Phys - GI Flashcards

1
Q

Functions of the Liver

A
  1. Formation and secretion of bile.
  2. Glycogen formation & short term storage.
  3. Urea synthesis.
  4. Fat & Cholesterol Metabolism
  5. Protein Synthesis - blood, immune, P450, Coagulation.
  6. Detox of drugs & poisons.
  7. Cleansing bacteria from blood (Kupffer)
  8. Pro-Hormone synthesis from cholesterol
  9. Vitamin D hydroxylation to Calcidiol 25 (OH) Vit D3.
  10. Volume reservoir for blood “sponge”.
  11. Hemoglobin & Raggy RBC break down.
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2
Q

What’s delivered via the Hepatic Artery?

A

Oxygen Rich blood w/fats from the Lymph System

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3
Q

What’s delivered via the Portal Vein

A

Nutrient/Toxin rich Deoxygenated Blood and Water drained from the Intestines

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4
Q

Effects of Obstruction of Portal Blood Flow In/Into Liver

A
  • Ascietes in Abdomen
  • Collateral Vessels form to hold backed up Blooe
  • Hemorrhoids form in Rectum AND Esophagus ( called Esophageal Varices)
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5
Q

Served by Branches of the Celiac Trunk

A

Liver (via Rt & Lt Hepatic Branch)
Stomach (Gastric & GastroEpiPloic Branches)
Spleen (Splenic Artery)
Pancreas (Pancreatic & Pancreato-Duodenal)
Duodenum (PancreatoDuodenal & GastroDuodenal)

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6
Q

Served by Branches of the Sup. Mesenteric Artery

A

Duodenem
Pancreas
Small Intestines
Colon (partial)

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7
Q

Served by Braches of the Inf. Mesenteric Artery

A

Colon

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8
Q

Rate Limiting Enzyme in Cholesterol Synthesis

A

HMG-CoA reductase

Supply of which controls rate of Mevalonate Pathway

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9
Q

Target of Statins

A

HMG-CoA Reductase

To prevent Chol. Synthesis and stop up the Mevalonate Pathway

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10
Q

Composition of Bile

A
Amino Acids
Cholesterol
Bile Salts
Bilirubin
Phospholipids
Water 
Electrolytes
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11
Q

Bile from liver to Intestine

A
  • Secreted by Hepatocytes into Bile Ducts via Canniculi
  • Travels down Hepatic Ducts to Cystic Duct and follows that into the Gallbladder where bile is concentrated
  • Bile released from Gallbladder into cystic/common bile duct, on stimulation of CCK, release of which from I Cells on Duodenal Villi is directed by Monitor Peptide, secreted from the pancreasin response to presence of Amino Acids in Duodenum.
  • Meets Pancreatic Duct in Pancreas and bile mixes with pancreatic secretions at sphicter of Odi and exits into the lumen of the small intestine via the Ampulla of Vater.
  • Combines with
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12
Q

Main Function of Bile Acid

A

To Facilitate formation of Micelles by free phospholipids in the duodenal/jejunal lumen

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13
Q

Micelle

A

compact double phospholipid bi-layer ball into which fats form upon exposure to bile acids in the sm intestine

Micelles are tinier than emulsion droplets as their phospholipids arrange in an orderly compact manner. They’re so small they may be absorbed by enterocytes on the brush border of intestinal villi. Enterocytes add a thread of protein, maybe some handy cholesterol and voila, a chyolmicron is formed

Enterocytes release chylomicrons into lymph lacteals as they’re too big to cross into the capillary bed and off they goe to the cisterna chyli and into the blood supply at the base of the left jugular

The chylomicron can be received by the brain and heart - any tissue that has Lipoprotein Lipase and excess is returned to the liver to have additional proteins added VLDL, LDL, HDL

Bile is reabsorbed by active transport in the ilium, 10% is lost to the feces. The liver recycles the reabsorbed bile back into the bile ducts 10-12X/day

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14
Q

CCK

A

Cholecystokin

Causes Gallbladder contraction and Sphincter of Odi relaxation

Secreted by I-Cells on duodenal villi brush border in response to lipids in the chyme Also activated by Monitor Peptide which moitors chyme for trypsin.

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15
Q

What happens to unused Liver Glycogen

A

It is turned into Triglyceride, packed into VLDL and shipped off to Adipose tissue for long term storage

Thus sugar becomes fat

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16
Q

Clotting Factors Synthesized in the Liver

A

Fibrinogen
Prothrombin
Factors V, VII, IX, X

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17
Q

Liver action on NH3 found in the blood?

A

Deamination - NH3 is toxic

Turns it into Urea - nontoxic, excretable & used in the countercurrent exchange system of the medullary loop of henle to cocentrate the tissue there and draw water in from the collecting tubules

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18
Q

How to get rid of cholesterol?

A

10% bile lost to feces

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19
Q

Endocrine Liver Products

A
Angiotensinogin
Thrombopoietan
Hepatocyte Growth Factor (HGF)
IGF-1
Hydrolyzes Vit D3 to 25 (OH) Vit D (Calcidiol)
CRP  (C-Reactive Protein)
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20
Q

Hepatocyte Growth Factor HCG

A

Causes cell replication/division in all tissues derived from embryonic mesenchyme: Hepatocytes, Epithelium, Endothelium, Neurons, Hematopoietic cells, Melaocytes

Target for cancer treatment for cancers in mesenchymal tissue

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21
Q

Insulin-like Growth Factor -1 IGF-1

A

Released in response to somatostatin (growth hormone) release by anterior pituitary

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22
Q

CRP

A

C-Reactive Protein

Syn & Released by Liver in response to Inflammation (specifically IL-6 from Macrophages and T-Cells)

It opsonizes dying self cells and some bacteria & activates complement

It is an infammation marker

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23
Q

Explain Liver Encephalopathy

A

If the liver is damaged (cirrhosis, Hep C..) it is unable to conjugate NH3 into Urea and toxic NH3 from protein consumption/breakdown builds up i the blood, causes brain swelling and altered mental status in end stage liver failure

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24
Q

Explain Jaundice

A

Excess Bilirubin is not broken down and recycled into bile in the damaged or immature liver. It accumulates in tissue and turns tissue orangy brown.

25
Q

Connection between edema and the liver?

A

Damaged Liver does not synthesize blood proteins and the concentration of the blood is not high enough to draw water out of the tissues so water and wastes stay put in the tissue, accumulate and cause swelling.

26
Q

Connection between Liver and Asceites

A

Damaged/Blocked liver backs blood up all along the GI tract. Fluid is forced out of blood vessels into surrounding tissue and essentially causes edema/swelling of the abdomen

27
Q

Steatorrhea

A

Failure to produce bile salts results in inability to absorb lipids which are thereafter excreted in feces which becomes urgent diarrhea

Can happen after Gallbladder removal
The Olestra “anal leakage”
Various malabsorption Diseases

28
Q

Bleeding & the Liver

A

Damaged liver doesn’t make clotting factors or normal liver can’t replace factors lost to hemorrhage fast enough

29
Q

CCK secreted from

A

I cells

specialized Entereoendocrine cells in the brush border of the duodenal epithelium

30
Q

Enterochromaffin Cells (EC Cells) loc, funct, stim

A

-Stomach, sm bowel, colon
-makes Serotonin from absorbed tryptophan, 90%
of body’s serotonin stored in EC cells
-Secrete Serotonin in resp to stretch/chemorecptor act
-Serotonin secreted by EC cells regulates:
+ Enteric NS Peristalsis
+ Stimulates Vagus to send afferent messages
to the brain (to vomit/nausea ctr- chemo
receptor signaling of toxins in the GI)

31
Q

Odansetron (Zofran)

A

5HT3 Blocker
Inhibits serotonin’s communication from gut to vomit ctr
Not sure if it works in gut, CNS or in between on vagus

  • Long QT Risk like Cisapride
  • CYP 3A4 and CYP2D6, not with macrocodes
32
Q

Cisapride (Prepulsid)

A

5HT4 Agonist
Promotes gastric motility via local effects of Serotonin
Rx for GERD & Diabetic Gastroparesis via excretion of feces

  • Long QT risk, like Zofran, banned in India for this
  • Cleared by CYP 3A4 - no cadmic w/ macrocodes (claithro, erythro, azithro)
33
Q

EnteroChromaffin-Like Cells (ECL Cells)

A

-Gastric Mucosa, beneath epithelium, near parietals in pits
-Secrete Histamine in response to Gastrin binding H1 Recpt
-Also stim chief cells to secrete pepsinogen
-Inhibited by Somatostatin (which inhibits parietal
release of gastrin and directly inhibits ECL cells)

-Also stims Pancreas to make insulin, not release it,
just a warning that some will be used and to get ready to
replace it, via release of Chromogranin A (not only cell to
make this stuff)

34
Q

B1

A

Thiamine
Yeast, Eggs, Liver nuts,veggies & Synth by Gut Flora
-Absorbed in Jejun & Ilium Folic Acid B9 required to
absorb
Deficiency = BeriBeri - neurological defecits
= Optic Neuropathy (DM often B1 def)
= Alcoholism, malnut, AIDS, DM

35
Q

B9

A

Folic Acid
Green Leafys, Avo, Yeast
Deficiency = Glossitis & Macrocytic anemia
= Neural Tube & Heart defect in fetus

36
Q

B12

A

Cobalamin
-Meat, Fish, Eggs, Milk, Bacteria produce it
-Intrinsic Factor from Parietals shepherds it thru to illiim for
Absorption

Deficiency = Pericious Anemia (loss of Intr Fact specifically)
= Megaloblastic anemia (req to ‘gather’ DNA i
RBC formation, the longer this takes the
more cytoplasm fills the RBC, hence Mega)
= Stocking Glove parasthesias
= Dementia/Alzheimers

Absorption impaired by Metformin, supplement IM or sublig

RX for Cyanide Poisoning IM Hydroxycobalamin

37
Q

B2

A

Riboflavin

-Yeast & Cereals

Deficiency= Stomatitis (PAINful red swollen tongue)
fissured mouth corners
= Cheilosis (chapped & fissured lips)
= Microcytic Anemia as req for Fe++ absorp

38
Q

Niacin

A

B3
Deficiency = Pellagra (Diarr/Dermatitis/Dementia
B3 supplementation is RX & works

               = Corn Based Populations (Africa)
                  (Masa Harina is treated and does suppl B3)

Skin Flushing “Niacin Flush” via Vaso Dilation

Increases HDL & is therefore used in hyperlipidemia

39
Q

B3

A

Niacin Meat, Fish Eggs, Seeds Avos NOT In CORN

well… it is in corn but not available unless treated with lyme first. This is the difference between Corn Meal and Masa, Masa Harina is treated with lime and B3 is bioavailable AND it makes a nice dough, whereas cornmeal does not

40
Q

B2

A

Riboflavin Yeast & Cereal

Pellagara w/o Pellagara (mouth sores not everywhere)

41
Q

Pellagara

A

Niacin Deficiency (B3)

Diarrhea, Dermatitis & Dementia

Alcoholism, Malnutrition

42
Q

B5

A

Pantothenic Acid

MEAT Royal Jelly, Whole Grain, Avos, eggs meat legumes

43
Q

Pantothenic Acid

A

B5

Req to synth Acetyl- CoA, (ACh)
(Autonomic neurotransmitter & Kreb cycle & Fatty Acid Metabolism)

May lower LDL, can’t OD on it so worth a try

Deficiency is rare: Malnutrition Neuropathy, Apathy

44
Q

B6

A

Pyridoxine

Organ Meats, Brewer’s Yeast, Avos & Eggs

45
Q

Pyridoxine (s) there are 6

A

B6

Absorbed by diffusion in Jejunum & Ilium

Essential for tryptophan conv to Serotonin

Deficiency = Serotonin Deficiency Symptoms
=Apathy/ Parkinsons Dementia

Good for Morning Sickness & Carpal Tunnel
Given to TB pts taking Isoniazid
Potentiates Levadopa

46
Q

B7

A

Biotin

Liver, Peanuts, raw egg yolks Raw egg white not good -
It binds up biotin and causes deficiency

47
Q

Biotin

A

B7

Produced by intestinal bacteria so deficiency is rare unless
gut flora are wiped out

Severe
Deficiency = Alopecia, Conjunctivitis & Dermatitis,
earning it the Vitamin H (H for hair) sobriquet

48
Q

CCK

A

I Cells secrete in duod

49
Q

Motilin

A

M Cells of duod during fasting

Stimulates MCC housekeeping waves

50
Q

Gastrin

A

G Cells Gastric Pits

51
Q

Somatostatin

A

Delta Cells, Gastric Pits

52
Q

EC Enterochromaffin Cells

A

Serotonin

stomach, sm intest and colon (and brain and lung…)

secreted in response to stretch receptor activation by a bolus, causes constriction of alimentary canal behind the bolus

Secreted extra if chemoreceptors detect toxins, whereupon it rides Afferent Vagus to the vomit ctr causing emesis and also super speeds the digestive contractions to speed toxic contents through the tract and OUT

Also to do with satiety- no need to eat more if our mechanoreceptors are already stretched to the max

53
Q

SSRIs
PPIs
Corticosteroids all linked to what condition

A

Osteopenia/porosis in post menopausal women

Yike!!, SSRI is WORSE than Steroids. Mice w/too much serotonin have osteoporosis

54
Q

CCK & Gastric Motility

A

CCK enters blood in duos, inhibits gastric motility while simultaneously causing gallbladder and pancreas to contract, flooding duodenum with the bicarb, insulin, bile and other pancreatic secretions that Secretin told them to make.

CCK reduces gastric motility by initiating inhibitory impulses at vagus.

55
Q

Serotonin and Gastric Motility

A

Increases Motility via enteric peristalsis

Can increase gastric emptying from both ends if chemoreceptors detect toxins: vomit ctr via vagus and increased contraction to get it out via enteric NS and Vagus

56
Q

MHC class II antigen HLA-DQ2.

A

celiac disease , antigen for gluten

57
Q

indirect bilirubin

A

RBC breakdown in spleen yields Heme, broken further by splenic macrophages to indir. Bilirubin, insoluble, so attached to albumin to transport and sent to the liver for either recycling into bile or conjugation into direct bilirubin for excretion via urine or feces.

58
Q

direct bilirubin

A

Conjugated in Liver to become water soluble for transport without albumin

Most is recycled into bile and is reabsorbed again and again in the ilium. 10% of bile is lost to feces though and colon bacteria ‘un-congugate’ the conjugated bilirubin in bile into UroBilirubin, the yellow brown color of feces

A small amount of conjugated/direct bilirubin is lost to urine, the pale yellow color. It gets unconjugated in the kidney into urobilirubin.

Lots of urobilirubin in the urine means there is an increased source of Heme being properly broken down -think macrocytic anemia or other source of raggy blood cells.

If there is lots of direct bilirubin in the blood- the liver is functioning but bile is probably backed up and the bilirubin is being squeezed out of the bile ducts due to increased pressure caused by blockage.

If there is indirect/unconjugated bilirubin in urine, there are holes in the nephron big enough to admit the large bilirubin-albumin complex and you should look to nephritis or ckd