageal sphincter
Esophageal body
Lower esophageal sphincter
172
What are the components of the upper esophageal sphincter?
One of the two inferior muscles of the pharynx with the circular fibers of the upper esophagus
173
Where is the upper esophageal sphincter located?
At the pharyngeal esophageal junction
174
What is the resting pressure of the upper esophageal sphincter?
15-60cmH2O
175
What is the function of the UES?
Prevents air from entering the esophagus under normal circumstances, seals esophagus from the hypopharynx in preventing aspiration
176
What causes loss of tone in the UES?
Impaired during sleep and anesthesia
177
What is the lower esophageal sphincter?
3-4cm ring of smooth muscle surrounding the lower end of the esophagus
178
What pressure is the resting tone of the LES?
10-15cmH2O
179
What factors affect the sphincter pressure of the LES?
Intrinsic nerve plexus and gastrin release
180
What are typically the causes of esophageal disorders?
Altered motor function (intrinsic or extrinsic)
Disordered peristalsis
Increased LES tone
Decreased LES tone
181
What is the most common esophageal abnormality?
Decreased LES tone
182
What is achalasia?
Increased LES tone due to impaired smith muscle relaxation
183
What is the triad of symptoms associated with Achalasia?
Incomplete LES relaxation
Increased LES tone
Aperistalsis of esophagus
184
What causes primary achalasia?
Failure of the distal inhibitory neurons
185
What is the cause of secondary achalasia?
Chagas disease, parasite ("kissing bug") causes destruction of myenteric plexus
186
What is the treatment for achalasia?
Laparoscopic myotome to release the spasm or pneumatic balloon dilation
Botox has also been shown to be effective
187
What are symptoms of achalasia?
Swallowing is difficult and the patient can regurgitate undigested food as they cough
188
What is gastroesophageal reflux disease?
Persistent repetitive acid exposure to the esophagus
189
What typically prevents a patient from reflux?
The LES
190
What hormones are secreted in the proximal and distal ends of the esophagus that are protective to the mucosal lining?
Mucin and Bicarbonate
191
What abnormalities of the GI tract can cause GERD?
Increased intraabdominal pressure
Delayed gastric emptying
Increased acid production
Increased gastric volume dilation
192
How should the LES accommodate increased intraabdominal pressures in a healthy adult?
LES pressure should ride in response to increase intragastric pressure
193
What is the primary cause of GERD?
40% of patients with GERD have delayed gastric emptying
194
What are the most common causes of delayed gastric emptying?
```
Neurologic disorders (ALS, MS)
Autonomic neuropathy (DM)
Collagen-vascular disorders (RA, SLE, Scleroderma)
```
195
What condition is associated with recurrent reflux?
Barrett's Esophagitis
196
What can develop in conjunction with Barrett's Esophagitis?
Epithelium changes from squamous to columnar and can transition to adenocarcinoma
197
What population is Barrett's Esophagitis most common?
White males 40-60yrs/o
198
What is a Hiatal hernia?
A portion of the stomach protrudes through the hiatus of diaphragm into the thoracic cavity
199
How does a hiatal hernia contribute to acid reflux?
Produces defect in esophageal propulsion resulting in inadequate acid clearance and longer transit time
200
What are the two types of hiatal hernias?
Type I: sliding
| Type II: paraesophageal
201
What surgical interventions are typically done for patients with a hiatal hernia?
Surgical correction of hernia and Lap Nissen
202
What is an esophageal diverticula?
A pouch in the esophagus that can trap food particles
203
What are complications associated with esophageal diverticula?
Predispose the patient to pulmonary aspiration even in the absence of recent food intake
204
What are the three classifications of esophageal diverticula?
Zenker (upper)
Traction (mild)
Epiphrenic (near LES)
205
What is commonly associated with the formation of an esophageal carcinoma?
Alcohol and tobacco abuse
206
What procedure is performed for esophageal carcinoma?
Ivor-Lewis/McKeowen Esophagectomy
207
What are the most common complications associated with the Ivor-Lewis/Mckeowen Esophagectomy procedure?
Bleeding
RLN injury
Injury to the trachea
208
What are the two parts of the stomach?
The fundus and the antrum
209
What is the primary function of the fundus?
Storage
210
What is the primary function of the antrum?
Mixes food and slowly releases via pyloric sphincter into the duodenum
211
What is the function of the antral glands?
Contain endocrine cells that secrete gastrin to stimulate luminal acid secretion by the parietal cells
212
What factors cause gastric motility?
Increased tone in proximal stomach
Strength of antral contractions
Opening of pylorus
Inhibition of duodenal segmental contractions
213
What determines the rate of gastric motility?
Rate influenced by chemical composition of chyme entering duodenum
214
What do parietal cells secrete?
HCL and intrinsic factor
215
What do peptic cells secrete?
Pepsinogen
216
What is the purpose of the mucous secreting cells of the stomach?
Protection of the stomach
217
What are the functions of HCL in the stomach?
Kills bacteria
Aids protein digestion
Releases pepsin from pepsinogen
218
What is the function of intrinsic factor in the GI tract?
Required for efficient absorption of B12 in terminal ileum
219
What class of drugs inhibit gastric acid secretion?
H2 receptor antagonists
PPI
Prostaglandin analogue
220
Where do PPIs work in the GI tract?
Inhibit the H/K ATPase pump
221
Why aren't H2 antagonists as effective in treating GERD as PPI?
H2 still allows many paths for acid creation:
Ach
Gastrin
Prostaglandin
222
What is an ulceration of the GI tract?
Focal damage that extends beyond the mucosal layer into the submucosa and muscularis epithelial layer
223
What are the two main causes of gastric ulcer disease?
H pylori is number 1
| NSAID induced is 2
224
What population are acute stress ulcers typically seen?
Seriously ill patients, plasma volume reduced sloughing of gastric mucosa precipitated by shock and SNS response
225
What are curling ulcers?
Ulcers in proximal duodenum associated with severe burns or trauma
226
What are cushings ulcers?
Gastric, duodenal and esophageal ulcers associated with intracranial disease (high incidence of perforation)
227
What is thought to be the cause of cushing's ulcers?
Elevated ICP probably stimulates basal nuclei which causes a vagal response to stimulate Ach, receptors on parietal cells cause H secretion
228
What is Zollinger-Ellison Syndrome?
Gastrin secreting tumor
229
What pathology is Zollinger-Ellison syndrome often associated with?
```
MEN1 syndrome:
Parathyroid
Pancreas
Pituitary
Metastatic disease involving three organ sites
```
230
What are anesthetic implications for Zollinger-Ellison syndrome?
Esophageal reflux -RSI
IV volume depletion and electrolyte abnormalities
Maintain PPI and H2 therapy
231
What is the most common gastric neoplastic disease?
Adenocarcinoma
232
What form of cancer is becoming more common probably due to an increase in Barretts esophagitis?
Cancer of the gastric cardia
233
What are the components of the small intestine?
Duodenum
Jejunum
Ileum
234
What connects the duodenum of the small intestine to the diaphragm?
Ligament of treitz
235
What is the primary purpose of the small intestine?
Digestion and absorption
236
What part of the small intestine does majority of Na absorption occur?
Jejunum
237
What metabolic processes occur in the ileum?
Bicarbonate excretion and chloride absorbed
| K absorption
238
What is the primary function of the large intestine?
Store and expel waste products, absorption of water and electrolytes
239
What electrolyte is lost when a patient has colitis?
Potassium loss
240
What are the four main causes of intestinal obstruction?
Herniation
Adhesion
Volvulus
Intussusception
241
Where are intestinal obstruction most likely to take place?
Small intestine due to small lumen
242
What are clinical manifestations of an intestinal obstruction?
Abdominal pain, distention, vomiting and constipation
243
What are common characteristics of IBS?
Alternating diarrhea and constipation
Abdominal pain
Bloating
244
What is thought to influence symptoms of IBS?
Thought to be caused by intense intra-abdominal response to emotional stress
245
What are additional symptoms associated with vasomotor instability in relation to IBS?
Tachycardia
Hyperventilation
Diaphoresis
Headaches
246
What is splenic flexure syndrome?
Air trapped in splenic flexure of the colon, pain in left shoulder (laparoscopic cases)
247
What is the prominent feature of inflammatory bowel disease?
Malabsorption
248
What is ulcerative colitis?
Severe ulcerating inflammatory disease that is limited to the colon and rectum and extend into the mucosa and submucosa
249
What is crohn's disease?
May involve any area of the GI tract and is typically transmural
250
Where does Crohn's diseases most frequently occur?
Distal ileum and colon
251
What hereditary disorders can Crohn's disease also be associated with?
Cystic fibrosis and Ankylosing spondylitis
252
What are complications that can occur as a result of Crohn's disease?
Perforation, fistula formation, access formation, small bowel obstruction
253
What are additional symptoms that are associated with Crohns disease?
```
Amyloidosis
Thromboembolic disease
Migratory arthritis
Inflammatory disorders of the skin, eye and mucous membranes
Nephrolithiasis
```
254
What are the anatomical borders of the duodenum?
Begins pyloric sphincter and extends to the ligament of Treitz
255
Where is the jejunum?
Proximal 2/5 of the small intesting
256
What are the anatomical borders of the ileum?
Distal 2/5 of small intestine ending with ileocecal valve
257
What is ulcerative colitis?
Inflammation restricted to mucosa of colon and rectum
258
What medications can be given to patients with ulcerative colitis?
Glucocorticoids and Sulfasalazine
259
What is a complication of ulcerative colitis?
Toxic megacolon, increased risk of perforation
260
If infected what can diverticulosis develop into?
Diverticulitis
261
What are early signs of appendicitis?
Mild visceral abdominal pain, poorly localized in the periumbilibal and epigastric areas with the urge to defecate or pass flatus
262
What are later symptoms of appendicitis?
Steady somatic pain as inflammation processes
Severe, aggravated by motion or cough
Temperature slightly elevated and moderate leukocytosis
263
What is mesenteric station syndrome?
Facial flushing, sudden tachycardia, HoTN and cutaneous hyperemia from surgeon tugging on the bowel
264
What medications are used to treat mesenteric traction syndrome?
NSAIDs
H1 & H2 receptor antagonists
(Since reactions is thought to be histamine, prostacyclin, thromboxane and COX activation)
265
Why might the provider mistake mesenteric tractions syndrome for the patient being light?
Same symptoms however if the patient was light from anesthesia would be HTN not HoTN
266
What are the most important factors in determining severity of pulmonary insult?
Volume
pH
Presence or absence of particulate matter
267
What factors are associated with the most severe pneumonitis?
Gastric volume greater than 25mL and pH less than 2.5
268
What can be done to minimize aspiration risk on induction of anesthesia?
Minimize intake
Increase gastric emptying
Reduce gastric volume and acidity
Airway management and protection (cricoid pressure and cuffed ETT)
269
What can use of N2O cause in large abdominal cases?
Excessive distention of bowel
Possible bowel ischemia
Difficulty with surgical exposure
Difficulty with closure
270
How does increased intra-abdominal pressure affect CO?
Decreases CO
271
If nitrous oxide is used for longer than four hours, how does that affect the volume of the bowels?
After 4hrs 100-200% increase in volume
272
What percentage of the pancreas function is exocrine?
80-85%
| Digestive enzymes
273
What percentage of the pancreatic function is endocrine?
1-2%
| Insulin, glucagon and somatostatin
274
What are the borders of the pancreas?
C loop of the duodenum to the hilum of the spleen
275
What are the most significant disorders of the exocrine cells?
```
Cystic fibrosis
Congenital anomalies
acute/chronic pancreatitis
Pseudocysts
Neoplasms
```
276
What are the exocrine functions of the pancreas?
Adjusts pH of the duodenal contents to optimize pancreatic enzyme activity
Secretion control
277
If exocrine function is decreased leading to decreased secretions what metabolic disturbance can occur?
Impaired fat and protein digestion
278
What is the primary endocrine function of the pancreas?
Regulates plasma glucose
279
What is secreted by the alpha cells of the pancreas?
Glucagon
280
What is secreted by the beta cells of the pancreas?
Insulin
281
What is secreted by the delta cells of the pancreas?
somatostatin to control plasma levels of insulin and glucose
282
What inhibits insulin secretion?
Alpha adrenergic stimulation
| Beta adrenergic and cholinergic blockade
283
What enhances insulin secretion?
Vagal stimulation
B2 adrenergic activation
Cholinergic drugs
284
What is pancreatitis?
Inflammation or injury to the exocrine parenchyma
285
What is the difference between acute and chronic pancreatitis?
In acute the pancreas returns to normal if underlying cause is removed where chronic is irreversible loss of exocrine parenchyma
286
What is normally the cause f acute pancreatitis in western countries?
Biliary tract disease and alcoholism
287
What percentage of patients with acute pancreatitis have gallstones?
35-60%
288
What are the three proposed pathways of acute pancreatitis?
Pancreatic duct obstruction
Primary acinar cell injury
Defective inracellular transport
289
What is the cardinal characteristic of acute pancreatitis?
Abdominal pain, constant, intense referred to upper back or left shoulder
290
How is acute pancreatitis typically diagnosed?
Elevated plasma levels of amylase and lipase
291
What electrolyte abnormality is often seen in acute pancreatitis?
Hypocalcemia (tetany)
292
What effects doe pancreatic kinin peptides have when released during acute pancreatitis?
Enhanced vasodilation
Enhanced vascular permeability
Impair myocardial contractility
293
What CV complication can result from acute pancreatitis?
Pericardial effusions
Alteration in rhythm
Thombophelbitis
Cardiac depression
294
What are anesthetic implications for acute pancreatitis?
Correction of significant intravascular volume deficits
Aspiration precautions
Electrolyte imbalances
295
What is the triad of symptoms from chronic pancreatitis from alcoholism?
Steatorrhea
Pancreatic calcification
DM
296
What lab values differ in acute versus chronic pancreatitis?
Amylase levels are elevated in acute and normal in chronic pancreatitis
297
Why are patients with chronic pancreatitis malnourished?
They are unable to absorb and utilize fats and proteins once secretions are decreased to the point where enzymes entering the duodenum 10-20% of normal
298
What hepatic complications are often seen with chronic pancreatitis?
Jaundice, ascites, esophageal varices, altered coagulation and serum albumin
299
Why are patients with chronic pancreatitis predisposed to pericardial and pleural effusions?
Because they have lost protein, they can't generate albumin
300
What is a pancreatic pseudocyst?
Mass of proteolytic enzymes
301
Why are pseudocysts potentially lethal?
If they erode or rupture wth spillage into abdominal cavity
302
What are predisposing factors of pancreatic cancer?
Genetic, Chronic DM, Alcoholism, Chronic pancreatitis, heavy tobacco use and heavy caffeine use
303
What is the most common surgical procedure in an attempt to cure pancreatic cancer?
Pancreaticoduodenectomy (Whipple)
304
What components of the digestive system are involved in the Whipple?
Head of pancreas taken off, Gallbladder, part of the stomach, duodenum and portion of the bile duct
305
What electrolyte abnormalities are often seen with a whipple procedure?
Hypocalcemia, Hypokalemia, Hypomagnesemia and possible hypochloremic metabolic alkalosis
306
Where is the spleen located?
Left upper quadrant
307
What are the borders of the spleen?
Surrounded by stomach fundus medially, colon interiorly, let kidney and adrenal gland posteriorly and the diaphragm superiorly
308
Where does the splenic artery arise?
Celiac plexus
309
Where does the splenic vein empty?
Joins mesenteric vein to contribute to portal venous blood flow
310
Approximately how much blood circulates in the splenic vascular structures?
300mL/min
311
What are the functions of the spleen?
Fetal hematopoiesis
Blood filtering
Immune processing of blood borne foreign antigens
Minor role as platelet reservoir
312
What are causes of splenomegaly?
Hyperplenism
Nonspecific acute splenitis
Congestive splenomegaly
Splenic infarctions
313
What pathology can cause hyperplenism of the spleen?
Anemia, Leukopenia, Thrombocytopenia
314
What can occur if there is venous obstruction from the spleen?
Portal vein HTN
315
What is the main cause of massive congestive splenomegaly?
Cirrosis
316
What is usually the cause of splenic rupture?
Blunt force trauma
317
What are non traumatic predispositions to splenic rupture?
Infectious mono
Malaria
Typhoid fever
Lymphoid neoplasms
318
What conditions may cause an individuals to have an elective splenectomy?
Hodgkin's and non Hodgkins lymphoma
Leukemia
Myeloid metaplasia
319
What are usually the first signs of a carcinoid tumor?
Asymptomatic, usually have abdominal pain, diarrhea, intermittent intestinal pain and bleeding
320
What cells make up carcinoid tumors?
Composed of enterochromaffin cells
75% GI
22% lung
321
What are carcinoid tumors?
Non metastatic tumors usually secrete hormones that are usually activated and transporter to the liver through the portal vein
322
Where is a high incidence of carcinoid tumors located?
Appendiceal region
323
What two factors release carcinoid hormones?
Direct physical manipulation
| B-adrenergic stimulation
324
What is carcinoid syndrome?
Massive amounts of hormone released by tumor causing cutaneous flushing of the head neck and thorax, bronchocontriction/spasm, profuse diarrhea, labile arterial BP and supra ventricular dysrhythmias
325
What can carcinoid syndrome indicate?
Pulmonary or hepatic metastasis
326
In carcinoid heart disease what components make up carcinoid triad?
Cardiac involvement
Flushing
Diarrhea
327
What causes right sided heart failure in carcinoid heart disease?
Valvular (tricuspid regurg) and myocardial plaque formation
328
Why is the left heart protected from failure in carcinoid heart disease?
Lung metabolism of serotonin
329
What is the most effective treatment in carcinoid tumors?
Surgical excision
330
What drugs should be avoided in carcinoid tumor disease?
Drugs that cause histamine release and catecholamines
331
What are the most common clinical signs of carcinoid tumors?
Flushing, wheezing, BP and HR changes
332
If a patient with carcinoid tumor disease how should this be treated?
A-receptor agonist, not beta
333
Why is GA preferred over regional in patients with carcinoid tumor?
Increased serotonin levels may prolong recovery
334
Why are patients with carcinoid tumor disease treated with octreotide?
It is a somatostatin analogue that blunts vasoactive and bronchoconstrictive effects of carcinoid products
Mimics inhibitory action of somatostatin on release of many GI hormones/carcinoid tumors
335
What dose of octreotide is given prior to surgery?
100mcg SQ TID x 2 weeks
336
What is the intraoperative dose of octreotide?
Infusion 100mcg/hr
| 100-200mcg IV if intraoperative crisis
337
What factors can cause intraoperative carcinoid crisis?
Physical or chemical stimulation (succinylcholine)
Stress
Tumor necrosis following hepatic artery ligation
Embolization
Chemotherapy
338
What are the functions of the kidneys?
Regulate the volume and composition of extracellular fluid
Endocrine functions
Regulation of BP
339
What are the functional units of the kidney?
Nephron
340
What are the borders of the kidney?
Extends from the 12th thoracic vertebrae to the third lumbar vertebrae
341
Why is the right kidney slightly lower than the left kidney?
Hepatic displacement
342
What are the two regions of the kidney?
Outer cortex and inner cortex
343
What serves as the major reservoir for urine?
Renal pelvis
344
How does the renal pelvis connect to the bladder?
Ureters
345
What are the components of the nephron?
```
Proximal tubule
Loop of Henle
Distal tubule
Collecting ducts
Juxtaglomerular apparatus
```
346
What is the function of the proximal tubule?
Reabsorption of Na Cl H2O HCO3 glucose, protein, amino acids, K, mag, calcium, phosphate, uric acid and urea
Secretion of organic anions and cations
Ammonium production
347
What is the function of the loop of Henle?
Reabsorption of Na, Cl, H2O, K, Ca, Mg
| Establishes concentration gradient with renal medulla
348
What is the function of the Distal Tubule?
Reabsorption of Na, Cl, H2O, K, Ca, HCO3
| Secretion of H, K and Ca
349
What is the function of the Collecting duct?
Reabsorption of Na, Cl, H2O, K, HCO3,
Secretion of H, K
Ammonium production
350
What is the function of the JG apparatus?
Renin secretion
351
How much of the CO do the kidneys receive?
20%
352
What is the normal GFR?
120mL/min
353
What does the renal plasma flow dependent on?
Hct of blood, viscosity is important
354
How does viscosity impact renal plasma flow?
Greater viscosity decreases renal plasma flow
355
What is the filtration fraction?
GFR/RPF
| It is the percent of total blood that is actually filtered
356
How is GFR determined?
It is the product of the net driving pressure forcing fluid out of the glomerular capillaries and the permeability of the filtration barrier
357
What forces determine GFR?
Hydrostatic pressure in Bowmens space
Glomerular capillary plasma oncotic pressure
Hydrostatic pressure in glomerular capillary
358
How does afferent arteriole constriction affect renal blood flow?
```
RBF --> Decreased
End hydrostatic pressure --> Decreased
GFR --> Decreased
Functional fraction --> No change
End proximal fluid delivery --> Decreased
```
359
How does efferent arteriole constriction affect renal blood flow?
```
RBF --> Decreased
End hydrostatic pressure --> Increase
GFR --> Increase
Functional fraction --> Increase
End proximal fluid delivery --> No change
```
360
How does afferent arteriole dilation affect renal blood flow?
```
RBF --> Increase
End hydrostatic pressure --> Increase
GFR --> Increase
Functional fraction --> No change
End proximal fluid delivery -->Increase
```
361
How does Efferent arteriole dilation affect renal blood flow?
```
RBF --> Increase
End hydrostatic pressure --> Decreased
GFR --> Decreased
Functional fraction --> Decrease
End proximal fluid delivery --> No change
```
362
What determines blood flow to the kidneys?
CO however the kidneys are autoregulated
363
What response by the kidneys occur when hypotension and decreased perfusion occurs?
Falling BP increases SNS activity and releases the renin cascade
364
What processes are required for the renal system to concentrate urine?
Adequate GFR
Na reabsorption without water reabsorption in the ascending loop of Henle
Water permeability in the collecting ducts must be variable
365
How does afferent arteriole constriction affect renal blood flow?
```
RBF --> Decreased
End hydrostatic pressure --> Decreased
GFR --> Decreased
Functional fraction --> No change
End proximal fluid delivery --> Decreased
```
366
How does efferent arteriole constriction affect renal blood flow?
```
RBF --> Decreased
End hydrostatic pressure --> Increase
GFR --> Increase
Functional fraction --> Increase
End proximal fluid delivery --> No change
```
367
What indirect effects of anesthesia affect RBF?
CV due to decrease BP
Neural from SNS activation
Endocrine RAAS
368
How does Efferent arteriole dilation affect renal blood flow?
```
RBF --> Increase
End hydrostatic pressure --> Decreased
GFR --> Decreased
Functional fraction --> Decrease
End proximal fluid delivery --> No change
```
369
What determines blood flow to the kidneys?
CO however the kidneys are autoregulated
370
What response by the kidneys occur when hypotension and decreased perfusion occurs?
Falling BP increases SNS activity and releases the renin cascade
371
What processes are required for the renal system to concentrate urine?
Adequate GFR
Na reabsorption without water reabsorption in the ascending loop of Henle
Water permeability in the collecting ducts must be variable
372
What is the most likely cause of renal damage in anesthesia?
Decreased GFR from hypoperfusion
373
How does anesthesia affect the kidneys?
Reversible decrease in RBF, GFR, urinary flow and sodium excretion
374
What criteria place a patient at risk for renal failure?
Increased serum creatinine by 1.5 or GFR decreased by greater than 25%
Urine output less than 0.5mL/kg/hr for greater than 6hrs
375
Why are the kidneys so vulnerable to toxicity?
Rich blood supply
Concentrated excretion
Medullary hyperosmolality
376
What factors affect the amount of renal damage?
Concentration of toxins
Degree of binding to proteins
Length of exposure
377
What component of volatile anesthetics is harmful to the kidneys?
Fluoride ion
378
How does fluoride ion cause toxicity?
Interferes with active transport of Na and Cl in the medullary portion of the loop of Henle
Potent vasodilator
Inhibits ADH nephron water reabsorption
379
How is compound A created?
CO2 absorbent degrade Sevo
380
What factors increase compound A production?
High concentration of the agent
Increase temperature in the CO2 absorbent
Low fresh gas flows
Increase CO2 production
381
What criteria place a patient at risk for renal failure?
Increased serum creatinine by 1.5 or GFR decreased by greater than 25%
Urine output less than 0.5mL/kg/hr for greater than 6hrs
382
What criteria is known to cause renal injury?
Increased serum creatinine by 2 or GFR decreased by greater than 50%
Urine output less than 0.5mL/kg/hr for greater than 12hrs
383
What is acute glomerulonephritis?
Inflammation and damage to the glomerular membrane
384
What tools are used to stage renal injury?
RIFL --> GFR
| AKIN --> Serum Cr levels
385
What surgical procedures place a patient at risk for an acute kidney injury?
Cardiac surgery
Aortic Surgery
Liver transplantation
Any procedure the patient will be on cardiac bypass (cross clamping of the aorta)
386
What are the three types of acute renal failure?
Pre renal
Post renal
Intrinsic
387
What causes pre renal failure?
Transient renal hypo perfusion:
HoTN
Decreased CO
Decreased blood volume
388
What causes post renal failure?
Due to obstruction of the urinary tract:
Tumor
Kidney stones
Positional
389
What are the causes of intrinsic renal failure?
Acute glomerulonephritis
Acute Interstitial nephritis
Acute tubular necrosis
390
What is acute glomerulonephritis?
Inflammation and damage to the glomerular membrane
391
What is interstitial nephritis?
Allergic reaction caused by a variety of drugs
392
What interventions should be performed in order to decrease the risk of a CI-AKI?
Decrease the dose
Consider not making NPO for prolonged period of time
Adequate hydration before/during/after
Close monitoring
393
What components of GA cause decreased CO and hypoerfusion to the kidneys?
Bleeding
Positive pressure ventilation
Volume loss
394
What is the goal of patients under GA to avoid acute kidney injury?
Renal perfusion
395
What non depolarizer would the provider want to avoid if kidney function decreased?
Vecuronium
396
What medications impair renal function?
```
Anti rejection medications
Anti microbial agents (aminoglycocides)
NSAIDs
ACE inhibitors
Contrast
```
397
What is considered a contrast induced acute kidney injury?
Acute renal toxic event that results in acute tubular necrosis and apoptosis of renal cells from iodinated contrast injection
398
What procedures are associated with CI-AKI?
Cardiac cath, and PCI
399
What can be done to overcome diuretic resistance?
Restore normal hemodynamics
Higher dose of diuretic
Restore hypo albumin with albumin
400
What is the first step in identifying intraoperative oliguria?
Identify the patient is producing less than 0.5mL/kg/hr
| Mannitol will be less than 1-2mL/kg/hr
401
Once intraop oliguria has been identified what should the provider do first?
Check for low sodium, assess hemodynamics and urine response to fluid challenge
402
If a patient does not respond to a fluid challenge after oliguria has been identified what should be done next?
Institute invasive hemodynamic monitoring: CVP, TEE, PAC
403
What can be done to maximize a patients CO to insure adequate renal perfusion?
Normal rhythm/rate
Optimize preload
Inotropic support
After load reduction
404
Why aren't diuretics the first line of treatment when oliguria has been identified?
Greater mortality rate when loop diuretics given when patients are in acute renal failure
405
What causes diuretic resistance?
Acute tolerance induced by hypovolemia
Chronic tolerance
Refractory status such as renal insufficiency, CHF and cirrhosis
406
What can be done to overcome diuretic resistance?
Restore normal hemodynamics
Higher dose of diuretic
Restore hypo albumin with albumin
407
What are characteristics of chronic renal failure?
Diminished function of the nephrons
Decreased RBF and GFR
Decreased tubular function and reabsorptive activity
408
What physical changes of the kidney may be seen in chronic renal failure?
Decreased size and apparent granulations
409
What does stage five end stage renal disease consist of?
GFR less than 15 or on dialysis
410
What does stage one end stage renal disease consist of?
GFR greater than 90
| Normal kidney function but urine findings, structural abnormalities or genetic trait point to kidney disease
411
How should stage one end stage renal disease be treated?
Observation and control of BP
412
What does stage two end stage renal disease consist of?
GFR 60-89
| Mildly reduced kidney function and other findings point to kidney disease
413
How should stage two end state renal disease be treated?
Observation, BP control and risk factors
414
What differentiates stage 3A from 3B of end stage renal disease?
GFR
3A: 45-59
3B: 30-44
415
What does stage four end stage renal disease consist of?
GFR: 15-29
| Severely reduced kidney function
416
What is not a good indicator of fluid status or renal function in patients with chronic renal disease?
Urine output
417
How might the provider differentiate pre renal from intrinsic acute renal failure from looking at the BUN to Cr ration?
Greater than 20:1 pre renal
| Less than 20:1 intrinsic
418
How does uncontrolled HTN cause chronic renal disease?
Prolonged increased pressure on renal vasculature can lead to glomerularsclerosis and changes in renal blood flow auto regulation
419
What is a normal BUN?
10-20mg/dL
420
What is a normal serum creatinine?
0.7-1.5 depending on muscle mass
421
What is a normal creatinine clearance?
95-150mL/min
422
What are the two types of dialysis?
Peritoneal and Hemodialysis
423
What is not a good indicator of fluid status or renal function in patients with chronic renal disease?
Urine output
424
How might the provider differentiate pre renal from intrinsic acute renal failure from looking at the BUN to Cr ration?
Greater than 20:1 pre renal
| Less than 20:1 intrinsic
425
What is the most frequent chromosomal aberration?
Down Syndrome/Trisomy 21
426
What do PFTs look like in a patient with CF?
Obstructive disease, increased FRC, decreased FEV1, decreased peak expiratory flow rate and decreased VC
427
What airway considerations should be assessed in children with down syndrome?
Atlantoaxial inststability
OSA
Subglottic stenosis
428
What cardiac consideration should be taken into account for anesthesia in children with down syndrome?
Prone to bradycardia on induction
| Consider antibiotic for endocarditis prophylaxis
429
What occurs in cystic fibrosis?
A membrane glycoprotein chloride channel that contributes to regulation of ion flux at various epithelial surfaces
Decreased Cl is accompanies by decrease transport of Na and water = dehydration, viscous secretions and electrolyte abnormalities
430
What is indicative of cystic fibrosis?
Elevated sweat chloride concentrations
| Greater than 80mEq/L
431
Why are children with CF generally small?
Malabsorption and malnutrition due to pancreatic insufficiency
Increased caloric demand due to severe lung disease
432
What is the main cause of morbidity and mortality in patients with CF?
Lung disease
433
What do PFTs look like in a patient with CF?
Obstructive disease, increased FRC, decreased FEV1, decreased peak expiratory flow rate and decreased VC
434
What are the most common surgeries associated with CF?
Polypectomy
Functional endoscopic sinus surgery
Bronchoscopies
Lung transplant
435
What are the goals in treating patients with CF?
```
To alleviate symptoms:
Treat malnutrition --> g-tube
Relief of airway obstruction
Correct Organ dysfunction
Clearance of airway secretions
Bronchodilators
Reduce viscous sputum
Antibiotics for infection
```
436
What pharmacologic considerations should be made on patients with CP taking anti seizure meds?
Avoid acute withdrawal
Hepatic enzyme induction
Lethargy/sedation
437
Why are inhalation inductions prolonged in children with CF?
Large FRC, small tidal volumes and V/Q mismatch
438
What drugs should be avoided in patients with CF?
Anticholinergics, dry up even more, thicker secretions
439
What is cerebral palsy?
A collective term for a variety non-progressive condition resulting from an insult early in life or lesion/anomalies of the brain
440
What neurologic deficits to patients with CP have?
Varying degrees of developmental delays and varying degrees of muscular function (spastic to quadriplegia)
441
How does the sickled cell cause damage?
The distorted shape of the RBC leads to occlusion of the vessel causing infarctions in the lungs, bones and brain
442
What types of surgeries are common in patients with CP?
Orthopedic corrective procedures
Dental restoration
Anti reflux operations
443
What pharmacologic considerations should be made on patients with CP taking anti seizure meds?
Avoid acute withdrawal
Hepatic enzyme induction
Lethargy/section
444
What are important anesthetic considerations for patients with CP?
Aspiration risk --> RSI
Increased secretions
anti seizure meds may make child resistant to NMBA
Contractures make positioning difficult
445
What globulin chain is altered in sickle cell anemia?
A beta is replaced by Hgb S
446
What occurs when Hgb S becomes acidotic?
Hgb S undergoes a conformation change exposing a hydrophobic region of the molecule which will polymerize with other Hgb S molecules to form intracellular strands resulting in a sickle shape
447
How does Hgb S affect the RBC?
Oxidative damage, deformation and shortened life span
448
How does the sickled cell cause damage?
The distorted shape of the RBC leads to occlusion of the vessel causing infarctions in the lungs, bones and brain
449
What end organ damage occurs in sickle cell anemia?
Spleen, kidneys, lungs and brain
450
What damage occurs from vaso-occlusion in sickle cell anemia?
Episodic pain characterized by bone and joint pain, CVAs, retinopathy and osteomyelitis
451
Why do patients with MD require dextrose infusions while NPO?
Impairment of the beta oxidation of fat leading to ketosis, acidosis and hypoglycemia
452
What determines the severity of sickle cell anemia?
Depends on the percentage of HbS present and the presence or absence of other abnormal forms of Hgb
453
What is the difference between sickle cell trait and sickle cell disease?
```
Trait = heterozygous, sickling rare unless sever hypoxemia
Disease = homozygous more than 75% HgbS
```
454
What conditions are likely to cause sickle cell crisis?
Anemia, acidosis, HoTN, dehydration, septic or hypothermic
455
Why are children with sickle cell anemia often admitted the night before surgery?
Pre op transfusion Hgb greater than 10 and hydration with IVF for optimization
456
What is mitochondrial disease?
Defects in the protein alpha or beta chains or in enzyme activity, impairs ATP production
457
Why should the provider used less NMBA in patients with mitochondrial diseases?
Myopathies may have exaggerated sensitivity to neuromuscular blockade
458
Why shouldn't propofol infusions be used on patients with MD?
Propofol infusion syndrome
