Hematology, GI, Renal and Peds Flashcards Preview

Pathophysiology II > Hematology, GI, Renal and Peds > Flashcards

Flashcards in Hematology, GI, Renal and Peds Deck (458):
1

What are the two components of blood volume?

Plasma 55%
Cellular components 45%

2

What are the components of the Plasma?

91% water
7% blood proteins
2% Nutrients, Hormones and Electrolytes

3

What are the cellular components in blood volume?

Buffy coat & RBCs

4

What are the two components that make up the buffy coat of the blood?

WBC and Platelets

5

What causes erythropoietin to be released from the kidneys?

Hypoxia, reduced O2 levels in blood

6

What is the function of erythropoietin once released by the kidneys?

Stimulates red bone marrow to produce more RBCs

7

What is the name for immature erythrocytes in the blood stream?

Reticulocytes

8

What is the lifespan for a RBC?

120 days

9

What cellular structures does a erythrocyte lack?

Nuclei, mitochondria and ER

10

How do erythrocytes create ATP?

Cytoplasmic enzymes (anaerobic glucose metabolism)

11

What is the normal range of Hgb in adult males?

13.5-17.5g/dL

12

What is the normal range of Hgb for adult females?

12-16g/dL

13

What can indicate if enough red blood cells are being produced in the bone marrow?

Reticulocyte count

14

How would the provider calculate the reticulocyte index?

(Ret% x Hct)/(0.45)

15

What vitamins are required for Hgb synthesis?

B12, B6, B2, E, C, folic acid, pantothenic acid and niacin
B12 DNA synthesis, maturation
Folate DNA/RNA synthesis, maturation

16

How is Hgb formed?

Fe released into erythroblast mitochondria

17

What removes RBS from circulation?

Macrophages (spleen), broken down

18

What conditions shift the oxyhemoglobin dissociation curve to the left?

Decrease temperature, PaCO2, 2,3 DPG and increased pH
More likely to hang on to O2

19

What conditions shift the oxyhemoglobin dissociation curve to the right?

Increased temperature, PaCO2, 2,3 DPG and decreased pH
More likely to release O2 at the site

20

What is anemia?

It is a decrease in O2 carrying capacity that can lead to tissue hypoxia

21

What are common symptoms of anemia?

Fatigue, weakness, dyspnea and pallor

22

What are the causes of anemia?

Impaired erythrocyte production
Actue/chronic blood loss
Increased erythrocyte destruction

23

When does WHO suggest the diagnosis of anemia?

Non pregnant females Hgb less than 11
Males less than 13

24

Why might a patients spleen be enlarged from anemia?

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