LEC 3-T Exam.txt
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1. ★ Know the location of the organs of gastrointestinal tract (intra or retroperitoneal)
- Transverse Colon
- Small intestine
- Rectum (Titi: colon)
- Kidneys (urinary, not gastrointestinal)
2.1 ★ Gallbladder functions?
- Store bile that enters it by way of hepatic and cystic ducts.
- Concentrate held bile five- to ten-fold.
- Eject bile into duodenum when digestion occurs in the stomach and intestines.
- Bile salts and lecithin, components of bile, facilitate the emulsification of fats for digestion.
2.2 ★ What is the surgical removal of gallbladder.
2.3 ★ What is Cholecystitis?
- Gall Stones or infection…
3. ★ What gallbladder hormone stimulates bile release?
- CCK (cholecystokinin) and Secretin
4. ★ How does bile facilitate fat emulsification?
- It, and lecithin (both phospholipids), mechanically break up large drops into smaller ones by forming micelles around smaller drops. These phospholipids are arranged so that their water-loving heads are outward, which also makes the smaller fat droplets water soluble.
5. ★ Know the steps of starch digestion.
- Starch (polysaccharide or carbohydrate) digestion begins to some degree in the mouth where it is mixed with saliva containing amylase, which can hydrolyze them into disaccharides. But the time available to salivary amylase before it is destroyed by stomach acids and enzymes make this function relatively unimportant.
- Therefore, it is mostly pancreatic amylase that completes the hydrolysis to disaccharides in the intestine.
- There, “brush border” enzymes, sucrase, lactase, and maltase bond to the disaccharides and further hydrolyze them into monosaccharaides (mostly glucose)where they can be immediately absorbed, e.g. contact digestion.
6. ★ Know the steps of protein digestion.
- Proteins, large molecules of amino acids are
- Hydrolyzed into intermediate compounds called Peptides & Proteoses by an army of proteases:
- Pepsin in gastric juice.
- Trypsin & Chymotrypsin in pancreatic juice.
- Peptidases from the intestinal brush border
- Finally, more unique proteases - depending on the type of peptide bond to be broken will further hydrolyze these intermediate compounds into amino acids.
- As with sodium and glucose, these are absorbed into the blood via sodium cotransport into the intestinal epithelium and then passively into the capillaries.
7. ★ Know the steps of carbohydrate digestion and the final products.
- Starting with polysaccharides which contain many saccharide groups (C6H10O5) we have:Disaccharides:Finally Monosaccharides:
8. ★ Know how the glucose is absorbed into intestinal epithelial cells.
- Sodium (Na+) cotransport.
9. ★ Know the histology of alimentary canal and be able to list the layers.
- Mucosa Mucus, enzymes & ectopic hormones
- Sub Mucosa Blood & Lymphatic vessels, with nerves in Connective tissue
- Thick layer of Muscularis consisting of 2 layers
- Inner Circular, which becomes a sphincter in some locations, and serves both Peristalsis and Segmentation
- Outer Longitudinal
10. ★ Know the phases of gastric (stomach) secretion.
- Cephalic triggered by sight, smell, taste or thought. Vagal nerve impulses also stimulate endocrine G cells in gastric mucosa to secrete gastrin, which stimulates gastric secretion.
- Gastric stretch reflexes in stomach release 2/3 of the gastric juice. Products of protein digestion that have reached the pyloric portion of the stomach stimulate its mucosa to secrete gastrin where after circulating to the gastric glands greatly accelerates the secretion of gastric juice, high in pepsinogen and HCl.
- Intestinal has both a brief excitatory phase, and an inhibitory phase for gastric secretions. Chyme with fats, carbohydrates and acid in the duodenum inhibit gastric secretions via GIP, secretin, and CCK. Also, the enterogastric reflex, which reduces gastric peristalsis, may also inhibit gastric secretions.
Gastrin: Source & Action:
Formed by gastric mucosa in presence of partially digested proteins, when stimulated by the vagus nerve, or when the stomach is stretched.
Stimulate secretion of gastric juice rich in pepsin and hydrochloric acid.
Secretin: Source & Action:
Formed by intestinal mucosa in presence of glucose, fats, and perhaps other nutrients.
Inhibits gastric secretion; stimulates secretion of pancreatic juice low in enzymes and high in alkalinity (bicarbonate); stimulates ejection of bile by the gallbladder.
Gastric Inhibitory Peptide (GIP): Source & Action:
Formed by intestinal mucosa in presence of glucose, fats, and perhaps other nutrients.
Inhibits gastric secretion and motility; enhances insulin secretion by pancreas.
Cholecystokinin (CCK): Source & Action:
Formed by intestinal mucosa in presence of fats, partially digested proteins, and acids.
Stimulates ejection of bile from gallbladder and secretion of pancreatic juice high in enzymes; opposes the action of gastrin, raising the pH of gastric juice.
11. ★ Know the unique features of the mucosa of stomach; 5 basic cell types; what do they produce.
: mucus & HCl
- Cardius portion
- Parietal HCl (needed to activate pepsinogen) and Intrinsic Factor, that binds with vitamin B12 to protect it from digestive juices until it reaches the SI.
- Mother & Stem CellsBOOK:
- Mucus – digestive enzymes and HCl
- Chief – enzymes of gastric juice
- Parietal – HCl & Intrinsic factor
- Endocrine – ghrelin (GHRL) a hormone that stimulates the hypothalamus to secret growth hormone and increase appetite, as well as gastrin.
12. ★ Know the anatomical parts of the stomach.
- Cardius – near heart and esophagus
- Fundus – dome shape to the left of esophageal opening
- Body – middle
- Pylorus – near the opening to the duodenum.
13. ★ Be able to tell what the condition of heartburn (acid reflux) and hiatal hernia represent, the factors which can aggravate the conditions.
- Heartburn is the backward flow of stomach acid up into the esophagus. Hiatal Hernia is a weakening of the LES (lower esophageal sphincter) such that part or even all of the stomach can protrude into the thoracic cavity. This condition also causes GERD. Causes are:
- Spicy Food
14. ★ Know the anatomical parts of the small intestine.
- Duodenum, 25 cm (10”)
- Jejunum, 2.5 m (8’) – primary site of absorption & digestion
- Ileum, 3.5 m (12’) – absorbs vitamins & electrolytes
15. ★ Know the anatomical parts of the large intestine.
- Cecum, 5-8 cm 0 blind pouch
- Ascending Colon
- Hepatic or Right Colic Flexure
- Transverse Colon
- Splenic or Left Colic Flexure
- Descending Colon
- Sigmoid Colon
- Rectum, 7-8”
- Anal Canal, 1”, with 2 sphincters
16. ★ Know the lobes of the liver.
- Caudate (posterior next to inferior vena cava)
- Quadrate (anterior, next to gallbladder)
17. ★ Know the components of the portal triad.
- Hepatic Artery
- Hepatic Portal vein
- Bile Duct
18. ★ Know the circulation of blood in the liver.
- Blood flows FROM portal triad TO central vein.
19. ★ Know how the bile flows (the ducts).
- Bile flows from hepatocytes in the liver lobule through Bile Canaliculi to the Bile Ducts in the Portal Triad to:
- Left & Right hepatic Ducts to
- Common hepatic Duct where it meets bile from delivered from or to) the
- Cystic Duct, then joins the
- Common Bile Duct, which joins the Pancreatic Duct the form the
- Hepatopancreatic Ampulla before emptying into the duodenum through the
- Major Duodenal Papilla.
20. ★ The role of enzymes in the process of digestion.
- These are Inorganic catalysts which speed up the digestion process.
21. ★ Know the exocrine functions of the pancreas (the components of pancreatic juice)
- Digestive enzymes are secreted by Acinar cells in the form of zymogens or inactive enzymes and contain:
Duct cells secrete a watery, bicarbonate-rich solution to neutralize the acidity of chime.
- Proteases for proteins
- Lipases (for fat digestion)
- Amylases (pancreatic for carbohydrates)
22.1 ★ Hiatal Hernia:
- Weakening or stretching of the LES (lower esophageal sphincter), which is intrinsic to the esophageal hiatus through the diaphragm. This can allow part or all of the stomach up into the thoracic cavity.
22.2 ★ Gastric Ulcer:
- Erosion of the stomach wall. Most ulcers are caused by an infection with spiral-shaped bacterium Helicobacter pylori, NOT excess stomach acid.
22.3 ★ Hemorrhoids:
- Varicose veins of the anus.
22.4 ★ Constipation:
- Excess water absorption leading to dry packed feces.
22.5 ★ Diarrhea:
- Decreased water and electrolyte absorption in the SI resulting from increased motility.
22.6 ★ Peritonitis:
- Inflammation of the covering of the organs of the abdominal cavity.
23. ★ Know the functions of the urinary system.
- Primary – regulation of
- Blood Volume, i.e. BP
- Chemical makeup of blood
- Metabolism of Vitamin D
- Production of Renin, which is released by JG (Juxtaglomerular cells) by detection of the increased reabsorption of Na+ & Cl-, resulting from decreased arterial BP. Renin sets in motion the release of a vasoconstrictor to raise BP.
- Production of EPO (erythropoietin) to stimulate RBC generation.
- Gluconeogenesis from amino acids and possibly fatty acids. Though primarily a liver process, it does occur in the cortex of the kidneys.
24.1 ★ Be able to trace urine flow.
- Renal papilla of medullary pyramid.
- Minor Calyces
- Major Calyces
- Renal Pelvis.
24.2 ★ Normal urine contents.
- 95% water
- 5% solutes
- Uric acid from nucleic acid breakdown.
- Creatinine from skeletal muscles
- Urea from protein catabolism
- Ions: Na+, K+, Cl-, Ca, Mg, and HCO3-
25.1 ★ Know the blood supply to the kidneys.
- Abdominal aorta
- Renal arteries
- (5) Segmental arteries
- Lobar and then Interlobar arteries
- Arcuate arteries, which arch over the base of the renal pyramids
- Interlobar radiate arteries to Renal Cortex
- Afferent arterioles (larger lumen than efferent)
- Efferent arterioles
- Peritubular capillaries or vasa recta
- Interlobular veins, etc. (Note: there are no "lobar" or "segmental" veins)
25.2 ★ What is a “Renal Corpuscle”?
- Bowman Capsule plus the Glomerulus
26. ★ Know the role of the nephron as the functional unit of kidney.
- It is THE site of:
- It is composed of:
- The Renal Corpuscle (Bowman Capsule & Glomerulus)
- PCT (Proximal Convoluted Tubule)
- Loop of Henle
- DCT (Distal Convoluted Tubule)
- CD (Collecting Ducts)
27. ★ Know the processes, which result in the formation of urine.
28. ★ Know the mechanisms and pressures involved in the process of filtration.
- The primary driving force behind filtration is Hydrostatic pressure specifically of the Glomerulus. But the Glomerular osmotic Pressure and Capsular (Bowman) Hydrostatic Pressure have an impact on the Effective Filtration Pressure
- The smaller lumen of the Efferent Arteriole (compare to the Afferent Arteriole boosts the pressure in the Glomerulus to about 80 mm Hg.
29. ★ Know the processes of reabsorption and secretion; the mechanisms involved; role of the sodium in tubular reabsorption.
- Major portion of water & electrolytes and (normally) all nutrients are reabsorbed in the PCT.
- Na+ is reabsorbed via active transport (requires ATP). It has the following effects:
- Creates an electrical gradient, which passively pulls negative ions such as chloride (Cl-) and phosphate (PO4-3)
- As the ions concentration increases in the Interstitial fluid and peritubular blood, an Osmotic gradient is also created, which creates an obligatory reabsorption of water.
- Along with the active transport of Na+, glucose and amino acids bind to the Na+ and are reabsorbed via sodium cotransport
30. ★ Know the process of transport maximum (saturation) in the reabsorption of a substance.
- The ability to move glucose back into the peritubular blood from the nephron is limited by the number of cotransport carriers; in this case sodium. This limit is the transport maximum.
- It is the highest concentration of a substance before it cannot be reabsorbed due to limited protein carriers and it appears in the blood (should be urine).
- Normal blood glucose is 70-110 mg/Dl. Tmax or saturation is 180 per Titi, but about 300 per book.
31.1 ★ Hypoalbuminemia:
- Albumin, the most abundant plasma protein, never normally leaves blood plasma. But with Hypoalbuminemia – holes in damaged glomeruli, it is secreted in the urine and results in low oncotic pressure (protein osmosis gradient) resulting in widespread edema because of water leaving the blood stream.
31.2 ★ Nephritis:
- Is a general term referring to kidney disease; especially inflammatory conditions. More specifically is Pyelonephritis (pelvis nephritis), or inflammation of the renal pelvis.
31.3 ★ Renal failure:
- Cannot eliminate UREA, a nitrogen–containing waste product from the catabolism of proteins. Diagnosed via high BUN (blood urea nitrogen) Renal failure can be acute or chronic.
31.4 ★ Urethritis:
- An inflammation of the urethra that is commonly the result of a bacterial infection, often gonorrhea. Nongonococcal infections are usually Chlamydia. Males suffer more often than females.
31.41 ★ Uremia:
- Titi: “Toxins of meat digestion”. Book indicates that it is essentially high UREA in the blood.
31.5 ★ Lithotripsy:
- Ultrasonic waves via “Lithotriptor” to dissolve kidney stones.
31.6 ★ Acute glomerulonephritis:
- the most common form of kidney disease. It may be caused by a delayed immune response to a streptococcal infection – the same mechanism that causes damage to heart valves in rheumatic heart disease. For this reason, it is sometimes called postinfectious glomerulonephritis.
31.7 ★ Cystitis:
- Infection of the urinary bladder. (It is a “cyst” like the gallbladder.)
31.8 ★ Renal calculi:
- Or Kidney Stones, these are crystallized mineral chunks that develop in the renal pelvis or calyces.
32.1 ★ Proteinuria:
- Presence of proteins (especially albumin) in the urine. It abnormally leaves the blood through damage glomeruli and is not reabsorbed by the kidney tubules.
32.3 ★ Oliguria:
- Reduced urine formation. Titi: less than 1 liter/day
32.4 ★ Glycosuria:
- Glucose in the urine; a sign of diabetes mellitus.
32.5 ★ Incontinence:
- Involuntary voiding of urine. Usually from loss of nervous control (stroke or accident), e.g. neurogenic bladder.
32.6 ★ Anuria:
- NO urine. From dehydration, renal failure or obstruction.
32.7 ★ Ketonuria:
- Medical condition in which ketone bodies are present in the urine. It is seen in conditions in which the body produces excess ketones as an alternative source of energy. It is seen during starvation or more commonly in type I diabetes mellitus. Production of ketone bodies is a normal response to a shortage of glucose, meant to provide an alternate source of fuel from fatty acid.
32.8 ★ Hematuria:
- Blood in urine – likely cause
- It may be idiopathic and/or benign, or it can be a sign that there is a kidney stone or a tumor in the urinary tract (kidneys, ureters, urinary bladder, prostate, and urethra), ranging from trivial to lethal. If white blood cells are found in addition to red blood cells, then it is a signal of urinary tract infection.
32.9 ★ Polyuria:
- Unusually large amounts (or frequent) urination.
32.10 ★ Dysuria:
- Painful urination, usually indicative of an infection
33. ★ Know the characteristics of mucosa of urinary bladder.
- The inner-most layer of the bladder is the mucosa, which is composed of transitional epithelial cells, which are extensible. In addition to this capability, the mucosa is formed into Rugae, or folds, that give it further ability to stretch. There is a submucosal layer as well.
- The 2nd layer is a thick Muscularis of smooth muscle with bundles running in all directions. It is often called detrusor muscle.
- The 3rd layer is an adventitia of connective tissue.
- the outermost layer is the serosa, a retroperitoneum, lying under the parietal peritoneum.
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