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Unit 4 GNA > LGS Week 1 & 2 > Flashcards

LGS Week 1 & 2 Flashcards

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1
Q

**

Outline the pathway and outcomes of GCPR G-alpha-q in the GI tract

A

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

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2
Q

Outline the pathway and outcomes of GCPR G-alpha-s in the GI tract

A

Activates adenylyl cyclase –> stimulates cAMP –> activates PKA –> vesicle release, upregulation and activation of transporters and channels, smooth muscle relaxation

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3
Q

Outline the pathway and outcomes of GCPR G-alpha-i in the GI tract

A

Inhibits adenylyl cyclase –> downregulation of cAMP –> counteracts Gas

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4
Q

What receptors in the GI are Gas? What receptors in the GI are Gaq?

A

Gas - H2 receptors

Gaq - M1 and M3

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5
Q

What is the role of serotonin in the enteric nervous system?

A

Stimulates contraction

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6
Q

What is the role of dopamine in the enteric nervous system?

A

Inhibits contraction

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7
Q

What is the role of ACh in the enteric nervous system?

A

Stimulates smooth muscle contraction on muscarinic receptors

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8
Q

What is the role of NO in the enteric nervous system?

A

Inhibits smooth muscle contraction

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9
Q

What is the role of Calcitonin gene-related peptide (CGRP) in the enteric nervous system?

A

increases activity of inhibitory neurons - released from afferent neurons

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10
Q

What are the mechanisms by which a bolus of food can get through the LES?

A

Peristaltic movement pushes bolus down
Negative pressure from the stomach pulls bolus in
Inhibitory NT (NO or VIP) relaxes the LES

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11
Q

Is Achalasia a structural or functional cause of dysphagia? Why?

A

Functional - it has nothing to do with the anatomy - it’s due to either a hypersensitivity of ACh or dysfunction of NO inhibition

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12
Q

What should normal scintigraphy (gastric emptying test) results look like?
What might you suspect if they are slower?

A

70% remaining at 1hr, 30% remaining at 2hr, 0% at 4hr

Slower gastric emptying could indicate gastroparesis

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13
Q

What is the function of Interstitial cells of Cajal?

A

Pacemaker cells - keep cells slightly depolarized to allow easier induction of action potentials to have a response

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14
Q

Explain receptive relaxation

A

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

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15
Q

What else besides receptive relaxation triggers NO release in the fundus of the stomach?

A

Distention of the duodenum

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16
Q

What is the function of I cells?

A

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

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17
Q

Relate the pathophysiologic mechanism involved in diabetic gastroparesis to his early satiety and bloating

A

Afferents or parasympathetics could be damaged due to diabetic neuropathy –> no proper release of ACh or NO –> impaired receptive relaxation, impaired mixing and grinding

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18
Q

What is the best medication to use for someone with gastroparesis and nausea/vomiting?

A

Metaclopramide - it’s prokinetic and an antiemetic

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19
Q

Outline Metaclopramide MOA and AE

A

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

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20
Q

Outline Erythromycin MOA and AE

A

Binds directly to motilin receptors on muscle cells –> directly stimulates contraction
AE: GI distress, only used when other meds have failed

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21
Q

Outline Neostigmine MOA and AE

A

AChE inhibit –> increased ACh –> more stimulation for contraction
AE: cholinergic effects, bradycardia

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22
Q

Which antiemetic is best for motion sickness?

A

Scopolamine - it acts on the vestibular system

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23
Q

Explain what effect the Seven Countries Study had on dietary recommendations and practices

A

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

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24
Q

Compare and contrast popular diets with high feasibility

A

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

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25
Q

Compare and contrast popular diets with moderate feasibility

A

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

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26
Q

Compare and contrast popular diets with low feasibility

A

Ketogenic - for diabetics
Low carbs, high proteins and fats

Raw Food diet - possible health wellness

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27
Q

What are the challenges of incorporating botanicals into medicine?

A

Lack of standardization
Variation in plants
Risk of contamination
Limited scientific evidence due to underfunding
Not much FDA oversight
Consumer confusion/misconception

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28
Q

What botanicals are helpful with chronic inflammatory diseases?

A

Ginger
Tumeric
Garlic
Chamomille

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29
Q

Outline the source, MOA and healthy effects of polyphenols

A

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

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30
Q

Outline the source, MOA and healthy effects of Terpenes

A

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

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31
Q

Outline the source, MOA and healthy effects of Sulfurs

A

Source: cruciferous vegetables
Health effects: phase II liver detoxification, anti-cancer

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32
Q

Outline the MOAs of Flavonoids

A

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

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33
Q
A
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34
Q

What is the number one most common disease amongst children, and 6th most prevalent of mankind?

A

Periodontal disease

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35
Q

How can poor dentition lead to malnutrition?

A

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

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36
Q

Explain how not brushing properly can lead to dental caries

A

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

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37
Q
A
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38
Q

What’s the difference between a periapical abscess and a peridontal abscess?

A

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

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39
Q

What complications can arise from an untreated dental abscess?

A

Bacteremia, sepsis
Infection travels to brain
Osteomyelitis
Lymph node infection
Cellulitis

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40
Q

Explain how biofilm + excessive inflammation leads to periodontitis

A

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

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41
Q

What oral bacteria should you treat with amoxicillan-clavulanate?

A

All aerobes
Strep oralis, strep mutans - gram (+) anaerobes
Porphyromaonas gingivalis - gram (-) anaerobe
Aggregatibacter actinomycetemcomitans - gram (-) anaerobe

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42
Q

What oral bacteria should you treat with Clindamycin?

A

Treponema denticola - gram (-) anaerobe
Fusobacterium nucleatum - gram (-) anaerobe

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43
Q

What causes aphthous stomatitis?

A

Oxidative inflammation - too many oxidative species –> inflammatory response

Nutritional deficiency (B12, folate, vitamins)

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44
Q

Outline carbohydrate digestion in the mouth

A

Salivary amylase secreted by salivary glands - breaks down starch by cleaving a(1-4 bonds) into:
Glucose
Maltose
Maltotriose
Oligosaccharides
a-Dextrins

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45
Q

Outline the carbohydrate digestion in the stomach

A

Only mechanical digestion in the stomach (mixing and grinding)

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46
Q

Outline carbohydrate digestion in the small intestine

A

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

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47
Q

Where does carbohydrate digestion conclude?

A

Small intestine brush border

48
Q

What is the role of Glucoamylase in carbohydrate digestion?

A

Cleaves (1-4) bonds

Breaks down Starch, Glycogen, and Maltose into:
Glucose
Isomaltose

49
Q

What is the role of Sucrase-Isomaltase in carbohydrate digestion?

A

Sucrase: breaks down Sucrose, Maltose, Maltotriose into:
Glucose
Fructose

Isomaltase: breaks down a-Limit Dextrins, Maltose, Maltotriose into:
Glucose

50
Q

What is the role of B-Glycosidase in carbohydrate digestion?

A

Contains two active sites: Lactase and Glucosylceramidase

Lactase - breaks down Lactose into:
Glucose
Galactose

Glucosylceramidase - breaks down Glucocerebroside and Galactocerebroside into:
Glucose
Galactose
Ceramide

51
Q

Explain the pathophysiology of Lactose Intolerance, and how you would confirm a diagnosis

A

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)

52
Q

Characterize Primary Lactose Intolerance / Non-persistence

A

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

53
Q

What are the types of Lactose Intolerance?

A

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

54
Q

Explain the receptors used for Glucose, Fructose and Galactose transport across an enterocyte

A

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

55
Q

How does Galactose Oxidation contribute to Glycolysis?

A

Galactokinase pathway –> G6P –> Glycolysis

55
Q

How does Fructose Oxidation contribute to Glycolysis?

A

Muscle and adipose: Hexokinase pathway –> F6P –> glycolysis

Liver: Fructokinase pathway –> DHAP or Glyceraldehide –> glycolysis

56
Q

Compare and Contrast Classic Galactosemia from Galactokinase deficiency

A

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

57
Q

Compare and Contrast Hereditery Fructose Intolerance from Essential Fructosuria

A

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

58
Q

Glycogenesis is a (high/low) energy process

A

High - requires hydrolysis of 2 high-energy bonds

59
Q

What is the primary enzyme of Glycogenesis?

A

UDP-Glucose
Glycogen Synthase

Glycogen primer/chain + UDP-Glucose –> (Glycogen Synthase) –> Glycogen primer/chain + Glucose + UDP

60
Q

What is the role of Glycogen Branching Enzyme?

A

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

61
Q

What is the role of Glycogen Debranching Enzyme?

A

Cleaving off glycogen chains of Glucose residues and transferring to nonreducing end of other glycogen chain - leaving one glucose remaining and cleaving it

62
Q

What is the role of G6P Complex?

A

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

63
Q

Explain the downstream effects of Glucagon in Hepatic Glycogen Metabolism

A

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

64
Q

Explain the downstream effects of Epinephrine in Hepatic Glycogen Metabolism

A

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

65
Q

Explain the downstream effects of Epinephrine in Muscle Glycogen Metabolism

A

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

66
Q

Explain the downstream effects of Insulin in Hepatic and Muscle Glycogen Metabolism

A

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

67
Q

Glycogen provides feedback inhibition to Glycogen Synthase a –> downregulate Glycogenesis when it has enough

This is stronger in (liver/muscle)

A

Muscle

68
Q

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.

A

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

69
Q

Compare and contrast Pompe disease in different stages of life

A

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

70
Q

Outline McArdle Disease

A

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

71
Q

What non-carbohydrate precursors can be converted into glucose?

A

Lactate
Pyruvate
Glycerol
Glucogenic AA
Odd-chain FA
Branched chain FA

All converted to OAA/DHAP before entering gluconeogenesis

72
Q

How does the PPP create Glucose?

A

G6P –> reduction reactions –> –> –> F6P + GAP –> Glycolysis or Gluconeogenesis

73
Q

What byproducts fo you get from PPP?

A

NADPH (from NAD+)
H+ (from H2O)
CO2 (from NAD+ reaction)
R5P (for nucleotide biosynthesis)

74
Q

What’s the most important nucleotide sugar? Why?

A

UDP-glucuronate

Solubilizes Bilirubin for excretion/conjugation
Solubulizes Glucuronides for excretion
Creates GAGs, proteoglycans, glycoproteins

75
Q

Contrast the health effects of different fiber types

A

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

76
Q

How is gastric acid produced by the parietal cell?

A

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

77
Q

Will a weak acid with a pKa of 3.5 be absorbed in a pH of 1?

A

Yes, it will stay protonated in the acidic pH –> remains unionized.

Unionized gets absorbed better than ionized.

78
Q

Will a weak acid with a pKa of 3.5 be absorbed in a pH of 5?

A

No, it will be deprotonized in the more basic pH –> ionizing it

Ionized don’t get absorbed as well

79
Q

Will a weak base with a pKa of 8 be absorbed in a pH of 1?

A

No, the acidic pH will protonate the weak base causing it to ionize

Ionized don’t get absorbed very well

80
Q

What are the regulators of Parietal Cell H+ secretion?

A

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

81
Q

What are the regulators of ECL cells and what does it secrete?

A

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+

82
Q

What are the regulators of Chief cells and what does it secrete?

A

Histamine, ACh, Gastrin –> stimulate

Secretes pepsinogen and gastric lipase

83
Q

What medications are used to inhibit H+ secretion?

A

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

84
Q

Explain the MOA of Omeprazole

A

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

85
Q

What medications directly protect mucosal lining?

A

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

86
Q

How do exocrine pancreas secretions differ from hepatic canalicular secretions?

A

Both secrete: water, HCO3-

Pancreas: Na+/K+/Cl- ions, pancreatic enzymes, mucins

Hepatic canalicular: ions, urea, AAs, glucose, GSH, bile acids, bilirubin, cholesterol

87
Q

What enzymes from the pancreas break down carbohydrates?

A

Pancreatic amylase

88
Q

What enzymes from the pancreas break down proteins?

A

Trypsin
Chymotrypsin
Carbopeptidase
Elastase

89
Q

What enzymes from the pancreas break down lipids?

A

Lipase-colipase
Phospholipase A2
Cholesterol ester hydrolase

90
Q

Explain the physiology of the alkaline tide?

A

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

91
Q

The blood pH is normal when the ratio of [HCO3-] to [H2CO3] is

A

20:1

92
Q

What mechanisms are used to power ion movement from an endothelial cell into the lumen to draw water?

A

Concentration gradient
Na+/K+ ATPase
CFTR

93
Q

What transporters or channels are used to create the concentration gradient inside the endothelial cell

A

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

94
Q

What pathways does water take to get into the lumen? What draws it there?

A

Between cells (through junctions) or through cells (aquaporins)

Cl- being secreted into the lumen –> attracts Na+ –> attracts H2O

95
Q

How does Cl- exit the ductal cell to start the process of pancreatic secretions?

A

through CFTR channel

96
Q

Outline the regulation of Pancreatic secretion

A

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

97
Q

What are the duct cells of hepatobiliary canals called?

A

Cholangiocytes

98
Q

What is actively secreted from hepatocytes into canaliculi?

A

Bile salts
Phosphatidylcholine
Conjugated bilirubin
Xenobiotics

99
Q

What is passively secreted from the interstitial space into canaliculi?

A

Water
Glucose
Electrolytes
Glutathione
AAs
Urea

100
Q

What transporter is responsible for the uptake of bile acids and xenobiotics from the blood?

A

Organic anion transporting proteins receptor (OATP) located on BL membrane

101
Q

What transporter is responsible for the secretion of conjugated bile acids into bile?

A

Bile Salt Export Pump (BSEP) on the canalicular membrane

102
Q

What transporter is responsible for the secretion of sulfated lithocholic acid and conjugated bilirubin into bile?

A

Multiple organic antion transport protein (MRP2) located on canalicular membrane

103
Q

What is the most powerful stimulator to put Bicarb into the bile duct and why?

A

Secretin –> activates AC –> stimulates cAMP –> stimulates PKA –> phosphorylates CFTR

104
Q

What is CCK responsible for regulating?

A

Stimulates contraction of the gallbladder
Stimulates acinar secretion
Slows gastric emptying
Relaxes Sphincter of Oddi

105
Q

What is rebound hyperacidity?

A

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

106
Q

Compare and contrast Soft Tissue technique and MFR

A

Both passive

ST: primarily direct
MFR: either direct or indirect

ST: rhythmic alternating forces
MFR: steady engagement of fascia

107
Q

Label each nerve fiber

A
108
Q

What are the landmarks for collateral ganglion palpation?

A

Celiac - 1 in below xyphoid process
SMG - halfway between celiac and inferior
IMG - one inch above umbilicus

109
Q

How do we assess for positive Viscerosomatic reflexes at the collateral ganglia?

A

Bogginess and tenderness with palpation

110
Q

What are two symptoms that can lead to do suspect an upper GI bleed?

A

Hematemesis (vomiting blood)
Melena (black tarry stool)

111
Q

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

A

Esophageal cancer

112
Q

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

A

Esophageal dysmotility

113
Q

What’s a key symptoms of oropharyngeal dysphagia?

A

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

114
Q

What are the abdominal pain red flags?

A

Hematemesis
Melena
Bright red blood
Fever
Unintended weight loss
Sudden onset of pain - awakened by GI symptoms
Diarrhea w/ blood or mucus

Unit 4 GNA (6 decks)

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