Physio Flashcards
What are 6 differences between smooth and skeletal muscles?
1) Smooth: non-striated; Skeletal: striated
2) Smooth: Fusiform; Skeletal: Cylindrical
3) Smooth: Involuntary; Skeletal: Voluntary
4) Smooth: Slow contraction; Skeletal: fast
5) Smooth: phasic; Skeletal: deliberate
6) Smooth: sustained tonic contraction; Skeletal: unsustained tonic
Smooth activity of stomach and intestines are _________ active.
Phasically active
What are 4 functions of mastication?
1) Dissolve chemicals in saliva (taste)
2) Lubricate food to ease swallowing
3) Mix food with salivary enzymes (α-amylase)
4) ↑ SA of food by breaking into smaller pieces
Primary peristalsis is (voluntary/involuntary) while secondary peristalsis (voluntary/involuntary).
Primary: voluntary
Secondary: involuntary
What are the 3 phases of swallowing?
1) Oral (voluntary) phase
- chewing reflex
- food bolus formation
2) Pharyngeal phase (1-2s)
- swallowing reflex start
- respiration inhibited
3) Oesophageal phase
- 1° peristalsis
- 2° peristalsis
What happens during the pharyngeal phase of swallowing?
1) Soft palate pushes against nasopharynx
2) Food moves downwards → pushes against epiglottis to close trachea
3) Larynx moves up to meet bolus and close off airway
(respiration inhibited)
4) Upper oesophageal sphincter opens
What induces secondary peristalsis?
Stretching of esophageal wall by food bolus
What are 4 functions of the stomach?
Secretory:
1) Acid, mucous, enzymes, hormones
Motor:
2) Reservoir (proximal, fundus)
3) Churning (distal, antrum)
4) Antrum-pylorus-duodenum unit for emptying
What are 3 types of modalities of gastric relaxation?
1) Receptive (swallowing signal)
2) Adaptive (Vago-vagal)
3) Feedback (Small intestines)
Describe the pathway of adaptive gastric relaxation.
Vago-vagal:
Gastric stretch receptors → vagal afferents
→ medulla
→ vagal efferents
→ enteric nervous system
→ interneuronal circuits → inhibitory motor neurons (NO and VIP)
→ muscle relaxation
How does a vagotomy affect gastric filling?
Limits vago-vasal/adaptive gastric relaxation
→ ↑Intraluminal pressure @ ↑volumes
What are the 3 processes of gastric churning and trituration?
1) Propulsion
- bolus pushed towards closed pylorus
2) Grinding
- antrum churns the trapped material
3) Retropulsion
- bolus pushed back into proximal stomach
What are 3 intragastric factors that inhibit gastric emptying?
1) low pH
2) hypertonicity
3) fatty acids
The pyloric sphinter:
regulates ________
prevents ________
regulates gastric emptying
prevents duodenal-gastric reflux
Gastric motility is under what 2 mechanisms of control?
1) Neural
- Vagal nerve (eg. stress, nausea)
- vaso-vagal reflex
2) Hormonal
- gastrin (+)
- CCK, Secretin, GIP (-)
What are 3 hormones that affect gastric motility?
1) CCK (cholecystokinin)
2) GIP (Gastric inhibitory peptide)
3) Secretin
What is the most effective method of eliciting intestinal mobility/peristalsis?
Radial stretch of intestinal wall
What is segmentation in intestinal motility?
Local reflex
- bidirectional propulsion in propulsive segments
- mixing of bolus in receiving segments
What are migrating motor complexes?
Phases of 90-120mins of contractions
- stimulated by motilin
- occur during interdigestive period (no food)
- sweeps food and bacteria down towards colon
- inhibits migration of colonic bacteria into distal ileum
What hormone triggers the migrating motor complex during interdigestive period?
Motilin
What are the 3 phases of MMC?
Phase 1: No spike potential, no contraction
Phase 2: Irregular spike potentials, no contractions
Phase 3: Regular spike potentials, contractions
Where is the ileocaecal sphincter?
Terminal ileum
What are 2 functions of the ileocaecal sphincter?
1) regulate flow past ileocaecal junction
2) prevent reflux of colonic bacteria
What are 2 stimuli that affect the contraction and relaxation of the ileocaecal sphincter?
Relaxation: Ileum distension
Contraction: Proximal colon distension
The large intestine partakes in (propulsive/non-propulsive) segmentation.
Non-propulsive
- mix colonic contents
- slow progressive of contents
- retrograde movements
When would there be mass peristalsis within the large intestine?
1) after meal (gastrocolic reflex)
2) Defecation
3) Opiates (morphine, codeine, pethidine)
How is the gastrocolic reflex initiated?
Distension of stomach and duodenum
(vago-vagal gastro/duodenal colic reflex)
What happens when defecation is not desired?
Involuntary reflex by sacral nerves → keep external sphincter contract
What happens when defecation is desired?
1) Relaxation of external sphincter
2) Relaxation of pelvic wall muscles
3) Contraction of abdominal muscles
What happens as feces move towards the rectum?
rectum distension →
1) rectosphincteric reflex
→ relaxation internal sphincter
2) sensation to “void” (defecate)
Differentiate between active and passive distention of the rectum.
Passive: by filling of rectum
Active: triggered by threshold pressure in rectum by passive distention → active contraction of rectal smooth muscles
Differentiate within the internal and external anal sphincter.
Internal: ANS
- circular and longitudinal muscle
- high resting tone
External: voluntary
- striated muscle
What is the term for problems with swallowing?
Dysphagia
What is the term for pain on swallowing?
Odynophagie
What are 4 causes of dysphagia?
1) Abnormal coordination
2) Obstruction
3) Stricture
4) Dysmotility
5) Achalasia
What are 4 gastric secretions that are secreted into the gastric lumen?
1) HCl (Parietal)
2) Pepsinogen (Chief)
3) Intrinsic factor (Parietal)
4) Mucous and electrolytes
What are 2 gastric secretions secreted into the blood stream?
1) Gastrin
2) Ghrelin
When is ghrelin secreted?
When stomach is empty
What is the difference between satiety and satiation?
Satiety: lack of desire to eat between meals
Satiation: “fullness” after a meal
What is the effect of destruction of the ventromedial nucleus?
Ventromedial nucleus: Satiety signals
Destruction → Hyperphagia → Obesity
What is the effect of destruction of the lateral nucleus?
Lateral nucleus: Hunger center
Destruction → starvation
What is the effect of ghrelin?
Travels in bloodstream to hypothalamus → ↑ appetite
What is the effect of gastrin?
Travels in bloodstream to hypothalamus → ↑acid secretion and antral motility
How do the different parts of the stomach differ in their function?
Proximal → reservoir function
Distal → Churning function
Antrum-pylorus-duodenum unit → gastric emptying
What do parietal cells secrete?
HCl and intrinsic factor
What do enterochromaffin-like cells secrete?
Histamine
What do the chief cells secrete?
Pepsinogen and lipase
What do D cells secrete?
Somatostatin
What do G cells secrete?
Gastrin
How are parietal cells stimulated and what are the morphological changes to the cells?
Stimulated by:
i) Gastrin (CCK-B → Ca2+)
ii) ACh (M3 → Ca2+)
iii) Histamine (H2 → cAMP)
Changes:
↑ expression of apical H+/K+ ATPase (from tubulovesicles)
↑ expression of canaliculi
What is an alkaline tide in gastric acid production?
Activation of carbonic anhydrase:
H2CO3 → ↑H+ and ↑HCO3-
H+ pumped out by H+/K+-ATPase to gastric lumen (apical)
HCO3- pumped out by HCO3-/Cl- ATPase to blood (basolateral)
**all pumps driven by Na+/K+ ATPase
What are the factors that promote the activation of pepsinogen?
1) Low pH (optimal <3)
2) Pepsin (autocatalytic)
Which part of the stomach are the cells producing intrinsic factor found?
Parietal cells mainly in fundus
What is the function of intrinsic factor?
Absorption of vit. B12
- forms complex with B12 in intestine → resistant to digestion
- IF-B12 absorbed at terminal ileum
What are the factors that stimulate intrinsic factor secretion?
1) Gastrin
2) Histamine
3) ACh
Do PPIs reduce intrinsic factor secretion?
No
What are the neuronal factors involved in the stimulation of gastric secretion?
1) CNS (vagal): 30%
2) Local gastric(local reflex, vagal, gastrin-histamine): 60%
3) Intestines (nervous and hormonal): 10%
What are 4 effects of gastrin?
1) ↑HCl secretion
2) ↑Gastric and intestinal motility
3) ↑pancreatic secretion
4) Growth of GI mucosa (Trophic effect)
How does smelling good food stimulate gastric acid secretion?
Olfactory receptors → higher centers in CNS
i) ACh to parietal via vagus
ii) Vagus stimulate gastrin → parietal
How does distension of the antrum stimulate gastric acid secretion?
Local reflex → gastrin → parietal
How do gastrin related peptides/amino acids stimulate gastric acid secretion?
Stimulate G cells → gastrin → parietal cells
How does somatostatin reduce gastrin acid secretion?
Inhibits G cells → ↓gastrin
What is the functions of mucin in the gastric mucosal barrier?
Large molecules → R to digestion
→ Coat and lubricate mucosal surface
What are 2 factors that physiologically stimulate mucin expression on the gastric mucosa?
1) ACh
2) Mechanical (food)
What are 4 functions of prostaglandins in the gastric mucosal barrier?
1) Epithelial restitution (stem cells)
2) Regulate mucosal HCO3- and mucosa
3) Inhibit parietal cell secretion
4) Mucosal blood flow
What is the main defence of the gastric mucosal barrier against abrasion, HCl and pepsin?
Thick mucous layer (mucins, HCO3-)
The unstirred later of the gastric mucosal barrier, there is an inward diffusion of _______ and an outward diffusion of __________.
Inward: H+
Outward: HCO3-
What are 3 exocrine secretions of the pancreas, and the cells that secrete them?
1) Enzymes (Acinus cells)
2) Electrolytes (Ductal cells)
3) Mucin (Goblet cells)
What are 4 endocrine secretions of the pancreas, and the cells that secrete them?
Islets of Langerhans
1) Glucagon (α)
2) Insulin (ß)
3) Somatostatin (δ)
4) Pancreatic polypeptide (F cells)
Describe the 4 factors that contribute to the “autoprotection” of the pancreas.
1) Package as zymogens (inactivated)
2) Protease inhibitors (pancreatic trypsin inhibitor)
3) Compartmentalisation
4) Condensation of secretory proteins @ low pH
Acinar cell secretions are stimulated by _________.
CCK (cholecystokinin) from I cells
Ductal cell secretions are stimulated by ___________.
Secretin from S cells
What are 3 active enzymes secreted by the pancreas (do not require trypsin for activation)?
1) Pancreatic α-amylase (polysaccharide (except cellulose) → disaccharides)
2) Pancreatic lipases
- water-insoluble esters → need bile salts to work
- water-soluble esters dont need
3) Nucleases
What 4 examples of zymogens secreted by the pancreas and how are they activated?
Activated by: Enterokinase in pancreatic juice
→ cleave trypsinogen → trypsin
→ activates other enzymes
1) Trypsinogen
2) Chymotrypsinogen
3) Proelastase
4) Procarboxypeptidase A/B
What are 4 functions of CCK in the GIT?
TLDR: match nutrient delivery to digestive and absorptive capacity
1) Gall bladder contraction
2) Pancreatic acinar secretion
3) ↓ stomach emptying
4) Sphincter of Oddi relaxation
Describe the hormonal control of pancreatic secretions.
1) Cephalic and gastric (30%)
- ACh to M3 on ductal and acinar cells
- gastrin → CCK-A on acinar cells
2) Intestinal (70%)
- H+ → S cells → secretin
- protein/lipids → I cells → CCK
Describe the neuronal control of pancreatic secretions.
Vagal (+)
Where do CCK-RP and Monitor peptides come from and how do they regulate pancreatic secretion?
CCK-RP: stimulated by digested AA/FA
Monitor peptide: secreted by pancreas
Both can bind to I cells → ↑CCK secretion
- broken down by trypsin
- so when ↑food → ↓trypsin →↑CCK-RP/Monitor peptide → ↑CCK from I cells
- vice versa
In the liver, _____ cell-thick epithelial hepatocytes separates two fluid compartments: ________________
One-cell thick
- canalicular lumen (bile)
- sinusoids (blood)
The apical membrane of hepatocytes face the ___________ while the basolateral membrane faces the ___________.
Apical: canalicular lumen
Basolateral: peri-sinusoidal space (space of Disse)
The blood flow in the sinusoids and the bile flow in the cannaliculi is (parallel/countercurrent).
Countercurrent flow
Describe the flow of bile from the liver to the intestines.
Produced in liver → R/L hepatic ducts →common hepatic duct
→ gallbladder (via cystic duct)
Cystic + Common hepatic duct → common bile duct
common bile duct + pancreatic duct → sphincter of oddi → duodenum
What are 2 sources of bile secreted into the duodenum?
Hepatic and gall bladder
What are 5 components of bile?
1) Bile acids
2) Bile pigments (bilirubin)
3) Lecithin/phospholipids
4) Cholesterol
5) Proteins
6) Electrolytes
Describe the regulation of bile release.
FA in duodenum → ↑CCK
i) gall bladder contraction → ↑ bile into common bile duct
ii) sphincter of oddi relaxation → bile flow into the duodenum
What are 2 classes of bile acids?
1) 1° bile acids (cholic, chenodeoxycholic acid)
- produced in liver
2) 2° bile acids (deoxycholic, lithocholic acids)
- converted from 1° by intestinal bacteria
How are bile acids converted to bile salts?
Bile acids conjugated to glycine/taurine
What is the difference between conjugated and unconjugated bile acids?
1) More amphipathic
- easier to form micelles → aid fat absorption
- poor reabsorption → stays longer in gut
2) R to hydrolysis by pancreatic enzymes
What are 3 functions of bile acids?
1) Promote bile flow
2) Solubilse cholesterol, phospholipids in gall bladder
3) ↑ dietary lipid digestion and adsorption by mixed micelle formation
Where and how are bile acids reabsorbed?
@ terminal ileum by active Na+ dependant process
Why is bile acid reabsorption so important?
80-90% is reabsorbed (too much loss, synthesis cant keep up → ↓fat absorption)
Where is most of dietary fluid absorbed?
Small intestine
(much less in colon, very little normally excreted in feces)
What are 2 ions that are secreted in the small intestine?
1) Cl- secretion
2) HCO3- secretion
How does Cl- secretion occur in the small intestine?
Basolateral Na/K/Cl co-transporter
- driven by Na/K ATPase
Apical CFTR (Cystic fibrosis transmembrane conductance regulator)
- water follows the change in osmolarity via paracellular transport (space between cells)
How does HCO3- secretion occur in the small intestine?
HCO3- and H+ from carbonic anhydrase
HCO3- also from NBC1 (HCO3-/Na+ co-transporter)
- driven by Na/K ATPase
Apical:
1) CFTR HCO3-/CL- co-transporter
2) PAT (HCO3-/Cl- antiport)
What are 2 functions of small intestinal secretions?
1) Maintain fluidity of chyme
2) Akalinise contents (enzyme activity)
What are the components of intestinal juice, where does it come from and what is it driven by?
Intestinal juice: water, electrolytes, mucous
- driven by CFTR (Cl-secretion)
What are 4 stimulants of intestinal juice secretion?
1) Mechanical irritation of mucosa
2) Distension of gut
3) ACh (vagal), prostaglandin, guanylin
4) 2nd messenger (cAMP, cGMP, Ca)
What are 3 ions secreted in the colon?
1) Cl-
2) HCO3-
3) K+ secretion
How does the intestinal fluid in the colon differ from that of the small intestine?
Higher K+ and HCO3- secreted in colon (to buffer H+ produced by bacterial fermentation)
What are 2 stimuli that promote colonic secretion?
1) Parasympathetic nerve impulses
2) Mechanical/chemical irritation of mucosa
How is K+ secreted in the colon?
Aldosterone → Na+ influx from lumen into colonic epithelial cells
change in electrical gradient → K+ efflux into colonic lumen
What is the main driver of water and electrolyte absorption in the small intestine?
Na
What are the differences between the ions absorbed and secreted in the small vs large intestine?
Small intestine
net abs: H2O, Na, Cl, K
Secrete: HCO3
Large intestine
net abs: H2O, Na, Cl
Secrete: K, HCO3
Paracellular transport of solutes and water in the intestines is highest in ________ and decreases in __________ direction. The greatest limiting factor is the __________________.
Paracellular transport highest in duodenum, decreases arborally (down the GIT).
Limiting factor: permeability of tight junction
In transcellular transport of solutes and water in the intestines, there is higher _________________ R than in paracellular transport and may require ______________.
Higher transepithelial R, need active processes (co-transporters, exchangers: secondary active)
What is solvent drag absorption?
Solute movement coupled to fluid movement for absorption
How is K+ absorbed in the GIT?
In small intestine
- via paracellular (solvent drag)
What is the difference between the water and solvent absorption in the distal ileum/proximal colon vs the distal colon?
Distal ileum/proximal colon
- driven by electroneutral Na/Cl absorption
Distal colon
- driven by electrogenic Na absorption (aldosterone)
(tighter tight cell junctions → ↓paracellular)
How is iron absorption in the GIT adaptive?
↑Fe in Liver/Reticuloendothelial system → ↑Hepcidin production
Hepcidin → ↓ferroportin activity → ↓Fe in blood/↑Fe in ferritin in enterocytes (can be excreted in feces if enterocyte is sloughed off)
What are the 2 ways iron can be absorbed in the the GIT?
1) Heme → heme transporter → broken down into Fe2+
2) Fe3+ → reductase → Fe2+ (if needed) → DMT1
Then either:
1) Fe2+ → Ferroportin → blood → Fe3+ → Fe3+-Transferrin
2) Fe2+ → Fe3+-ferritin (stored in cell
How is B12 absorbed in the GIT?
B12 bound to food → released by enzymes/acid
→ haptocorrin from gastric glands bind to B12
→ transported to intestines
→ B12 released from haptocorrin by proteolysis
→ B12 bound to IF from parietal cells to form complex
→ IF receptors on terminal ileal enterocyte → endocytosis
What are 2 specific parts of the GIT where carbohydrate digestion occurs, each with their specific enzymes?
1) Luminal: salivary and pancreatic amylase
2) Mucosal: disaccharidases
What are the 3 products of luminal digestion of carbohydrates?
1) α-limit dextrins
2) Maltose
3) Maltotriose
(α-1,4 and 1,6 linkages that cannot be cut by amylase)
What are the 2 key transported in brush border digestion of carbohydrates?
1) SGLT (sodium-linked glucose transporter)
2) GLUT (glucose transporter)
- eg. GLUT 5 → fructose
How are (i) lactose, (ii) sucrose and (iii) amylase products (eg. maltose, maltotriose, α-limit dextrins) broken down and absorbed in the GIT?
i) Lactose → Lactase → Glucose + Galactose → SGLT1
ii) Sucrose → Sucrase → Glucose (SGLT1) + Fructose (GLUT5)
iii) Maltose, Maltotriose, α-limit dextrins → Isomaltase → glucose →SGLT1
Which part of the GIT has the highest capacity for carbohydrate absorption?
Duodenum and upper jejunum
How do the absorption of glucose and fructose differ?
Glucose: SGLT (2° active transport)
Fructose: GLUT5 (facilitated diffusion)
- most fructose rapidly converted into glucose and lactic acid within epithelial cells
How are absorbed sugars transported into the bloodstream?
Via basolateral GLUT2 (facilitated diffusion)
What are 3 types of proteases that aid in the digestion of proteins in the GIT and where are they located?
1) Gastric luminal pepsin
2) Pancreatic luminal proteases
3) Enterocyte peptidases
Where is most of dietary protein absorbed?
Duodenum and jejunum (50%)
- 20-50% in ileum
- 10% colon → digested by micro-organisms
True or false: most of the protein found in stools is a result of inefficient protein digestion in the GIT.
False.
- protein in stools is from bacterial and cellular debris
What are 2 methods of apical peptide/amino acid absorbtion?
1) Na+-dependent for L-amino acids
2) Carrier transport for Tri/Dipeptides → broken down by intracellular peptidases
How are oligopeptides absorbed in the GIT?
Via PEPT1 (peptide transporter 1)
- oligopeptide/H+- symport
What are 2 cells that partake in whole protein absorption?
1) Enterocytes
- 10% direct → intact protein
- 90% indirect → processed proteins
2) M cells
- 50/50 direct/degradative
How does lecithin and bile aid in the digestion and absorption of fats?
Bile → detergent → emulsify fats
lecithin → ↑detergency of bile
What are 3 parts of the GIT where lipases are secreted?
1) Pancreas
2) Stomach
3) Mouth (lingual lipases)
Gastric lipases work under what conditions compared to pancreatic lipases?
Gastric lipase: acidic (pH 4.5-6)
Pancreatic lipase: basic (pH >7)
Lipolysis by pancreatic lipase (glycerol ester hydrolase) is enhanced by __________ because _________
Colipase dependent
- bind tgt to form complex
→ btr access to lipids in emulsion & micelle
→ expose active site to substrate
→ target fat-water interface
What are 3 pancreatic lipases?
1) Glycerol ester hydrolase (main lipase)
2) Cholesterol esterase
3) Phospholipase A2
Micelles are very small (5nm in diameter) and contain ________________ within the interior, requiring a minimum amount of _______________.
Interior: extremely hydrophobic material (cholesterol, fat soluble vit.)
Need min. amount of bile salts
Why are micelles crucial in fatty acid absorption??
Fatty acids are highly insoluble in water
→ cannot pass through aqueous “unstirred” layer of eg. mucous
Micelles have ↑solubility in water → can pass through the “unstirred” layer to come into contact with the enterocyte membrane and diffuse into cells
What is the rate limiting step of lipid absorption from micelles?
Migration of micelle from chyme to microvilli surface
Once the micelles come into contact with the microvilli surface, lipid absorption can occur by:______________
Diffusion or carrier proteins
True or false: most of the lipid found in stools is a result of inefficient protein digestion in the GIT.
False.
Fat in stools is physiologically from colonic bacteria and desquamated intestinal cells
Where are short chain fatty acids derived from?
Synthesised by bacteria in the colon (not dietary)
- eg. acetate, propionate, butyrate
- butyrate is primary nutrient for colonic epithelial cells
Absorption of short chain fatty acids by colon also stimulate ______________.
Na and water absorption
Rank the fatty acid (short, medium, long chain) by their solubility in water.
Short > Medium > Long
True or false:
Medium chain fatty acids do not require micelle formation, hydrolysis, re-esterification nor chylomicrons and are found in the portal blood.
True
Describe the re-esterification/post-absorptive phase of long chain fatty acids.
1) Hydrolysed lipids in lumen in micelles absorbed at brush border
2) Re-esterification of free fatty acids to form cholesterol, triglycerides, phospholipids → chylomicrons
3) Exocytosis of chylomicrons into interstitial space → lymphatics (lacteals) → systemic circulation
Describe the structure of chylomicrons.
Phospholipid sphere (w apolipoproteins) with Cholesterol and triglyceride core
What are 4 classification of causes for diarrhoea?
1) Hypermotility of intestine (inflammation)
- ↓absorption and transit time
2) Hyperosmolarity (osmotic diarrhoea)
- unabsorbed nutrients (eg. lactose intolerance)
→ malabsorption
3) Loss of absorptive capacity
- loss of villi and length
→ malabsorption
4) Enhanced secretion of water and electrolytes (secretory diarrhoea)
- enterotoxins, tumours, Cl- channels
What is the definition of diarrhoea?
3 or more watery stools a day
What are 10 functions of the liver?
Synthesis:
1) Serum protein synthesis
2) Cholesterol synthesis/homeostasis
3) Bile and bile salts synthesis
Metabolic:
4) Metabolic and heat production
5) Detoxification of lipophilic compounds
6) Excretion of lipophilic waste
Storage:
7) Nutrient storage and regulation (glucose buffer)
8) Vitamin, Fe and Copper storage
9) Blood Reservoir
Immunity:
10) Immune function (Kupffer cells)
What are 3 key organs/tissues involved in nutrient/energy homeostasis?
1) Liver
2) Adipose Tissues
3) Skeletal muscles
Describe how the liver contributes to a “glucose buffer”.
Fed state: First pass
- all nutrients absorbed (except FFA by lymphatics) → released into portal vein → drain into liver
1) Liver “mops up” excess blood glucose
2) Stores glucose as glycogen
Fasting:
- ensure continual supply of blood glucose
1) Liver glycogen stores → glucose
2) Gluconeogenesis
Why do skeletal muscles lack glucose 6 phosphatase unlike that of hepatocytes?
So Glucose-6-phosphate is shunted into metabolic pathways for energy production rather than export into the bloodstream as in the liver
What are the main precursors for gluconeogenesis?
Glucogenic amino acids (eg. alanine)
Why is urea produced in the liver?
Amino group of amino acids→ ammonia → processed in urea cycle → urea
The liver is able to _______ and _________ ribonucleotides and deoxyribonucleotides.
Synthesise and salvage
What are 4 processes taht amino acids can partake in in the liver?
1) Deamination → detoxification
2) Interconversion
3) Biosynthesis (proteins)
4) Gluconeogenesis
Describe the differences in fatty acid/cholesterol metabolism in a (i) fed and (ii) starved state.
i) Fed state:
- FA synthesis → Triacylglycerides → secreted as VLDL
- Cholesterol and bile salt synthesis
ii) Starved:
- FA from adipose tissue → liver → acetyl CoA → ketone bodies
The liver detoxifies _____________ (eg. alcohol, drugs, food additives) and _________________ (eg. bilirubin) for excretion.
Xenobiotics
Endogenous compounds
What is the Cori Cycle?
Liver and muscle/non-hepatic tissue to handle lactate
Muscles/RBC:
Glucose → glycolysis → pyruvate → lactate dehydrogenase → lactate → blood
Liver:
Lactate → pyruvate → gluconeogenesis → glucose → blood
What is the glucose-alanine cycle?
Liver and muscle/non-hepatic tissue handle amino group on amino acids
Muscles:
Glucose → glycolysis → pyruvate → transamination → alanine → blood
Liver:
Alanine → NH4+ (detoxified to urea) + Pyruvate → gluconeogenesis → glucose → blood
In transamination of pyruvate, pyruvate is converted to _______ as _________ is converted to __________.
Pyruvate → Alanine
α-amino acid → α-keto acid
What are 6 chemicals measured in a liver function test?
1) Albumin
2) Coagulation tests (PTT, PT, INR)
3) Bilirubin
4) ALT (alanine aminotransferase)
5) AST (aspartate aminotransferase)
6) ALP (alkaline phosphatase)
7) GGT (ɣ-glutamyltransferase)
