LGS Week 1 & 2 Flashcards
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Outline the pathway and outcomes of GCPR G-alpha-q in the GI tract
Stimulates PLC –> stimualtes PIP2 –> stimulates IP3 –> increase Ca2+ –>** smooth muscle contraction**, vesicle release, upregulation of transporter and channels
Stimulates PLC –> stimulates PIP2 –> stimulates DAG –> activates PKC –> upregulation and activation of transporters and channels
Outline the pathway and outcomes of GCPR G-alpha-s in the GI tract
Activates adenylyl cyclase –> stimulates cAMP –> activates PKA –> vesicle release, upregulation and activation of transporters and channels, smooth muscle relaxation
Outline the pathway and outcomes of GCPR G-alpha-i in the GI tract
Inhibits adenylyl cyclase –> downregulation of cAMP –> counteracts Gas
What receptors in the GI are Gas? What receptors in the GI are Gaq?
Gas - H2 receptors
Gaq - M1 and M3
What is the role of serotonin in the enteric nervous system?
Stimulates contraction
What is the role of dopamine in the enteric nervous system?
Inhibits contraction
What is the role of ACh in the enteric nervous system?
Stimulates smooth muscle contraction on muscarinic receptors
What is the role of NO in the enteric nervous system?
Inhibits smooth muscle contraction
What is the role of Calcitonin gene-related peptide (CGRP) in the enteric nervous system?
increases activity of inhibitory neurons - released from afferent neurons
What are the mechanisms by which a bolus of food can get through the LES?
Peristaltic movement pushes bolus down
Negative pressure from the stomach pulls bolus in
Inhibitory NT (NO or VIP) relaxes the LES
Is Achalasia a structural or functional cause of dysphagia? Why?
Functional - it has nothing to do with the anatomy - it’s due to either a hypersensitivity of ACh or dysfunction of NO inhibition
What should normal scintigraphy (gastric emptying test) results look like?
What might you suspect if they are slower?
70% remaining at 1hr, 30% remaining at 2hr, 0% at 4hr
Slower gastric emptying could indicate gastroparesis
What is the function of Interstitial cells of Cajal?
Pacemaker cells - keep cells slightly depolarized to allow easier induction of action potentials to have a response
Explain receptive relaxation
Distention on the wall of the stomach when recieving a bolus activates afferent neurons to relac the stomach with NO or VIP and allow stretching of the fundus to prepare for more food
What else besides receptive relaxation triggers NO release in the fundus of the stomach?
Distention of the duodenum
What is the function of I cells?
Located in the duodenum
Sense changes in chemicals –> when detecting high fats and proteins –> releases CCK, and helps trigger ENS through vasal afferents to release NO to the fundus
Relate the pathophysiologic mechanism involved in diabetic gastroparesis to his early satiety and bloating
Afferents or parasympathetics could be damaged due to diabetic neuropathy –> no proper release of ACh or NO –> impaired receptive relaxation, impaired mixing and grinding
What is the best medication to use for someone with gastroparesis and nausea/vomiting?
Metaclopramide - it’s prokinetic and an antiemetic
Outline Metaclopramide MOA and AE
D2 receptor antagonist - blocks dopamine inhibition –> increase of ACh to allow for contraction
AE: dystonic reactions (involuntary movement), stiffness, mood changes, increases prolactin –> gynomastia and milk development
Outline Erythromycin MOA and AE
Binds directly to motilin receptors on muscle cells –> directly stimulates contraction
AE: GI distress, only used when other meds have failed
Outline Neostigmine MOA and AE
AChE inhibit –> increased ACh –> more stimulation for contraction
AE: cholinergic effects, bradycardia
Which antiemetic is best for motion sickness?
Scopolamine - it acts on the vestibular system
Explain what effect the Seven Countries Study had on dietary recommendations and practices
Study of mass burden and epidemic of artherosclerotic diseases in seven countries: USA, Finland, Yugoslavia, Japan, Netherlands, Italy, Greece
Results suggested replacement of saturated fats with unsaturated
Ended up generalizing all fats as bad –> started replacing fats with starch
Compare and contrast popular diets with high feasibility
All highly feasible
DASH - Dietary Approach to Stop Hypertension
Lower BP, sodium, limits unhealthy good intake
MIND - Mediterranean and DASH for brain health - may reduce B-amyloids
10 foods to eat (Mediterranean), 5 to limit (butter, cheese, red meat, fried food, sweets)
Elimination diet - food intolerances
Eliminate foods and reintroduce one at a time
Compare and contrast popular diets with moderate feasibility
Complete opposites
Plant-based - general health and wellness, reversal of diseases
No or minimal animal products
Paleo - caveman diet - weightloss
Red and lean meats, grains, fruits, vegetables - avoid processes food
Compare and contrast popular diets with low feasibility
Ketogenic - for diabetics
Low carbs, high proteins and fats
Raw Food diet - possible health wellness
What are the challenges of incorporating botanicals into medicine?
Lack of standardization
Variation in plants
Risk of contamination
Limited scientific evidence due to underfunding
Not much FDA oversight
Consumer confusion/misconception
What botanicals are helpful with chronic inflammatory diseases?
Ginger
Tumeric
Garlic
Chamomille
Outline the source, MOA and healthy effects of polyphenols
Source: Fruits, vegetables, cereals, beverages, legumes, seed oils
MOA: secondary metabolite of plants - defense against UV radiation and pathogens –> suppresses inflammatory processes, moderates cell signaling pathways, proliferation, apoptosis
Health effects:
Protective against cancer, ND disorders, CVDs
Therapeutic properties: anti-oxidant, anti-inflammatory, anti-ND, anti-diabetic, anti-viral, skin photoprotective, anti-allergic
Outline the source, MOA and healthy effects of Terpenes
Source: green foods and grains
MOA: interaction with free radicals
Health effects: anti-bacterial, anti-fungal, anti-inflammatory, anti-leishmanial, cytotoxic, anti-tumor, anti-GH, apoptosis regulation
Outline the source, MOA and healthy effects of Sulfurs
Source: cruciferous vegetables
Health effects: phase II liver detoxification, anti-cancer
Outline the MOAs of Flavonoids
Angiotensin converting enzyme blockage –> lower BP
Inhibition of COX –> no inflammatory eicosanoids (PGE)
Prevents platelet aggregation
Inhibits estrogen synthesis
Scavenge free radicals and inhibit oxidative enzymes
What is the number one most common disease amongst children, and 6th most prevalent of mankind?
Periodontal disease
How can poor dentition lead to malnutrition?
No teeth –> not chewing properly –> maldigestion, malabsorption
Diet change to adjust to teeth issues –> less variety –> malnutrition
Liquid diets not good for general health
Dentures only 20% effective as teeth
Explain how not brushing properly can lead to dental caries
Brushing too hard –> injured enamel on teeth –> exposes surfaces to decay
Brushing too soft –> not ridding mouth of all food –> food is broken down by bacteria –> bacteria ferment simple carbs on the tooth surface into acid –> acids diffuse into enamel and dentine –> dissolve minerals –> regeneration with Ca2+, PO4, F
Caries occur when breakdown exceeds regeneration
What’s the difference between a periapical abscess and a peridontal abscess?
Periapical is a bacterial infection that comes from the root of apex of usually dead teeth
Peridontal occurs in living teeth, usually on the lateral side
What complications can arise from an untreated dental abscess?
Bacteremia, sepsis
Infection travels to brain
Osteomyelitis
Lymph node infection
Cellulitis
Explain how biofilm + excessive inflammation leads to periodontitis
increased flow of nutrient rich GCF leads to heme-iron-loving, periodontisitis associated speciies –> oxygen deprivation, favoring anaerobic bacteria
Dysbiotic microbiota destroy periodontal tissue, supplying new nutrients for increasingly destructive bacteria
What oral bacteria should you treat with amoxicillan-clavulanate?
All aerobes
Strep oralis, strep mutans - gram (+) anaerobes
Porphyromaonas gingivalis - gram (-) anaerobe
Aggregatibacter actinomycetemcomitans - gram (-) anaerobe
What oral bacteria should you treat with Clindamycin?
Treponema denticola - gram (-) anaerobe
Fusobacterium nucleatum - gram (-) anaerobe
What causes aphthous stomatitis?
Oxidative inflammation - too many oxidative species –> inflammatory response
Nutritional deficiency (B12, folate, vitamins)
Outline carbohydrate digestion in the mouth
Salivary amylase secreted by salivary glands - breaks down starch by cleaving a(1-4 bonds) into:
Glucose
Maltose
Maltotriose
Oligosaccharides
a-Dextrins
Outline the carbohydrate digestion in the stomach
Only mechanical digestion in the stomach (mixing and grinding)
Outline carbohydrate digestion in the small intestine
Pancreatic amylase secreted by exocrine pancreas - breaks down starch and a-Dextrins by cleaving a(1-4 bonds) into:
Glucose
Maltose
Isolamtose
a-Limit Dextrins
Where does carbohydrate digestion conclude?
Small intestine brush border
What is the role of Glucoamylase in carbohydrate digestion?
Cleaves (1-4) bonds
Breaks down Starch, Glycogen, and Maltose into:
Glucose
Isomaltose
What is the role of Sucrase-Isomaltase in carbohydrate digestion?
Sucrase: breaks down Sucrose, Maltose, Maltotriose into:
Glucose
Fructose
Isomaltase: breaks down a-Limit Dextrins, Maltose, Maltotriose into:
Glucose
What is the role of B-Glycosidase in carbohydrate digestion?
Contains two active sites: Lactase and Glucosylceramidase
Lactase - breaks down Lactose into:
Glucose
Galactose
Glucosylceramidase - breaks down Glucocerebroside and Galactocerebroside into:
Glucose
Galactose
Ceramide
Explain the pathophysiology of Lactose Intolerance, and how you would confirm a diagnosis
Lactose not broken down by Lactase enzyme –> Lactose enters intestinal lumen –> bacterial fermentation produces gas and lactic acid –> lactic acid increases osmotic gradient and draws fluid into lumen –> distention of intestinal walls –> increase peristalsis –> malabsorption and watery diarrhea
Hydrogen breath test to prove fermentation of bacteria (with Lactose as substrate)
Characterize Primary Lactose Intolerance / Non-persistence
Enzyme Lactase-Phlorizin Hydrolase (LPH) encoded by LCT gene
AD pattern - SNP’s in MCM6 regulatory region upstream from LCT
Enzyme very active during nursing but declines to < 10% by age 7
What are the types of Lactose Intolerance?
Primary Lactase deficiency - lactose enzyme non-persistence
Secondary Lactase deficiency - GI mucosal injury
Congenital Lactase deficiency - rare AR disorder mutation in LCT gene
Developmental Lactase Deficiency - underdeveloped GI tract in premature infant - typically self resolves
Explain the receptors used for Glucose, Fructose and Galactose transport across an enterocyte
Glucose - GLUT2 or SGLT1 brings into cell –> GLUT 2 sends out of cell on BL side
Fructose - GLUT5 brings into the cell –> GLUT2 or GLUT 5 sends out of cell on BL side
Galactose - SGLT1 brings into cell –> GLUT2 sends out of cell on BL side
How does Galactose Oxidation contribute to Glycolysis?
Galactokinase pathway –> G6P –> Glycolysis
How does Fructose Oxidation contribute to Glycolysis?
Muscle and adipose: Hexokinase pathway –> F6P –> glycolysis
Liver: Fructokinase pathway –> DHAP or Glyceraldehide –> glycolysis
Compare and Contrast Classic Galactosemia from Galactokinase deficiency
Both:
Onset in infancy
AR inheritance
Tested in NBS
Diagnostic: galactosuria and hyperbilirubinemia
Treatment: lifelong lactose and galactose free diets
(Galactose is a component of lactose)
Pathogenesis:
Classic Galactosemia: G1P-Uridyltransferase enzyme deficiency –> can’t convert Galactose-1-Phosphate –> UDP-Galactose –> accumulation of toxic substances in tissues
Galactokinase deficiency: can’t convery galactose –> Galactose-1-Phosphate –> accumulation of galactitol in tissues, also present in blood and urine
Clinical features:
CG: more severe - buildup up galactose 1-P in kidneys, brain, ovaries, hepatocytes –> failure to thrive, E Coli sepsis, Kidney damage, Cataracts, V/D, jaundice, HpSpMgly, Cognitive impairment, hypogonadism/POI in females
GKD: mild - cataracts, difficulty tracking objects with eyes
Compare and Contrast Hereditery Fructose Intolerance from Essential Fructosuria
Both:
AR genetic mutations
Diagnostic: detection of fructose in urine
Pathogensis:
Hereditery Fructose Intolerance: Aldolase B deficiency –> can’t convert Fructose-1-P to glyceraldehyde (G3P) and DHAP –> accumulation of F1P –> F1P inhibits phosphorylase –> decrease in available phosphates –> inhibition of glycogenolysis and gluconeogenesis
Essential Fructosuria: Fructokinase deficiency –> can’t convert fructose to F1P –> diverts to hexokinase pathway –> increased conversion of fructose to F6P by hexokinase –> unphosphorylated fructose does not stay in cells –> excess fructose excreted
Clinical features:
HFI: symptoms begin once infant begins consuming foods containing sucrose –> bloating, failure to thrive, renal failure, hepatic failure, jaundice, lactic acidosis
Essential fructosuria: asymptomatic
Further Diagnostics:
HFI: elevated LFTs, decreased PT/PTT, hypoalbuminemia,
definitive Dx - liver biopsy, DNA testing
Treatment:
HFI: lifelong cessation of fructose, sorbitol, sucrose
ES: no treatment
Glycogenesis is a (high/low) energy process
High - requires hydrolysis of 2 high-energy bonds
What is the primary enzyme of Glycogenesis?
UDP-Glucose
Glycogen Synthase
Glycogen primer/chain + UDP-Glucose –> (Glycogen Synthase) –> Glycogen primer/chain + Glucose + UDP
What is the role of Glycogen Branching Enzyme?
Removing segments 11+ Glc residues long from non-reducing end of chain and attaching it them to another chain at least 4 residues away via a(1-6) bonds
What is the role of Glycogen Debranching Enzyme?
Cleaving off glycogen chains of Glucose residues and transferring to nonreducing end of other glycogen chain - leaving one glucose remaining and cleaving it
What is the role of G6P Complex?
G1P –> G6P in the liver –> transported to the ER through G5PT1 –> encounters G6Pase –> Glucose + P –> Glucose exits ER through G6PT2 and P exits through G6PT3 –> both travel to blood to supply tissues
Explain the downstream effects of Glucagon in Hepatic Glycogen Metabolism
Glucagon binds to GCRP –> activates AC –> activates cAMP –> activates PKA
PKA –> phosphorylates Inhibitor-1 to activate it –> inhibits PP1
PKA –> phosphorylates Phosphorylase Kinase (PhK) which activates it
PhK phosphorylates Glycogen Phosphorylase –> upregulates Glycogenolysis
PhK phosphorylates Glycogen Synathase b –>downregulates Glycogenesis
Explain the downstream effects of Epinephrine in Hepatic Glycogen Metabolism
Binds to B2 Adrenoceptor GCRP –> same pathway as Glucagon in Liver –> upregulates Glycogenolysis, downregulates Glycogenesis
Binds to a1 Adrenoreceptor GCRP –> activates PLC –> activates DAG and IP3
DAG –> activates PKC
IP3 stimulates Ca2+ release from ER –> activates PKC
PKC –> phosphorylates Glycogen Synthase b –> downregulates Glycogenesis
Ca2+ release from ER –> activates Calmodulin –> activates PhK –> phosphorylates Glycogen phosphorylase a (upregulates Glycogenolysis), and Glycogen Synthase b
Explain the downstream effects of Epinephrine in Muscle Glycogen Metabolism
Binds to B2 Adrenoceptor GCRP –> same pathway as Glucagon in Liver –> upregulates Glycogenolysis, downregulates Glycogenesis
Increased AMP produced by muscle contraction –> activates AMPK –> Phosphorylates Glycogen Synthase b –> downregulates glycogenesis
Explain the downstream effects of Insulin in Hepatic and Muscle Glycogen Metabolism
Insulin binds to Insulin Receptor (RTK) –> activates signal cascade to activate PP1
PP1 dephosphorylates PhK, Glycogen Phosphorlyase b, Inhibitor 1 to inactivate them –> downregulates glycogenolysis
PP1 dephosphorylates Glycogen synthase a to activate it –> upregulates glycogenesis
Glycogen provides feedback inhibition to Glycogen Synthase a –> downregulate Glycogenesis when it has enough
This is stronger in (liver/muscle)
Muscle
A 6 week old previously healthy baby presents with vomiting and lethargy that began after trying to let the baby sleep through the night without feeding.
Elevated LFTs, hypoglycemia, and elevated lactic acid, alanine, and uric acid is seen on labs.
Von Gierke Disease - child can’t release glycogen from stores - can’t convert G6P to glucose during fasting
Type 1a - defective G6Pase from AR mutation in G6PC1
Type 1b - defective transporter/G6P translocate from AR mutation in SLC37A4
Clinical Features:
Hpmgly, protuberant belly with thin limbs
Nephromegaly/renal dysfunction
Doll facies
Poor growth
Labs:
Type 1a - hypoketotic hypoglycemia, elevates lactic acid, uric acid, TGs,
Type 1b - neutropenia
Dx: genetic testing
Treatment: high carb diet, corn starch, continuous feeds
Compare and contrast Pompe disease in different stages of life
Lysosomal a-glucosidase deficiency - can’t convert glycogen stores to glucose within lysosomes
AR mutation in GAA gene
Infantile: progressive muscle hypotonia, failure to thrive, cardiomyopathy, respiratory insufficiency - death within 2 years if not treated
Juvenile: later onset myopathy with variable cardiac involvement
Adult: limb-girdle muscular dystrophy type features, Glycogen deposits accumulate in lysosomes –> can progress to death by respiratory failure
Dx: on NBS in some states, confirm with genetic testing, enzyme activity
Treatment: ERT with a-glucosidase
Outline McArdle Disease
AR mutation in PYGM gene
Defect in Muscle Glycogen Phosphorylase
Seen first in 20-30yos, gets worse with age
Infantile type is fatal
Leads to stiffness, muscle pain, and fatigue with exercise that improve with rest
Dx: forearm non-ischemic exercise test –> flat lactic acid response –> low lactate/ammonia ratio –> no glucose to convert to lactic acid
Labs: Elevated CK due to rhabdomylosis
Treatment: high carb meals, moderate exercise intensity
What non-carbohydrate precursors can be converted into glucose?
Lactate
Pyruvate
Glycerol
Glucogenic AA
Odd-chain FA
Branched chain FA
All converted to OAA/DHAP before entering gluconeogenesis
How does the PPP create Glucose?
G6P –> reduction reactions –> –> –> F6P + GAP –> Glycolysis or Gluconeogenesis
What byproducts fo you get from PPP?
NADPH (from NAD+)
H+ (from H2O)
CO2 (from NAD+ reaction)
R5P (for nucleotide biosynthesis)
What’s the most important nucleotide sugar? Why?
UDP-glucuronate
Solubilizes Bilirubin for excretion/conjugation
Solubulizes Glucuronides for excretion
Creates GAGs, proteoglycans, glycoproteins
Contrast the health effects of different fiber types
Soluble, gel forming fiber:
Lowers blood sugar and raises insulin sensitivity
Lowers total and LDL cholesterol
Delays gastric emptying and small bowel transit to improve satiety
Insoluble fiber:
Doesn’t dissolve in water –> speeds up passage through GI tract
Helps with constipation and diverticular disease
How is gastric acid produced by the parietal cell?
CO2 gets in the cell from blood stream and mitochondria (ETC)
CO2 + H2O + Carbonic Anhydrase –> H2CO3 –> H + HCO3-
H+ transported through H+/K+ pump and Cl- is secreted through Cl- channel
Will a weak acid with a pKa of 3.5 be absorbed in a pH of 1?
Yes, it will stay protonated in the acidic pH –> remains unionized.
Unionized gets absorbed better than ionized.
Will a weak acid with a pKa of 3.5 be absorbed in a pH of 5?
No, it will be deprotonized in the more basic pH –> ionizing it
Ionized don’t get absorbed as well
Will a weak base with a pKa of 8 be absorbed in a pH of 1?
No, the acidic pH will protonate the weak base causing it to ionize
Ionized don’t get absorbed very well
What are the regulators of Parietal Cell H+ secretion?
Stimulate:
ACh on M3 receptor or Gastrin on CCK receptor –> Gq –> stimulate IP3/Ca2+ –> upregulate H+/K+ ATPase
Histamine on H2 receptor –> Gs –> stimulate cAMP –> stimulate binding of tubulo vesicles with H+/K+ ATPase to membrane
Inhibit:
Somatostatin on SST receptor or Prostaglandin on EP receptor –> Gi –> inhibit cAMP –> prevent binding of tubulo vesicles with H+/K+ ATPase to membrane
What are the regulators of ECL cells and what does it secrete?
Regulators of ECL cells:
ACh –> stimulates
Gastrin –> stimulates
Somatostatin –> inhibits
Histamine secreted from ECL cells
Histamine binds to Chief cells –> secrete Pepsinogen and Gastric Lipase
Histamine binds to Parietal cells –> secrete H+
What are the regulators of Chief cells and what does it secrete?
Histamine, ACh, Gastrin –> stimulate
Secretes pepsinogen and gastric lipase
What medications are used to inhibit H+ secretion?
Atropine –> inhibits ACh from binding M3
Famotidine –> Histamine antagonist inhibits H2
Octreotide –> Somatostatin analogue stimulates SST
Misoprotol –> Prostaglandin agonist stimulates EP
Omeprazole –> inhibits H+/K+ ATPase
Explain the MOA of Omeprazole
Absorbed into the blood stream from the intestine due to enteric coating protecting it from gastric acid degradation
Enters parietal cells to bind with membrane bound H+/K+ ATPase
Need new doses for new vesicles that bind
What medications directly protect mucosal lining?
Sucralfate - combination of AlH and Sucrose sulfate –> negative charged sulfate binds to positively charged ulcers –> creates paste to bind and protect
Bismuth Subsalicylate - stimulates PEG, mucus and bicarb secretion –> coats ulcers
How do exocrine pancreas secretions differ from hepatic canalicular secretions?
Both secrete: water, HCO3-
Pancreas: Na+/K+/Cl- ions, pancreatic enzymes, mucins
Hepatic canalicular: ions, urea, AAs, glucose, GSH, bile acids, bilirubin, cholesterol
What enzymes from the pancreas break down carbohydrates?
Pancreatic amylase
What enzymes from the pancreas break down proteins?
Trypsin
Chymotrypsin
Carbopeptidase
Elastase
What enzymes from the pancreas break down lipids?
Lipase-colipase
Phospholipase A2
Cholesterol ester hydrolase
Explain the physiology of the alkaline tide?
Happens in the basolateral vasculature of the stomach - parietal cells secrete H+ into the lumen and the HCO3- into the interstitium –> travels down to duodenum where opposite effect happens
Pancrease secretes HCO3- into duodenum to neutralize stomach acid and H+ into interstitium where it meets alkaline tide
The blood pH is normal when the ratio of [HCO3-] to [H2CO3] is
20:1
What mechanisms are used to power ion movement from an endothelial cell into the lumen to draw water?
Concentration gradient
Na+/K+ ATPase
CFTR
What transporters or channels are used to create the concentration gradient inside the endothelial cell
Na+/K+ pump - pushing 3Na+ out and pulling 2K+ into the cell
NKCC pump - pushing K+, Na+ and 2Cl- into the cell
K+ leak channels pull K+ out due to concentration gradient
What pathways does water take to get into the lumen? What draws it there?
Between cells (through junctions) or through cells (aquaporins)
Cl- being secreted into the lumen –> attracts Na+ –> attracts H2O
How does Cl- exit the ductal cell to start the process of pancreatic secretions?
through CFTR channel
Outline the regulation of Pancreatic secretion
Enzymes:
Fatty acids/small peptides stimulate I cells –> release CCK –> stimulate acinar cells –> intracellular signaling with IP3, Ca2+ –> secretion of enzymes
Aqueous fluid:
H+ stimulates S cells –> secretes Secretin –> stimulates intracellular signaling with cAMP –> aqueous Na+/ Bicarb secretion
What are the duct cells of hepatobiliary canals called?
Cholangiocytes
What is actively secreted from hepatocytes into canaliculi?
Bile salts
Phosphatidylcholine
Conjugated bilirubin
Xenobiotics
What is passively secreted from the interstitial space into canaliculi?
Water
Glucose
Electrolytes
Glutathione
AAs
Urea
What transporter is responsible for the uptake of bile acids and xenobiotics from the blood?
Organic anion transporting proteins receptor (OATP) located on BL membrane
What transporter is responsible for the secretion of conjugated bile acids into bile?
Bile Salt Export Pump (BSEP) on the canalicular membrane
What transporter is responsible for the secretion of sulfated lithocholic acid and conjugated bilirubin into bile?
Multiple organic antion transport protein (MRP2) located on canalicular membrane
What is the most powerful stimulator to put Bicarb into the bile duct and why?
Secretin –> activates AC –> stimulates cAMP –> stimulates PKA –> phosphorylates CFTR
What is CCK responsible for regulating?
Stimulates contraction of the gallbladder
Stimulates acinar secretion
Slows gastric emptying
Relaxes Sphincter of Oddi
What is rebound hyperacidity?
The body compensates for prolonged PPI use by making more gastrin
When medication is stopped abruptly, body is still making excess gastrin –> excess gastric acid
Compare and contrast Soft Tissue technique and MFR
Both passive
ST: primarily direct
MFR: either direct or indirect
ST: rhythmic alternating forces
MFR: steady engagement of fascia
Label each nerve fiber
What are the landmarks for collateral ganglion palpation?
Celiac - 1 in below xyphoid process
SMG - halfway between celiac and inferior
IMG - one inch above umbilicus
How do we assess for positive Viscerosomatic reflexes at the collateral ganglia?
Bogginess and tenderness with palpation
What are two symptoms that can lead to do suspect an upper GI bleed?
Hematemesis (vomiting blood)
Melena (black tarry stool)
When the pts has these symptoms, what should you be considering?
Trouble passing solids through esophagus but not liquids
Progessive
Weight Loss
Tobacco/Alcohol hx
Esophageal cancer
When the pts has these symptoms, what should you be considering?
Liquid and solids equally difficult to pass through esophagus
Symptoms episodic
No significant PMH
No weight loss
Esophageal dysmotility
What’s a key symptoms of oropharyngeal dysphagia?
Solids go down better than liquids - due to distention of esophagus with solids helps it prepare better
Liquids go down too fast for the body to react
What are the abdominal pain red flags?
Hematemesis
Melena
Bright red blood
Fever
Unintended weight loss
Sudden onset of pain - awakened by GI symptoms
Diarrhea w/ blood or mucus
