1.5.- Prácticas del Tema 1: Introducción
TEMA 2: EL CRECIMIENTO ECONÓMICO EN LA ERA PREINDUSTRIAL, SIGLOS X-XVIII
P.4. Lecturas complementarias
Greater saphenous vein – joins femoral vein near groin; runs medially No clamps on IVC → will tear
Left renal vein can be ligated near the IVC in emergencies because of collaterals (left gonadal vein, left
adrenal vein); right renal vein does not have these collaterals Dialysis access grafts
• Most common failure of A-V grafts for dialysis – venous obstruction secondary to intimal hyperplasia
• Cimino – radial artery to cephalic vein; wait 6 weeks to use → allows vein to mature
• Interposition graft (eg brachiocephalic loop graft) – wait 6 weeks to allow fibrous scar to form Acquired A-V fistula – usually secondary to trauma; can get peripheral arterial insufficiency, CHF,
aneurysm, limb-length discrepancy
• Most need repair → lateral venous suture; arterial side may need patch or bypass graft; try to place interposing tissue so it does not recur
Varicose veins
• Smoking, obesity, low activity
• Tx: sclerotherapy Venous ulcers
• Secondary to venous valve incompetence (90%)
• Ulceration occurs above and posterior to malleoli
• Ulcers < 3 cm often heal without surgery
• Tx: Unna boot compression cures 90%
• May need to ligate perforators or have vein stripping of greater saphenous vein (see below) Venous insufficiency
• Aching, swelling, night cramps, brawny edema, venous ulcers
• Edema – secondary to incompetent perforators and/or valves
• Elevation brings relief
• Tx: leg wraps, ambulation with avoidance of long standing
• Greater saphenous vein stripping (for saphenofemoral valve incompetence) or removal of perforators (if just perforator valves are incompetent; stab avulsion technique) for severe symptoms or recurrent ulceration despite medical Tx
Superficial thrombophlebitis – nonbacterial inflammation
• Tx: NSAIDs, warm packs, ambulation
Suppurative thrombophlebitis – pus fills vein; fever, ↑ WBCs, erythema, fluctuance; usually associated with infection following a peripheral IV
• Tx: resect entire vein
Migrating thrombophlebitis – pancreatic CA
Normal venous Doppler ultrasound – augmentation of flow with distal compression or release of proximal compression
Sequential compression devices (SCDs) – help prevent blood clots by ↓ venous stasis and ↑ tPA release
Deep venous thrombosis (DVT)
• Most common in calf
• Pain, tenderness, calf swelling
• Left leg 2× more involved than right (longer left iliac vein compressed by right iliac artery)
• Risk factors: Virchow’s triad → venous stasis, hypercoagulability, venous wall injury
• Calf DVT – minimal swelling
• Femoral DVT – ankle and calf swelling
• Iliofemoral DVT – leg swelling
• Phlegmasia alba dolens – tenderness, pallor (whiteness), edema
• Tx: heparin
• Phlegmasia cerulea dolens – tenderness, cyanosis (blueness), massive edema
• Tx: heparin; rarely need surgery
• DVT Tx: heparin, Coumadin
• IVC filter indications – contraindication to anticoagulation; PE while on Coumadin, free-floating ileofemoral thrombi; after pulmonary embolectomy
• Pulmonary embolism with filter in place – comes from ovarian veins, inferior vena cava superior to filter, or from upper extremity via the superior vena cava
Venous thrombosis with central line – pull out central line if not needed, then heparin; can try to treat with systemic heparin or TPA down line if the access site is important
LYMPHATICS
Do not contain a basement membrane
Not found in bone, muscle, tendon, cartilage, brain, or cornea Deep lymphatics have valves
Lymphedema
• Occurs when lymphatics are obstructed, too few in number, or nonfunctional
• Leads to woody edema secondary to fibrosis in subcutaneous tissue – toes, feet, ankle, leg
• Cellulitis and lymphangitis secondary to minor trauma are big problems
• Strep most common infection
• Congenital lymphedema L > R
• Tx: leg elevation, compression, antibiotics for infection Lymphangiosarcoma
• Raised blue/red coloring; early metastases to lung
• Stewart–Treves syndrome – lymphangiosarcoma associated with breast axillary dissection and chronic lymphedema
Lymphocele following surgery
• Usually after dissection in the groin (eg after femoral to popliteal bypass)
• Leakage of clear fluid
• Tx: percutaneous drainage (can try a couple of times); resection if that fails
• Can inject isosulfan blue dye into foot to identify the lymphatic channels supplying the lymphocele if having trouble locating
CHAPTER 28. GASTROINTESTINAL HORMONES
Gastrin – produced by G cells in stomach antrum
• Secretion stimulated by amino acids, vagal input (acetylcholine), calcium, ETOH, antral distention, pH > 3.0
• Secretion inhibited by pH < 3.0, somatostatin, secretin, CCK
• Target cells – parietal cells and chief cells
• Response – ↑ HCl, intrinsic factor, and pepsinogen secretion
• Omeprazole blocks H/K ATPase of parietal cell (final pathway for H+ release) Somatostatin – mainly produced by D (somatostatin) cells in stomach antrum
• Secretion stimulated by acid in duodenum
• Target cells – many; is the great inhibitor
• Response – inhibits gastrin and HCl release; inhibits release of insulin, glucagon, secretin, and motilin; ↓ pancreatic and biliary output
• Octreotide (somatostatin analogue) – can be used to ↓ pancreatic fistula output CCK – produced by I cells of duodenum
• Secretion stimulated by amino acids and fatty acid chains
• Response – gallbladder contraction, relaxation of sphincter of Oddi, ↑ pancreatic enzyme secretion Secretin – produced by S cells of duodenum
• Secretion stimulated by fat, bile, pH < 4.0
• Secretion inhibited by pH > 4.0, gastrin
• Response – ↑ pancreatic HCO3− release, inhibits gastrin release (this is reversed in patients with gastrinoma), and inhibits HCl release
• High pancreatic duct output – ↑ HCO3−, ↓ Cl−
• Slow pancreatic duct output – ↑ Cl−, ↓ HCO3− (carbonic anhydrase in duct exchanges HCO3− for Cl−)
Vasoactive intestinal peptide – produced by cells in gut and pancreas
• Secretion stimulated by fat, acetylcholine
• Response – ↑ intestinal secretion (water and electrolytes) and motility Glucagon – mainly released by alpha cells of pancreas
• Secretion stimulated by ↓ glucose, ↑ amino acids, acetylcholine
• Secretion inhibited by ↑ glucose, ↑ insulin, somatostatin
• Response – glycogenolysis, gluconeogenesis, lipolysis, ketogenesis, ↓ gastric acid secretion, ↓ gastrointestinal motility, relaxes sphincter of Oddi
Insulin – released by beta cells of the pancreas
• Secretion stimulated by glucose, glucagons, CCK
• Secretion inhibited by somatostatin
• Response – cellular glucose uptake; promotes protein synthesis
Pancreatic polypeptide – secreted by islet cells in pancreas
• Secretion stimulated by food, vagal stimulation, other GI hormones
• Response – ↓ pancreatic and gallbladder secretion Motilin – released by intestinal cells of gut
• Secretion stimulated by duodenal acid, food, vagus input
• Secretion inhibited by somatostatin, secretin, pancreatic polypeptide, duodenal fat
• Response – ↑ intestinal motility (small bowel; phase III peristalsis) → erythromycin acts on this receptor
Bombesin (gastrin-releasing peptide) – ↑ intestinal motor activity, ↑ pancreatic enzyme secretion, ↑ gastric acid secretion
Peptide YY – released from terminal ileum following a fatty meal → inhibits acid secretion and stomach contraction; inhibits gallbladder contraction and pancreatic secretion
Anorexia – mediated by hypothalamus Bowel recovery
• Small bowel 24 hours
• Stomach 48 hours
• Large bowel 3–5 days
CHAPTER 29. ESOPHAGUS
ANATOMY AND PHYSIOLOGY
Mucosa (squamous epithelium), submucosa, and muscularis propria (longitudinal muscle layer); no serosa
Upper ⅓ esophagus – striated muscle
Middle ⅓ and lower ⅓ esophagus – smooth muscle
Vessels directly off the aorta are the major blood supply to the thoracic esophagus
Cervical esophagus – supplied by inferior thyroid artery
Abdominal esophagus – supplied by left gastric and inferior phrenic arteries Venous drainage – hemi-azygous and azygous veins in chest
Lymphatics – upper ⅔ drains cephalad, lower ⅓ caudad
Right vagus nerve – travels on posterior portion of stomach as it exits chest; becomes celiac plexus;
also has the criminal nerve of Grassi → can cause persistently high acid levels postoperatively if left undivided after vagotomy
Left vagus nerve – travels on anterior portion of stomach; goes to liver and biliary tree
Thoracic duct – travels from right to left at T4–5 as it ascends mediastinum; inserts into left subclavian vein
Upper esophageal sphincter (UES; 15 cm from incisors) – is the cricopharyngeus muscle (circular muscle, prevents air swallowing); recurrent laryngeal nerve innervation
• Normal UES pressure at rest: 60 mm Hg
• Normal UES pressure with food bolus: 15 mm Hg
• Cricopharyngeus muscle – most common site of esophageal perforation (usually occurs with EGD)
• Aspiration with brainstem stroke – failure of cricopharyngeus to relax
Lower esophageal sphincter (40 cm from incisors) – relaxation mediated by inhibitory neurons;
normally contracted at resting state (prevents reflux); is an anatomic zone of high pressure, not an anatomic sphincter
• Normal LES pressure at rest: 15 mm Hg
• Normal LES pressure with food bolus: 0 mm Hg Anatomic areas of esophageal narrowing
• Cricopharyngeus muscle
• Compression by the left mainstem bronchus and aortic arch
• Diaphragm
Swallowing stages – CNS initiates swallow
• Primary peristalsis – occurs with food bolus and swallow initiation
• Secondary peristalsis – occurs with incomplete emptying and esophageal distention; propagating waves
• Tertiary peristalsis – non-propagating, non-peristalsing (dysfunctional)
• UES and LES are normally contracted between meals
Swallowing mechanism – soft palate occludes nasopharynx, larynx rises and airway opening is blocked by epiglottis, cricopharyngeus relaxes, pharyngeal contraction moves food into esophagus; LES
relaxes soon after initiation of swallow (vagus mediated)
Surgical approach
• Cervical esophagus – left
• Upper ⅔ thoracic – right (avoids the aorta)
• Lower ⅓ thoracic – left (left-sided course in this region) Hiccoughs
• Causes – gastric distention, temperature changes, ETOH, tobacco
• Reflex arc – vagus, phrenic, sympathetic chain T6–12 Esophageal dysfunction
• Primary – achalasia, diffuse esophageal spasm, nutcracker esophagus
• Secondary – GERD (most common), scleroderma
Endoscopy – best test for heartburn (can visualize esophagitis)
Barium swallow – best test for dysphagia or odynophagia (better at picking up masses) Meat impaction – Dx and Tx: endoscopy