Week 2 Flashcards

(117 cards)

1
Q

Describe Type 1 Diabetes

A
  • Autoimmune destruction of Beta cells
    • No insulin made
  • Insulin injections required or islet transplant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe Type II diabetes

A
  • Beta cell exhuastion because of hyperglycemia and more insulin is required to produce same effect
  • Decreased insulin (relative to high glucose)
  • hyperglycemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What can occur when blood glucose are chronically too high?

A
  • Blindness
  • Limb amputations
  • Kidney disease
  • Increases risk of heart disease
  • Neuropathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is glucose homeostasis?

A
  • ~5.5 mM and very stable
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Function of Glucagon

A
  • Secretion by alpha cells
    • stimulated by low insulin
  • Cause glucose secretion and raises blood sugar
  • Anti-hypoglycemic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Function of Insulin

A
  • Secreted by Beta cells
    • high insulin inhibits alpha cells
  • Causes glucose clearance and removal from blood and stored into tissues
    • no insulin = no glucose clearance = hyperglycemia
  • Anti-hyperglycemic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Function of Somatostatin

A
  • Secreted by Delta cells
  • Regulates both glucagon and insulin levels by preventing their secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How are blood insulin levels measured?

A
  • insulin and C peptide are secreted 1:1
  • C peptide isnt internalized as quickly so it stays in the blood longer and can be measured
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the life threatening acute problems in glucose homeostasis and metabolism that occur in type I diabetes?

A
  • Ketoacidosis - unopposed glucagon because there is no insulin
  • Hypoglycemia - too much insulin injected
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How are insulin and glucagon levels altered by both carbohydrate and protein meals?

A
  • [Insulin] changes by a lot (10x)
  • glucagon only changes a little
    • release during a high protein meal is stimulated by arginine

Ratio of insulin: glucagon is more important than the concerations themselves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does insulin affect fat cells?

A
  • insulin effects in adipocytes is much larger than muscle
    • have much fewer GLUT4 transporters on membrane
    • lower basal level and stimulation causes a huge increase when compared to muscle
  • very low levels of insulin will still inhibit lipolysis, so other hormones/stimuli are required to mobilize energy stored in fat during a fast
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the major site of glucose disposal after a meal?

A
  1. Muscle ~50g
  2. Liver ~17g
  3. Brain ~15g
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does insulin affect muscle?

A
  • High insulin increases glucose transport 4x
    • rate limiting but esstential for efficient glucose clearance from blood
    • exercise stimulates GLUT4 receptors to cell surface to increase blood clearance
  • Stimulates glycogen synthesis and inhibits glycogen breakdown
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Where is GLUT1 found and its affinity?

A
  • Pancreatic alpha cells and most other tissues
  • High affinity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Where is GLUT2 found and what is its affinity?

A
  • Pancreatic beta cells, liver, intestine
  • low affinity
    • allow glucose to flow down its concentration gradient
  • insulin sensing
    • small changes in [glucose] are amplified due to low affinity of GLUT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Where is GLUT3 found and what is it affinity?

A
  • Brain and placenta
  • VERY high affinity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Where is GLUT4 found and what is its affinity?

A
  • skeletal muscle, fat, heart
  • high affinity
  • insulin regulated
    • glucose is rate-limited by the total # of GLUT4 transporters which increases with insulin and exercise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe high affinity GLUTs

A
  • Nearly saturated at basal level
    • no change in glucose uptake under normal glucose fluctations unless total # of GLUTs on surface changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe low affinity GLUTs

A
  • Not saturated at normal blood glucose levels
  • glucose uptake changes over all ranges of [glucose]
    • is how glucose level sensed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What occurs to beta cells secreting insulin during fasting?

A
  • low (basal) glucose _<_5.5 mM
  • ATP/ADP ratio is low
    • ATP sensitive K channel activated (by low ATP)
    • inhibits Ca channel -> causes low (inhibited) insulin secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What occurs to beta cells secreting insulin at the fed state?

A
  • High Glucose levels >5.5mM
  • ATP/ADP ratio increases
    • ATP sensitive K channel inhibited by ATP
    • Activates Ca channel
  • Insulin release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How are alpha cells glucagon secretion altered?

A
  • GLUT1 has high affinity so changes in [glucose] on ATP/ADp are muted
    • receptors are saturated at basal [glucose] cant detect changes in glucose unless # of GLUTs change
  • Insulin regulates glucagon
    • low insulin ->stimulate alpha cells
    • high insulin-> inhibits alpha cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What do sulfoylureas do?

A
  • Oral hypoglycemic agent that inhibits Katp channels
  • Causes insulin to be secreted
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What do incretins do?

A
  • primes the vesicles to responed to increased Ca2+
  • results in insulin to be secreted
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What does metformin do?
* Activates AMPK in muscle (mimics exercise) * increases insulin sensitivity in muscle
26
What are the roles of cholesterol?
* make membranes more rigid * precursor to bile salts/acids * Precursors to hormones * progesterone * estrogens * testoterone * cortisol * aldosterone * Precursor to Vit. D
27
How is cholesterol carried in the blood?
* Cholesterol ester * combination of cholesterol and either Fatty Acyl-CoA or Lecithin * Concentration in blood 150-240 mg/dl, 2x glucose
28
How does Acetyl-CoA get into the cell to synthesize cholesterol?
* •Pyruvate \> OAA \> (add acetyl-CoA) \> citrate \> citrate transporter crosses inner/outer mito membrane to cytosol \> citrate \> (dumps acetyl-CoA) \> OAA \> malate \> (gives off NADPH) \> pyruvate \> crosses membrane back to matrix
29
What is special about cholesterol synthesis?
* humans synthesize a little less than half of cholesterol we have from Acetyl-CoA rest comes from diet * eat more, make less * eat less, make more * Sources of Acetyl-CoA: FA, carbs -\>pyruvate * NADPH made in last step will be used for HMG-CoA reductase
30
What is the first step of cholesterol biosynthesis?
* Acetoacteyl CoA + Acetyl-CoA -\> HMG-CoA * enzyme: HMG-CoA synthase * requires H2O
31
What is the second step of cholesterol?
* HMG-CoA -\> mevalonate * enzyme: HMG-CoA reductase * Requires: 2 NADPH + 2H+ * rate limiting step * statins work at this step
32
What are the types of regulation of HMG-CoA reductase?
* Feedback inhibtion * higher cholesterol, you make less * less cholesterol, you make more * Phosphorylation/dephosphorylation of HMG-CoA reductase * Phosphorylation (AMPK) -\> inactive * Desphorylation (by HMGRP) -\> more active * Control of gene expression (Sterol Receptor Element Binding Protein) * during normal levels SREBP is anchored in ER membrane. At low sterol levels, SREBP is cleaved and it enters nucleus and increases synthesis of HMG-CoA reductase * Rate of enzyme degradation
33
How do statins work?
* Lipitor and Mevacor are competitive inhibitors of HMG-CoA reductase * Side effects * can lead to decreased CoQ10 and can lead myopathy and rhabdomyolysis
34
Outline the conversion of mevalonate to cholesterol
* C5 to C10 to C15. Two C15s condense to C30 (squalene) to C27 (cholesterol) * 19+ steps between squalene to cholesterol
35
What is the major metabolic fate of cholesterol? How is it used?
* Conversion by liver cytochrom P450 to bile acids * stored in gall bladder * cholesterol still present in bile acids and can turn to gall stones * Transported to small intestine * **function**: solubilize lipids * 90% of bile salts are reabsorbed and recycled by colon
36
How are bile acids made in bile salts?
* CO2- is switched for SO3- * Salt conjugates make better solubilizing agents than acids * pka of conjugates 1-4 * pH of duedenum 3-5
37
What is cholestyramine?
* Not absorbed by the body * ionic binding ((-) bile acids bine to (+)-nitrogen on cholestyramine) * Removes cholestyramine and cholestrol from the body * more cholesterol is converted to bile salts, lowering cholesterol levels * Used to be main cholesterol drug before statins but causes gas and diarreha and makes people uncomfortable
38
Name the different types of pancreas regions and cells
* Exocrine * Pancreatic acinar cells * centroacinar cells * acinar vascular system * Endocrine * Islets of Langerhans * Insuloacinar portal system
39
Describe Pancreatic Acinar cells
* produce, store and release digestive enzmes * zymogen granules * each granule has a different combo of enzymes depending on diet * cell makes trypsin inhibitor to protect itself * release of enzymes drive by hormones and parasympathetic nerves
40
Describe Centroacinar cells
* Modified intercalacted duct cells * Located with the acinus * Produce bicarbonate - rich buffer * adjust acicic chime to optimal pH for pancreatic enzymes
41
Describe Islets of Langerhans
* scattered among exocrine secretory acini * principal cells * Alpha, Beta, and Delta cells * Minor cells * PP cell (F cell) * D-1 * EC cell
42
What do PP Cell (F cell) secrete?
* Pancreatic polypeptide * stimulates gastric chief cells * inhibits * bile secretion * intestinal motility * pancreatic enzymes * HCO3 secretion
43
What do D-1 cells secrete?
* Vasoactive intestinal peptide (VIP) * simliar to glucagon (hyperflycemia and glycogenolytic) * affects secretory activity and mitility in gut * stimulates pancreatic exocrine secretion
44
What do EC cells secrete in the pancreas?
* Secretin * locally stimulates HCO3- secretion * stimulates pancreatic enzyme secretion * Motilin * increases gastric and intestinal motility * Substance P * NT properties
45
How is there duel control of the secretion of pancreatic enzymes?
* peptides secreted by enteroendocrine cells (EC) in duodenum * peptide hormones synthesized in endocrin pancreas (islets of langerhans) * Stimulate secretion * VIP * Insulin * CCK * Inhibit secretion * Glucagon * PP * Somatostatin
46
What is the insuloacinar portal?
* Each islet is supplied by a network formed by afferent arterioles capillaries lined by fenestrated endothelial cells * islets puts all of its hormones in the insulacinar portal
47
What is the acinar vascular system?
* independent arterial system that supplies pancreatic acini
48
What are the major functions of the liver?
* Produce most circulating plasma proteins * albumin * lipoproteins * glycoproteins * store and convert several vitaminas and iron * involved in many metabolic pathways * degrades drugs and toxins * bile production (exocrine) * ability to modify structure of many hormones (endocrine)
49
What is the protal area?
* Hepatocytes are arranged in a hexagon shape, where three classic lobules join together * Portal area in the middle * Hepatic artery * portal vein * Interlobular bile duct * lymphatic vessels
50
What is the liver acinus (Acinus of Rappaport)?
* concept module of the hepatocytes arrangement based on blood flow * 3 poorly defind surrunding a distributing artery in center * Zone 1-3 * Provides best correlation between blood perfusion, metabolic and liver patholgy
51
Describe zone 3 in a hepatocyte
* Closest to central vein * most oxygen poor zone * first to show ischemic necrosis * first to show fat accumulation * Key glycolysis enzymes * key FA-synthesizing enzymes
52
Describe zone 1 in a hepatocyte
* Closest to portal triad * richest in oxygen, nutrients, and toxins * key glucose liberating enzymes * key FA oxidation enzymes * firs to show signs of morphological chnages after bile duct occlusion * in ischemia - last to die/first to regenerate
53
Describe the cellular contents of a hepatocyte
* lots of free ribosomes, rER and Golgi apparatus * some golgi near bile canaciculi * 2k mito * many endosomes, lysosomes, peroxisomes * Smooth ER * two domains * lateral (apical) * siusodial (basolateral)
54
What is the function of smooth ER in hepatocytes?
* important in detoxification * enzymes necessary for detox are in the sER membrane * sER highest in zone 3 * increases if more toxins present * detox inactivated by methylation, conjugation, or oxidation * detox can happen in peroisomes
55
Describe the lateral (apical) zone of the hepatocyte
* covered with microvilli * separated by elaborate intercellular spaces that form bile canaliculi that will eventually flow out of
56
Describe the sinusodial (basolateral) domain of hepatocytes
* microvilli project into space of Disse * increase surface area by a factor of 6 * facilitate exchange of material between hepatocyte and space of Disse
57
What are the two cell types that line the hepatic sinusoids?
* discontinuous endothelial cells * Kupffer's cells
58
Describe the purpose of hepatic sinusoids
* lie between hepatic plates * empty directly into central veins * hepatic portal veins and hepatic artery empties directly into sinusoids
59
What are Kupffer cells?
* differentiated phagocytic cell derived from monocytes * in hepatic sinusoids * phagocytosize blood-borne foreign paticulate matter and worn out RBCs
60
Describe the space of Disse
* site of exchange of materials and blood plasma between blood and hepatocytes * hepatocyte microvilli absorb nutrients, oxygen, toxins adn release thier metabolic products and endocrine secretions * serves as liver's lymphatic system (lymphatic drainage opposite of blood flow) * hepatic stallate cells
61
What are hepatic stallate cells (cells of Ito)?
* Store Vitamin A * in pathological conditions differentiate into myofibroblasts adn synthesize collagen, leading to liver fibrosis
62
What is the function of the gall bladder?
* concentration and store of bile between meals * release bile by contraction of muscularis in response to CCK from duodenum EC cells * regulation of hydrostatic pressure within biliary tract
63
Describe the mucosa of gall bladder
* simple columnar epithelium * apical microvilli * concentration of bile requires couped transport of salt and water * Na pump on lateral surface to facilitate h20 absorption from bile * typical lamina propria
64
Describe the muscularis layer of gall bladder
there is NO muscularis mucosae or submucosa muscularis in the gall bladder * Interwoven SM to contract complete * contraction trigged by dietary fat in duodenum and EC cells secrete CCK
65
Describe outer layer of the gall bladder
* Adventitia attaches gall bladder to liver * Serosa covers its free peritoneal surface
66
What is the gastro-esophageal junction just below the diaphragm?
cardiac orifice * this is where the stomach begins
67
What are the divisions of the stomach and what seperates them?
* Fundus * stomach aboce the cardiac orifice * Body * from cardiac orifice to Veing of Mayo * Antrum * from angular incisure (notch/indentation on lesser curve) to pyloric canal * where vein of mayo crosses stomach * Pylorus * canal and sphincter
68
How is a peptic ulcer disease treated?
* peptic ulcer more common in duodenum * surgical removal of acid forming portion of stomach (antrectomy) and a vagotomy (cutting the vagus nerves)
69
How is pyloric stenosis treated?
* seen in infants and have hypertrophy of pyloric muscle that causes gastric obstruction * treatment is pyloromytomy - cutting of muscle to open pyloric canal
70
What is the arterial supply of stomach?
* All three branches of celiac axis * Common hepatic artery * right gastric artery off the proper hepatic artery * antrum and pylorus * right gasro omental artery off the gastroduodenal artery * greater curvature from antrum to mid body * Splenic Artery * short gastric arteries * greater curvature from fundus to upper body * Left gastro-omental artery * anastomoses with R gastro-omental * greater curvature from fundus to upper body * Left Gastric Artery - supplies upper stomach and lower esophagus
71
What is the venous drainage of stomach?
* Parallels arterial supply of stomach * veins coalesce and drain into portal vein * r/l gastric veins -\> portal vein * R gastro-omental vein -\>SMV * L gastro-omental vein -\> splenic vein
72
Where is there lympathic drainage of stomach?
* Left gastric lymph nodes * Gastro-omental lymph nodes * Pyloric lymph nodes * pancreaticolienal lymph nodes * R gastric lymph nodes All lymph nodes drain into **celiac axis lymph nodes**
73
What is the cisterna chyle?
* celiac lymph nodes drain itno cisterna chyle * Cisterna chyle is a dilation of convergence of lymphatic channels and drains into thoracic duct * right crus of the diaphragm
74
How does the vagus nerve innervate the stomach?
* Procides motor nerves to stomach and stimulation for acid production * Left vagus nerve * anterior vagus trunk - enters along lesser curvature and banches to anterior stomach, liver, and duodenum * Right vagus nerve * posterior vagus truck - enters lesser curvature and branches to posterior stomach
75
What are the borders of the duodenum?
* After pylorus of stomach * Ends at ligament of Trietz
76
What are the portions of the duodenum?
* All portions except for first one is complete retroperitoneal * First portion * duodenal bulb * common bile duct, gastroduodenal artery and IVC run posterior to it * Second portioin * C loop * where the pancreatic and common bile duct drain into duodenum through ampulla of vater * Third portion * horizontal portion * where duodenum goes over spine from right to left and ends at SMA * Fourth portion * begins left of SMA * Ends at ligament of Trietz * ascending portioin
77
What is the blood supply to duodenum?
* superior pancreticoduodenal artery from gastroduodenal artery * Inferior pancreaticodudenal artery from SMA Drainage * Superior mesenteric vein entering portal system
78
What is malrotation?
* the small intestine does not return in a rotated position * present with bilious vomiting
79
What are some external features of the jejunum?
* usually thicker and more muscular * circular folds (plicae circulares) in mucous membrane are large and well developed * more absorptive surface * more proximal portion and resides in upper abdomen
80
What is the blood supply to the small intestine?
* entire blood supply from SMA * 15-18 branches to jejunum and ileum with collateral circulation through various branches
81
What is the lymphatic drainage in the small intestine?
* lacteals are lyphatics in intestinal villi * drain into lymph vessel plexus in mesentery * plexus drains into mesenteric lymph nodes * Next to intestine * along arterial arcades * along SMA * lymphatics will drain into cisterna chyli and into thoracic duct
82
What is the innervation of the small intestine?
* parasympathetic from vagus - stimulates motility * sympathtic from superior mesenteric ganglion * T9 and T10 * pain comes through thoracic segments
83
What is teniae coli?
three longitudinal muscle bands that run along the entire colon
84
What is haustra coli?
* permanent sacculations between teniae involving circular muscle but go away in the rectum
85
What are the fatty appendages attached to teniae?
appendices epiplociae
86
Describe the cecum
* begins at ileocecal valve * sac like structure * blood supply * ileocolic artery - branch of SMA
87
Describe Vermiform appendix
* function unknown * at base of cecum * blood supply - ileocolic artery * Appendicitis * periumbilical pain moving to r lower quadrant * nausea +/- vomiting * fever is a later finding
88
Name the portions of large intestine
* Ascending or right colon * retroperitoneal, right colic artery * Transverse colon * intraperitoneal, middle colic artery * Descending or left colon * retroperitoneal, left colic artery * Sigmoid colon * intraperitoneal, sigmoid arteries * Rectum * retroperitoneal, superior rectal artery, middle and inferior rectal arteries
89
What are the structural features of the rectum?
* internal folds * continuations of teniae * supports feces * since rectum goes through pelvic floor, there are no diverticuli
90
What is the lymphatic drainage of larges intestine?
* Cecum/appendix * periappendiceal LN -\> Superior mesenteric Ln * Ascending colon * paracolic LN -\> Superior mesenteric LN * Transverse * Superior mesenteric LN * Descending colon * inferior mesenteric LN * Sigmoid colon * inferior mesenteric LN * Rectum * Pararectal LN -\> inferior mesenteric LN * Internal iliac LN
91
What is the innervation of large intestine?
* Colon by Superior mesenteric plexus and inferior mesenteric plexus * Rectum by middle rectal plexus from inferior hypogastric plexus
92
Describe the anus
* Begins at puborectalis muscle * internal (involuntary) and external (voluntary) anal sphincter * external innervated by inferior rectal nerve * superior and inferior portions seperated by petinate line * S/I rectal arties/veins * internal hemorrhoids - superior rectal vein * external hemorrhoids - inferior rectal vein
93
What are the borders of the lesser omentum?
* epiploic foramen - opening to lesser sac * Gastrosplinic ligament * attaches stomach and spleen together * Splenorenal ligament * attaches spleen and kidneys together
94
What is the bare area of the liver?
* where there is no periotenium * made up of the r/l triangular ligaments
95
What is the renal blood supply?
* Renal arteries come off of the aorta at the level of the SMA * divide into anterior and posterior segmental branches as it reaches hilum * can be polar branches * left kidney has collateral blood flow, right doe snot
96
What is the renal drainage?
* Renal veins to the IVC * left is longer and has to pass under the SMA
97
What are the three sites where the ureter narrows?
* renal pelvis to ureter * pelvic brim * entrance to the bladder (enters diagonally)
98
Innervation of kidneys
* sympathetics from lesser and least and lumbar splanchnics * synapse in ganglia * Parasympathetics come from pelvic splanchnics, vagus and synapse in renal sinus * sensory fibers from kidneys * vagus * sympathetics * Sensory fibers from ureters * similar as kidneys but can return to DRG via T12-L2 spinal nerves as the pain can move down the ureter
99
What is the blood supply to the supradrenal glands?
* Superior suprarenal off inferior phrenic * middle suprarenal directly off aorta * inferior suprarenal off renal
100
What is the innervation to the adrenal gland?
* Only just one neuron * preganglionic sympathetic fibers innervate secretory cells * cells respond to stimulation by secreting epinephrine adn norepinephrine
101
Describe hypogastric nerves
* where the pre-vertebral ganglia split, arise from superior hypgastric plexus and supply inferior plexus * contains * ascending and descending nerves * afferents * parasympathetics (from pelvic nerves reaching colon)
102
Identify these muscles
* yellow - quadratus lumborum * green - psoas major
103
Identify
104
Name the branches off the aorta
* inferior phrenics * celiac trunk * common hepatic artery, splenic artery, left gastric artery * middle suprarenal * SMA * renal * gonadal * IMA * numberous lumbar arteries * common iliacs * median sacral artery
105
identify
* middle white area with hole - central tendinous area * muscular part of diaphragm - peripheral muscular area * black line - medial arcuate ligament * where diaphragm abuts psoas major muscle * yellow line - lateral arcuate ligament * blue line - crura
106
The esophagus opening is usually formed entirely by fibers from
right crus
107
Lumbocostal trigone
* Defect in the diaphragm, normally posterior later * formed by imcomplete closure of pericardioperitoneal canals by pleuroperitoneal membrane * can cause a congential diaphragmatic hernia
108
What are the four embryonic structures that the diaphragm comes from?
* Septum transversum * pleuroperitoneal membranes * dorsal mesentery from esophagus forms crura * body wall from cervical somites
109
What is Cholelithiasis?
* prescence of gall stones * fat, fertile, female, forty * Diagnosis * Ultrasound
110
What is biliary colic?
* occurs when the gallstones move * symptoms * intermittent upper right quadrant pain * lasts few mins to hours * occurs aftter eating fatty, greasy meal * more frequent the attacks the higher the risk of complications
111
What is cholecystitis?
* inflammation of gallbladder - acute or chronic * calculus vs. acalculous cholecystitis * gallstones cause 80-90% of acute cholecystitis * treatment is the same * worse the inflmmation, the higher the risk of complication * Diagnosis * ongoing pain in RUQ * Elevated LFTs * Ultrasound findings
112
How is a pancreatitis diagnosed?
* same as cholecysititis * Labs: amylase, lipase * Imaging * CT scan * MRCP * ERCP
113
What is Ranson's creiteria?
* Acutely * age in years \>70 * WBC \> 18000 cells/mm3 * Blood glucose \> 12.2 mmol/L (\>220 mg/dl) * Serum AST \>250 IU/L * Serum LDH \> 400 IU/L * Score 0 to 2 - 2% mortality * Score 3-4 15% * Score 5 to 6 40% * Score 7 to 8 100%
114
What is cholangitis?
* primary * chronic autoimmune disease affecting the extra and intrahepatic bile ducts * leads to cirrhosis requiring liver transplant * Ascending * infection of common bile duct from obstrcutions * Charcots triad: fever, RUQabd pain, jaundice * Reynolds pentad - plus confusion and hyptension * treatment is immediate ERCP sphincterotomy after resuscitation and antibiotics
115
Name theses posterior wall nerves
116
What is the oxidative branch of PPP?
* G6P -\> ribulose 5-phosphate * G6P DeH * Generates NADPH * Generates biosynthetic precursors (ribulose 5-phosphate)
117
What is the non-oxidative branch PPP?
* ribulose 5-P -\> 2x F6P or G3P * transketolase/transaldolase * TPP dependent