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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