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GI II: Test 1 > GI PHYS review ** > Flashcards

GI PHYS review ** Flashcards

1
Q

Salivary glands and composition?

A

submandibular gland: serous/mucous - 70%

sublingual gland: serous mucous - 5%

parotid gland (largest): serous - 25%

composition: water, mucus, alpha amylase, lysozymes, igA, bicarbonate***
- bicarb is imp. b/c it minimizes tooth decay (neutralizes bacterial acid) and it neutralizes gastric acid refluxed in lower esophagus (GERD)

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2
Q

anatomy of salivary glands?

A

two types of glands:

  1. serous: (parotid gland) - secretes nonviscous saliva composed of water, electrolytes and enzymes
  2. mixed: submandibular, sublingual- secretes viscous saliva rich in mucin glycoproteins
  • acinar cells: primary secretion-saliva, plasma (H2O, Na+, Cl-, K+, HCO3-, amylase)
  • Myoepithelial cells: motile, contracts, expels saliva
  • Ductal cells: modifies secretion by modifying electrolytes, Na+/ Cl- reabsorbed K+, HCO3- is secreted
  • Ductal cells are water impermeable, water is not absorbed along with the solute, water remains in lumen and saliva is secreted hypotonic relative to plasma

Saliva is hypotonic with low osmolality!

Net absorption of Na + & Cl causes - NaCl in saliva lower than in plasma

Net secretion of K + and HCO 3 causes - K + and HCO 3 in saliva higher than in plasma

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3
Q

how does salivary rate/composition change?

A

Duct cells modify the composition of saliva as the rate changes -

At highest flow rates (4 mL/min), final saliva resembles plasma (high Na+, Cl-, low K+) as the ductal cells have less time to modify the saliva

At lowest flow rates (< 1 mL/min), final saliva is dissimilar to plasma (low Na+, Cl-, high K+) as saliva has more contact time with ductal cells, more Na+ and Cl- are reabsorbed, which decreases their concentration and more K+ is secreted (hypotonic)

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4
Q

Xerostomia

A

dry mouth due to absence of saliva production (drugs, radiation treatment, autoimmune disease).

buccal infections/dental caries

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5
Q

Sjogren’s syndrome

A

autoimmune process-targets salivary and lacrimal glands

glandular atrophy and decreased saliva production (xerostomia), dry eyes (keratoconjuctivitis sicca)

difficulty in chewing, swallowing and speech.

dry oral mucosa, superficial ulceration, buccal infections/dental caries

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6
Q

Addison’s

A

increase Na+ in saliva (↓ Na+ reabsorbed because there is no aldosterone)

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7
Q

Primary aldosteronism & Cushing’s

A

decrease Na+ in saliva (↑ Na+ reabsorbed), salivary NaCl is zero, increase K+ levels

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8
Q

achalasia

A

failure of ES to relax, results in food in LES

  • can be causd by nerve degeneration, lack of NO synthase or ** chagas disease

On barium radiography, achalasia is characterized by esophageal dilatation with the classic “bird’s beak” appearance distally and the to-and-fro movement of barium
(loss of peristalsis).

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9
Q

incompetent LES

A

failure of LES to contract

  • The LES acts like a guard that prevents anything that gets into the stomach from refluxing into the esophagus, it acts as a pressure barrier at the gastro-esophageal junction
  • Incompetent LES or transient relaxation of LES are the most common symptoms of reflux.

cessation of excitatory cholinergic activity and release of NO and VIP leads to LES relaxation

GERD is secondary to an incompetent lower esophageal sphincter

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10
Q

diffuse esophageal spasms

A

uncoordinated esophageal contraction

  • characterized by contractions that are of normal amplitude but are uncoordinated, simultaneous, or rapidly propagated
  • these spasms can prevent food from reaching the stomach, leaving it stuck in the esophagus
  • it can cause dysphagia, regurgitation and chest pain
  • may caused by disruption of the nerve activity that coordinates the swallowing action of the esophagus

on barium swallow see “corkscrew appearance” of esophagus

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11
Q

hiatal hernia

A

moves LES into thoracic cavity, increased GERd

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12
Q

GERD

A

: the most common symptom of
heartburn due to stomach acid reflux
into esophagus

is not a disease but a normal physiological process

stomach contents leak backwards from the stomach into the esophagus and irritates the lining of the esophagus

this occurs when the lower esophageal sphincter (LES) does not work properly

weak squamous lining of the lower esophageal section

decrease secretion of mucus and bicarbonate in saliva

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13
Q

Barrett’s esophagus

A

it is most often diagnosed in people who have long-term GERD (chronic inflammation)

this condition is recognized as a complication of GERD

a condition in whichcolumnar cells replace squamous cell in themucosa of esophagus
‘
the main cause of Barrett’s esophagus is thought to be an adaptation to chronic acid exposure fromreflux esophagitis

its importance lies in its predisposition to evolve into esophagealcancer

it develops in about 10–20% of patients withchronic GERD.

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14
Q

dysphagia

A

difficulty in swallowing due to abnormalities in:

  1. structural - anatomical structures
    - abnormal tongue, cannot propel bolus backward
    - diverticula (outpouchings of pharyngeal or esophageal wall) in which food is trapped.
  2. functional - abnormal swallowing reflex
    - neurological defect and control of oropharyngeal swallowing, peristalsis, and esophageal sphincter relaxation, or to defects in muscle layers.
  3. disease state:
    - neurological disorders
    - stroke
    - Parkinson’s disease
    - myasthenia gravis
    - xerostomia
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15
Q

Oxyntic glands

A

located in fundus and body

  1. parietal (oxyntic cells): secrete HCl and IF
  2. Peptic (Chief cells): secrete pepsinogen
  3. Mucous cells
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16
Q

pyloric glands

A

located in the antrum/pyloric region of stomach

  1. G cells: secrete gastrin (hormone) that stimulates parietal and peptic cells
  2. Mucous cells
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17
Q

oxyntic cells secrete?

A

= parietal cells - secretion stimulated by Ach, gastrin and histamine

  1. Gastric Acid (HCl): activates pepsinogen; kills bacteria
  2. Intrinsic Factor: complexes with Vitamin B12 to permit absorption

after a meal, stimulated by gastrin and histamine the secretion is

  • high in H + and Cl -
  • low in Na + and K +
  • there is an inverse relationship b/w luminal concentration of H+ and Na+ as a fn. of gastric acid secretion
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18
Q

Peptic cells secrete?

A

= chief cells: stimulated by Ach, acid, secretin

  1. Pepsinogen: digests proteins
  2. Gastric lipase: digests fats
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19
Q

Mucus neck cells secrete?

A
  1. mucus: stimulated with irritation of mucosa and serves as physical barrier b/w lumen and epithelium
  2. bicarb: acts as buffer to gastric acid to prevent damage to epithelium
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20
Q

Enterochromaffin like cells secrete?

A

stimulated by ACh and gastrin to secrete Histamine - which stimulates gastric acid secretion

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21
Q

D cells secrete?

A

stimulated by acid in the stomach to secrete Somatostatin (which inhibits gastric acid secretion)

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22
Q

G cells secrete?

A

G cells are stimulated by ACh, peptides and AA’s to secrete Gastrin –> which stimulates gastric acid secretion

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23
Q

how does acid secretion from parietal cells occur?

A

Cl- is brought into cells and HCO3- diffuses out into plasma

Cl- diffuses out into the gastric lumen

H+/K+ ATPase: K+ is pumped into parietal cells from the lumen while H+ is pumped out (requires a lot of ATP)

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24
Q

agonists/antagonists of parietal cells?

A

Agonists: ACh, Gastrin and Histamine all stimulate parietal cell to secrete acid

  1. ACh: released from vagus n. binds to M3 receptors
  2. Gastrin: released from G cells, binds to CCKB receptors
  3. Histamine released from ECL cell, binds to H2 receptors

Inhibitors: Somatostatin and PGs directly binds to parietal cell and inhibits Histamine

  1. Somatostatin binds to SST receptors
  2. PGs binds to PGs receptors
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25
Q

Three phases of gastric secretion?

A
  1. Cephalic Phase: 30% of total gastric acid secretion - impulses from vagus n –> ACh to be released which stimulates
    - parietal cells to release acid
    - ECL cells to release histamine
    - G cells to release gastrin
    - Chief cells to release pepsinogen
    - inhibits D cells, reduced release of somatostatin
  2. Gastric Phase: 50-60% of total gastric acid secretion
    - caused by food distension in the stomach –> activates vagus and ENS reflexes to increase acid and pepsinogen secretion
  3. Intestinal Phase: 10% of total acid secretion
    - peptides in duodenum, stimulate gastrin secretion
    - chyme in duodenum inhibits acid secretion
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26
Q

Vagotomy?

A

Vagotomy (cutting of vagus nerve):

  • inhibits gastric acid secretion
  • used to treat peptic ulcers
  • side effects: delay in gastric emptying, diarrhea
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27
Q

IF is secreted by? Vit B12 deficiency?

A

parietal cells located in fundus area

VITB12 deficiency caused by?

  1. decreased dietary intake
  2. decreased absorption: gastric resection, or AI disease
28
Q

what agents cause mucosal damage?

A
  1. H. pylori
  2. Zollinger-Ellison syndrome - tumor that causes excessive secretion of gastrin, which stimulates acid hyper-secretion
  3. NSAIDs (aspirin) - inhibits COX1, inhibiting PGs (PGs protect gastric mucosa)
    - aspirin is a weak acid that is easily absorbed in low pH of stomach –> acts stimulating histamine release and disruption or local mucosa
  4. alcohol
29
Q

peptic ulcer disease

A
  • includes both gastric ulcers and duodenal ulcers
    1. Gastric ulcer disease: occurs in gastric mucosa- due to increased acid secretion (H. pylori, ZE syndrome, Gastrinoma)
    2. Duodenal ulcer disease: due to decreased bicarb secretion from pancreas
30
Q

pentagastrin challenge?

A
  1. normal: gastrin is 35, acid is 1-2, after pentagastrin acid output is 20-35.
  2. gastric ulcer (gastrinoma): serum gastrin is 500, basal acid ouput is 15-25 - after pentagastrin challenge goes to 30-75
    (pancreatic islet cell adenoma causes high gastrin secretion, results in high basal level of acid, with little change after pentagastrin challenge)
  3. duodenal ulcer: gastrin is 50, basal acid is 2-7, after pentgastrin goes to 25-60 (see increase after pentagastrin challenge)
  4. pernicious anemia: gastrin levels are 350, basal acid output is 0, not changed with pentagastrin
31
Q

H. pylori

A
  • gram negative bacterium w/ high urease activity: NH4+ damages epihtelial cells (GU) and increases acid secretion (DU)
  • H. pylori found in 95% patients with DU and 100% patients with GU (when alcohol, aspirin, NSAIDS are eliminated)
  1. invades mucus layer of gut
  2. neutralizes surrounding acid using enzymatic actvity of urease (producing NH3+)
  3. colonoizes the mucous layer
  4. causes inflammation, mucosal degredation and cell death - allows pepsin/H+ to degrade the epithelial layer
32
Q

Ductal cells

A
  • secrete aqueous NaHCO3- to neutralize acidic chyme and allow for proper fn. of pancreatic enzymes
  • stimulated by acid in duodenal lumen –> results in increased secretin release –> stimulates ductal cells to increase NaHCO3- secretion
33
Q

Acinar Cells

A
  • secrete pancreatic enzymes
  • stimulated by fat and protein products in duodenal lumen –> results in increased CCK release –> stimulates secretion of pancreatic enzymes
34
Q

Hormonal control of pancreatic exocrine secretion

A
  1. Chyme entering
    duodenum causes duodenal
    enteroendocrine cells to
    release CCK and secretin
  2. CCK and secretin enter blood stream : CCK induces secretion of enzyme rich pancreatic juice. Secretin causes secretion of HCO3- rich pancreatic juice
4. Bile salts and to a
lesser extent, secretin
transported via blood 
stream stimulate liver
to produce bile more
rapidly.
5. CCK (via blood stream)
causes gall bladder to 
contract and hepato-
pancreatic sphincter
to relax. Bile enters
duodenum.
35
Q

what are acinar secretory products?

A
  1. trypsinogen - activated by enteropeptidase
  2. chymotrypsinogens activated by trypsin
  3. amylase, lipase, etc.
36
Q

what causes CCK release?

A

release is modulated by body’s needs for CCK and controlled by CCK-RP (releasing peptide)

CCK-RP is released in response to fatty acids, aromatic amino acids, etc. into duodenum

CCK increases enzymatic secretion from pancreas acinar cells

with large quantities of proteins in duodenum, CCK is released by CCK-PR and MP

if the proteins are digested, then trypsin will start to digest CCK - thus eliminating its own signal for release

peptides regulate release of CCK so that it can match its need in the duodenum

What is the significance of peptide
factors regulating CCK release? CCK ends its own end – it is released due to presence of peptides, if there are no peptides then it won’t be released

37
Q

S cells

A

secrete secretin in the duodeneum in response to falling pH due to entering of acidic chyme

38
Q

what stimulates secretin? cck?

A

presence of acid in duodenum stimulates release of secretin –> increased ductal cell release

presence of fats in duodenum causes release of CCK –> stimulates acinar cells

39
Q

steatorrhea

A

: fat in the stool-early sign of pancreatic dysfunction

reduced pancreatic enzyme (lipase) and bicarbonate secretion

low pH inactivates lipase

40
Q

Pancreatitis:

A

retention of secretion in pancreas leads to autodigestion of pacreatic tissue

obstructive (gallstone occluding pancreatic duct, or a malignancy)-acute

hereditary-expression of a mutated trypsin molecule that is resistant by
trypsin inhibitors. Trypsin digests pancreatic tissue-chronic

inflammation of the pancreatic tissue (alcohol abuse)-chronic

41
Q

Cystic fibrosis

A

Lack chloride transporter at apical membrane

Leads to decreased water, HCO3, & Cl excretion, with concentration of protein in acinar ducts and blockage…. gland autodigestion/destruction

Progressive pulmonary and pancreatic insufficiency - chronic

42
Q

fat digestion?

A
  1. bile salts in duodenum emlsify large fat globules
  2. digestion of fat by lipase yields FFAs and monoglycerides, which associate with bile salts to form micelles which “ferry” them into intestinal mucosa
  3. FA’s leave micelles and diffuse into epithelial cells - they are recombined and packaged to form chylomicrons
  4. chylomicrons are extruded from epithelial cells by exocytosis and are carried in lymph away from intestine
43
Q

Hyperammonemia

A

In adults, caused by liver failure

Toxic effects of ammonia

Brain swelling due to osmotic imbalance
High ammonia and glutamate in astrocytes
Initiates glutamine synthetase and inhibits glutaminase

Astrocytes produce glutamine
Exacerbates osmotic imbalance
At high enough concentrations, opens mitochondrial permeability transition pore

Decreases glutamate concentration
An excitatory neurotransmitte

44
Q

Homocystinuria

A
  • autosomal recessive deficiency
  • defect in cystathione synthase (homocysteine –> cysteine): presents w/ low cysteine and elevated methionine/homocystine

Presentation:

cardiovascular disease:
Deep vein thrombosis
Thromboembolism
Stroke

dislocation of lens, mental retardation, marfanoid habitus

Vitamin B12 and folate: needed to remake methionine from homocysteine (if have these deficient then will have low serum methionine levels and elevated homocysteine)

45
Q

when do you expect positive nitrogen balance?

A

when there is a lot of growth/repairing tissue: puberty, infants, growth, hospitalized pts after surgery

Positive nitrogen balance occurs during growth
Amount incorporated into macromolecules each day exceeds the amount excreted

46
Q

when do you expect negative nitrogen balance?

A

malnutrition

Amount of nitrogen macromolecules excreted exceeds the amount incorporated

47
Q

Marasmus

A

generalized malnutrition
Reduction in the total number of calories in an infant’s diet

child’s weight falls below 60% for normal sex, height and age

significant loss of body fat and muscle occurs due to catabolism of fats and protein, an adaptive strategy to use lipids and amino acids as energy sources.

48
Q

Kwashiorkor

A

A protein-energy malnutrition (PEM)

Protein deprivation with adequate caloric intake

normal or nearly normal body weight and height for age

Often, the child has been weaned too early and subsequently fed a low-protein, high-carbohydrate diet.

Insufficient essential amino acid intake results in decreased protein synthesis.
- see Hypoalbuminemia and hypopigmentation

49
Q

essential AA’s?

A

arginine only essential AA needed during period of growth- not reqd for adults

all of the non-essential AAs can be made from glucose

50
Q

what coenzymes are needed to make methionine?

A

VitB12 and Folate

51
Q

Key coenzyme for amino acid metabolism that is required for transamination reactions?

A

Vitamin B6 (Pyridoxal Phosphate)

52
Q

Alcoholic Hypoglycemia

A

Metabolism of Alcohol:
Ethanol rapidly converted to acetaldehyde in liver then converted to acetate
- Both reactions require NAD+
- [NADH]/[NAD+] increases in the liver

NAD+ is needed for gluconeogenesis: : if there is no NAD then new glucose cannot be produced in the food starved state

53
Q

maintenance of blood glucose levels?

A

Glycogenolysis
During fasting
Mostly depleted after more than 12 hours

Gluconeogenesis
During starvation
Increases as glycogen reserves decrease
Only source after 24 hours of fasting

54
Q

low methionine vs. high methionine?

A

low methionine: seen in VitB12/folate deficiency b/c they are needed to convert homocysteine to methionine

if have high methionine and high homocysteine: then you know its because of a problem in cystathione sythase resulting in homocysteiniuria

55
Q

paneth cells

A

located at bottom of crypts – secrete antimicrobial peptides

56
Q

M cells

A

transport cells that sit on top of Peyer’s patches and bring in Ags

57
Q

Humoral immunity?

A

IgA is the most important factor

58
Q

most imp. adaptive immunity cytokines in gut?

A

IL17 and IL22 - seen with Th17 cells

59
Q

how to not mount vigorous response to bacteria in gut?

A

mucins are layer protection over epithelial cells allowing bacteria to live in the intestinal lumen and also protecting the mucosal surface

60
Q

Immunologic Abnormalities in IBD?

A
  1. Dysregulated innate immune response
    Defective defensin expression
    Inadequate negative immune regulation to commensal organisms
  2. Abnormal cell-mediated immunity
    - Overactive Th17 response
    - Granulomatous inflammation by IFN-γ-producing Th1 cells
  3. Defective regulatory T cell function
    - FoxP3 and IL-2 or IL-2R deficiencies result in inflammatory bowel disease
  4. Defective autophagy
61
Q

induction of oral tolerance?

A

Ags take up –> presented to T cells by CD103+ DC’s –> DC secretes TGFbeta and retinoic acid –> induces FOXP3 (TReg) cell to become tolerogenic to normal flora

62
Q

Celiac Disease

A

an immune-mediated disease mediated by T cells -which make Antibodies to tissue transglutaminase (IgA) and Anti-gluten

gluten is processed by TG2 making it fit better into certain HLADQ2/8 MHC complexes –> results in presentation to CD4 TH2 cells –> production of IgA antigluten Abs

–> results in lymphocytic destruction of epithelial cells due to gluten intake –> villous atrophy

Clinical symptoms can vary from abdominal pain, diarrhea, growth failure, anemia, osteoporosis, or asymptomatic

63
Q

genetics of celiac disease?

A

All Celiac disease patients have HLA - DQ2 or DQ8

64
Q

celiac disease antibodies?

A 
Tissue Transglutaminase (Antibody to TG)
IgA – sensitive and specific
IgG – check if IgA deficiency

Endomysium (IgA)

Gliadin (IgA & IgG)

Deamidated Gliadin

use MARSH score to rate increasing villous atrophy of intestinal lesions

65
Q

IPEX

A

Arises due to mutations in the transcription factor Foxp3

The phenotype in humans results in a loss of functional Treg cells

Lack of T cell inhibitory activity results in widespread autoimmunity

Symptoms include intractable watery diarrhea, failure to thrive, dermatitis, and autoimmune diabetes

Immunoglobulin levels are normal with the exception of IgE which is elevated

case presentation:Billy was born full term and developed atopic dermatitis shortly after birth. At 4 months of age Billy developed intractable watery diarrhea and at 6 months of age Billy was diagnosed with type 1 diabetes.

Genetic analysis shows lack of CD4+ CD25 T cells, and lack of FOXp3 gene

Treg cells and IgE production
Suppress Th1 and Th2 cytokines
Suppress IgE by inducing IL-10 and TGF-β

GI II: Test 1 (6 decks)

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