It is the persistent inflammation and necrosis of liver for 6 mnths.

Reference- a.k. tripathi for medicine


Clinical Features:-

  • Prodromal Symptoms- nausea, vomitting, abd. Pain, headache, fatigue, malaise
  • Icteric Phase- patients notice dark urine and yellowish discolouration of skin and eyes.
  • Recovery Phase- improvement of general symptoms and diminution of jaundice
  • Signs- sclera yellow, scratch marks due to pruritus, tender hepatomegaly, splenomegaly and lymphadenopathy


  • Physical activity restricted
  • High calorie diet intake. Good protein intake
  • Drugs which are hepatotoxic to be avoided.
  • Alcohol stopped
  • Bile sequestering agents for pruritus


Reference- a.k. tripathi for medicine


Anaesthetics – local & genral

Used as

👉 Percutaneous infiltration anaesthesia ,

👉 peripheral nerve block

👉Sympathetic nerve block
👉retrobulbar block ,

👉Cadual block

👉Lumbar epidural block

Brand names.

🙏Buloc by celon
Inj – 0.25 % & in 0.5 % ( 20ml )
🙏Bupivan by Sun pharma
Inj :- 0.25% (20ml)
0.5% ( 20ml )
0.5% ( 4ml )
🙏 Marcain by AHPL
Inj:- 0.5 % ( 20ml )
Inj :- 1 % ( 2ml )

  1. Halothane
    Inhalation anesthesia

👉 used in Induction & maintenance of general anaesthesia
🙏Fluothane by AhPL
I:vap :- 100% in ( 200 , 250 , 30, 50 ml ) soln
Inhalation anaesthesia

👉 Induction & maintenance of general anaesthesia
🙏 Forane by abbott
Inhalant :- 100% in ( 100, 250 ml )

🙏Isorane by AhPL
I:sol :- 5mg/5ml in ( 100,250,30 ml )

  1. Ketamine
    & Intravenous anesthesia

,🙏Ketam by sun
Inj 10mg/ ml (10ml )
Inj 50mg / ml ( 2ml )
🙏Ketmin by Themis medicare
Inj 50mg /ml ( 10 ml )
Inj 50 mg/ ml ( 2ml )
🙏Ketsia by celon
Inj 100mg ( 2ml )
Inj 500mg ( 10ml )

I sol :- inhalation solution
Ivap :- inhalation vapour

  1. Lidocaine ( used as )
    👉 as Epidural anesthesia
    👉Pulp dilatation during phaco-emulsification cataract surgery
    👉Spinal anaesthesia
    as Intravenous
    👉Intravenous regional anaesthesia
    👉 Sympathetic nerve block
    👉 Peripheral Nerve Block
    👉 Percutaneous infiltration anaesthesia
    👉Surface anesthesia
    Mouth / throat
    👉Surface anesthesia
    as for Opthalmic region
    👉Surface anesthesia
    Rectal & topical / cutaneous
    Company names


🙏Gesican 2% gelly by AHPL ( 30ml )

🙏Lidopatch by zydus cadila
T:patch- 5%

🙏Xylocaine by AstraZeneca
T:sol:- 2% 100ml
Oint :- 5% w/w ( 20mg )
Jelly :- 2% w/w ( 30mg )

🙏Xylocard 2 % by AstraZeneca
Inj (21.3mg/ml ) 50ml soln

🙏 Xylocaine viscous by astra zeneca
T:sol :- 21.3mg/ml ( 100ml )

🙏 Xylocaine topical 4% by AstraZeneca
T:sol :- 42.7mg/ml ( 30ml )

🙏Nummet by icpa
Spy :- 15% w/w ( 100g )

Some Combinations
Lidocaine + epinephrine

🙏 Lignosafe by stedman
( Lignocaine hcl 21.3mg & adrenaline 0.0125mg/ml )
Inj in 30ml

🙏 Xylocaine with adrenaline 2% by AstraZeneca
( Lidocaine hcl 21.3mg , adrenaline 0.005mg , nacl 6mg /ml )
Inj 30ml

Some other combination
🙏 Xylocaine 5% heavy ( lignocaine hcl 53.3mg/ml , Dextrose 75mg ) inj in 2ml

& Xylocaine soln ( same dosage as above ) T:Sol 100ml by AstraZeneca

🙏 Xylocaine spray by AstraZeneca
( Lidocaine hcl 100mg , ethanol 28.29% ) 500ml
🙏Xicaine by icpa
( Lignocaine 2 percent , adrenaline 0.022mg) inj 30ml
( Lignocaine hcl 2% , adrenaline 0.009 mg ) inj 30ml
🙏Asthesia by unichem
( Lidocaine 2.5% w/w , prilocaine 2.5% )
CRM (15,30,5 )g
Crm :- cream
Tsol :- topical solution


Muhad Noorman P, Team Dentowesome, Final year

Reference: Davidsons Internal medicine , Internet

Wilson’s disease, also known as hepatolenticular degeneration and progressive lenticular degeneration, is a rare genetic disorder that causes copper overload in the body.

Common cause of liver cirrohsis in children.

Etiology:- A mutation in the ATP7B gene, which codes for copper transportation, causes Wilson’s disease

Clinical Features:-

Liver related
Nausea, weakness, vomiting, jaundice, bloating, spider angiomas, muscle cramps etc..

Memory, Speech impairments. Altered gait, personality changes, headache, insomnia etc…

Characteristic clinical signs:- SUNFLOWER CATARACT AND KAYSER-FLEISCHER RINGS. KF rings are golden brown ring like discoloration of eyes due to copper deposition.

Lab investigation:- Altered Liver enzymes
Elevated Serum copper level
Increased urinary copper excretion. Low Serum ceruloplasmin level. Liver biopsy will reveal copper deposition. Imaging like MRI/CT for lenticular imaging.

Treatment:-. Copper chelating agents like d-penicillamine, Trientine etc.. can be used. Oral Zinz tetrathiomolybdate can be given ti reduce dietary absorption of Copper.


Muhad Noorman P, Final year, Team dentowesome

Abnormal accumulation of Iron in Liver , Pancreas and heart causing widespread damage of organs resulting in cirrohsis and diabetes mellitus.

Also known as Celtic Curse or Bronze diabetes

Autosomal recessive transmission due to HEF gene mutation.

Clinical features:-

Male : Female ratio = 10:1. Weaknesses, lethargy, diabetes mellitus, liver cirrohsis , arthralgia, skin hyperpigmentation, impotence, hepatomegaly, hypogonadism.

Lab investigation:- Serum Iron
Transferrin saturation > 45%. Plasma ferritin > 200 ng/ml. Liver biopsy (gold standard) > 1000 MCG/L. DNA Mapping study for gene mutation.

Treatment:- Venesection for all people with Iron biochemical overload. Chelating agents like Desferoxamine can be also taken.


Disorders of Fat Soluble Vitamins & Protein Energy Malnutrition


Fat-soluble vitamins

  • The fat-soluble vitamins are vitamins A, D, E, and K; they are stored in fat.

Water-soluble vitamins

  • The water-soluble vitamins are vitamins B and C; being water-soluble, they are NOT stored. The exception is vitamin B12, which is stored in the liver.

Fat malabsorption

  • Fat malabsorption is a key cause of vitamin A, D, E, and K deficiency.
    • Fat malabsorption commonly accompanies celiac disease, cystic fibrosis, pancreatic exocrine insufficiency, biliary obstruction, colitis, and can occur iatrogenically (albeit unintentionally) with laxative abuse via excess mineral oil intake, in particular.
    • Vitamins and minerals serve as coenzymes or hormones in key metabolic pathways, thus we can infer that their disorders lead to metabolic dysregulation of these pathways and dysfunctional assembly of key structural components.
  • Vitamin A (retinol) deficiency most notably causes night blindness.
  • Vitamin D deficiency most notably causes bone anomalies.
  • Vitamin E (tocopherol) deficiency most notably causes anemia.
  • Vitamin K deficiency most notably causes coagulopathy.



  • Indicate that it’s found in leafy vegetables (eg, carrots) meats, and dairy products.
  • It’s found as carotenoids that are metabolized in the body to active vitamin A where its stored in liver cells.

Clinical presentations

  • Indicate that night blindness is a key vitamin A deficiency.
    • To remember this, we draw a set of rod and cone photoreceptors because vitamin A is best known for its role in vision where it’s a key pigment in rods and cones.
  • It prevents the epithelia from undergoing squamous metaplasia – a further differentiation into keratinized epithelium.
  • Indicate that vitamin A deficiency manifests with ocular keratinization: specify the dry eyes (xerophthalmia), which specifically begins with drying of the cornea (xerosis conjunctivae) from keratinization of the lacrimal and mucus-secreting epithelium.
  • Show that, later, the keratin debris builds-up as Bitot spots (small opaque spots), which roughen and destroy the cornea.
  • Next, indicate that keratinization (squamous metaplasia) occurs in the mucus-secreting epithelium of the lungs and kidneys and, as well.
  • Vitamin A also has additional important metabolic effects, especially in fatty acid metabolism.
  • It plays a role in infection control, so indicate that immune deficiency is a consequence of vitamin A deficiency.
    • Thus infectious diarrhea in a newborn can be lethal because it can weaken the host’s immune system when it wastes the newborn’s low supply of vitamin A.


  • Now, consider that vitamin A is used to treat AML: acute promyelocytic leukemia; all-trans retionoic acid induces the ultimate apoptosis of acute promyelocyctic cells.
  • More commonly, it’s used to treat acne but can have significant teratogenicity.

Side Effects

  • Acutely, it causes:
    • GI upset
    • Visual disturbance
  • Chronically it causes:
    • Pseudotumor cerebri, which is a syndrome of pathologic increased intracranial pressure that manifests with headaches and a classic intermittent “rushing” sound.
    • Hepatotoxicity (remember it’s stored in the liver).
    • Alopecia.
    • Arthralgias.



  • Indicate that, for the most part, humans derive vitamin D in the form of vitamin D3 (cholecalciferol).
    • Vitamin D3 is derived from its endogenous synthesis in the skin from its precursor (7-dehydrocholesterol) in a photochemical reaction that involves solar/artificial ultraviolet light.
  • Write that vitamin D2 is the plant form, called ergocalciferol or ergosterol.
  • Indicate that the liver stores vitamin D as 25-OH-Vit. D (vitamin D undergoes 25-hydroxylation in the liver.)
    • Note that we use vitamin D without a subscript, here, because the source (D2 vs D3) is unidentified.
  • Draw a kidney and indicate that it releases 1-alpha hydroxylase, which fully activates vitamin D into 1-25 dihydroxyvitamin D [1,25(OH)2D] (calcitriol): it is the fully biologically activated form.
    • Vitamin D undergoes 1-alpha-hydroxylation in the kidney.
Note that Vitamin D2 is less bioactive than vitamin D3, so you’ll often see vitamin D3 used in reference to biologically active vitamin D.

Causes of vitamin D deficiency

  • Inadequate sunlight exposure
  • Malabsorption
  • Liver failure
  • Renal failure (renal osteodystrophy)

Clinical Presentation

  • Indicate that in children, vitamin D deficiency presents as rickets, which manifests with bowing of the legs and shortening of bones because of its impact during bone growth.
  • In adults it presents as osteomalacia, which manifests with softening of bones.

Vitamin D Toxicity

  • Regarding vitamin D excess, draw an osteoblast and show that vitamin D, along with PTH, is a key stimulus for osteoblast release of RANKL, which promotes osteoclast formation.
  • Thus, vitamin D excess promotes bone loss and excess calcium in the blood and urine, which manifests with stupor and coma.


  • Draw a RBC and indicate that vitamin E is an antioxidant that protects RBCs and membranes from free radical damage.

Clinical Presentations

Hemolytic Anemia

  • Indicate that deficiency of vitamin E manifests with hemolytic anemia.
    Spinocerebellar ataxia
  • Draw a cross-section of a spinal cord.
  • Indicate that vitamin E deficiency may present with spinocerebellar ataxia and most closely resembles Friedreich’s ataxia – so we draw an axial section of Friedreich’s ataxia, now.
  • Vitamin E deficiency presents in late childhood or early teens with symptoms of progressive ataxia and clumsiness, with exam findings of:
    • Large fiber sensory loss
    • Arreflexia with positive Babinski signs
    • Spinocerebellar/cerebellar signs of dysdiadochokinesia and dysarthria
  • Note that vitamin E deficiency is often mistaken for B12 deficiency because of the combination of motor and sensory findings but, importantly, in B12 deficiency there is a megaloblastic anemia with hypersegmented neutrophils and elevated serum methylmalonic acid levels – which are NOT present in vitamin E deficiency.



  • Indicate that vitamin K is derived from the diet (especially green, leafy vegetables) and from bacterial production in the proximal intestine.
  • Draw a liver and small intestine.
  • Show that vitamin K is integral for hepatic synthesis of prothrombin (which is factor II) and factors VII, IX, and X, and also protein C and protein S, which all contain 4-6-gamma-carboxyglutamate residues.
    • Vitamin K (hydroquinone) is necessary for the carboxylation of glutamate residues to form these rare amino acids.

Warfarin & Vitamin K Recycling

  • Indicate that vitamin K hydroquinone is oxidized to vitamin K epoxide via vitamin K epoxidase.
  • Then, show that the epoxide is reduced back to the hydroquinone in two steps vitamin K quinone as an intermediary.
  • Show that warfarin blocks each of these steps: the reduction of the vitamin K epoxide back to vitamin K quinone (via vitamin K epoxide reductase) and also the step back to the hydroquinone (via vitamin K quinone reductase).
    • Thus, warfarin promotes bleeding via inhibition of vitamin K epoxide reduction.
  • If there’s enough vitamin K in the diet, this recycling can be deemed irrelevant and the creation of coagulation factors will continue.
  • On the contrary, if the quantity of vitamin K present in GI tract is insufficient, or it is not properly absorbed and transported to the liver, thrombin production and clot formation will be impaired and bleeding disorders will ensue.

Vitamin K deficiency syndromes:

  • Neonatal hemorrhages occur secondary to sterile intestine and inadequate vitamin K in the breast milk.
    • Vitamin K is present only in very low concentrations in human milk and very little vitamin K actually crosses the placenta from mother to infant, so to prevent vitamin K deficiency in the newborn, intramuscular or oral vitamin K prophylaxis is necessary
    • Newborns are given an injection of vitamin K at birth to prevent vitamin K deficiency.
  • Indicate that prolonged antibiotic-use can also wipe-out intestinal bacteria and cause vitamin K deficiency.
  • Then, indicate that liver failure is a common cause of vitamin K deficiency because the coagulation factors, themselves, are synthesized in the liver, which commonly accompanies a prolonged PT/INR with normal fibrinogen concentration and normal platelet count.
    • In fact, a tip-off of liver failure is an elevated INR in a patient not already on warfarin.


  • Denote that in kwashiorkor there is malnutrition with severe protein depletion.
  • Denote that marasmus refers to malnutrition from generalized calorie deficiency.


  • Indicate that the loss of plasma oncotic pressure leads to peripheral edema, which, to some extent masks the visceral wasting, and is associated with:
    • Protuberant belly
    • Edematous feet
    • Fatty liver from loss of apolipoprotein synthesis
    • “Flaky paint” skin appearance so named because it alternates between hyper- to hypo- pigmentation
    • Shiny skin and alopecia


  • We show a classic picture of a purely wasted thorax from starvation.
  • There’s pure wasting.
  • Growth retardation.
  • Anemia.

Summary Distinction

  • Marasmus patients have an emaciated appearance rather than a swollen appearance because it is typified by a loss of body fat and muscle whereas kwashiorkor results in a loss in plasma oncotic pressure, which produces signs of swelling from edema.

Neural Control of GI Motility


Intrinsic control

  • The Enteric Nervous System (ENS):
    • Is intrinsic to the GI wall.
    • Runs the length of the GI tract.
    • Primarily coordinates local activity in the digestive tract via two key nerve plexuses:
  1. The submucosal plexus (aka Meissner’s plexus)
  2. The myenteric plexus (aka Auerbach’s plexus)

Extrinsic control

  • Parasympathetic innervation stimulates digestion: it stimulates GI motility and the secretion of hormones and digestive juices.
    • Remember its tagline is “Rest and Digest”.
  • Sympathetic nervous system inhibits digestive activity.
    • Remember its tagline is “fight or flight” – neither of which have anything to do with digestion.


Anatomy of the digestive tract.

From inside to outside:

  • The GI lumen
  • The mucosal layer
    • Epithelial layer
    • Lamina propria
    • Muscularis mucosae
  • The submucosal layer
    • The submucosal plexus (Meissner’s plexus) lies within the outer portion of this layer.
  • The smooth muscle (muscularis externa) layer.
    • The inner, circular layer.
    • The myenteric plexus (Auerbach’s plexus) lies in between the inner, circular and outer, longitudinal layers.
    • The outer, longitudinal layer.
The different orientations of the inner, circular and outer, longitudinal muscle layers allow us to distinguish them.
  • The adventitia/serosa layer; it’s serosa within the abdominal cavity.


Parasympathetic nervous system

  • Cranial nerve 10 (the vagus nerve) innervates the gut.
    • It innervates the upper 2/3 of the GI tract (ie, the foregut and midgut).
    • It is this wandering nature of the vagus nerve all the way to the gut that give it its name “vagus,” which is Latin for “wandering.”
  • Spinal neurons S2 to S4 of the intermediolateral cell column of the sacral spinal cord innervate pelvic splanchnic nerves, which innervate the gut.
    • They innervate the lower 1/3 of the GI tract (ie, the hindgut).

Sympathetic nervous system

  • Originates from the T5 to L2 neurons of the intermediolateral cell column.
  • Abdominopelvic splanchnic nerves innervate prevertebral ganglia, which innervate the GI tract.


Extrinsic neuronal input innervates the myenteric plexus

  • Show the extrinsic neuronal input converge on a neuron in the myenteric plexus.
  • Show it then innervate a neighboring neuron,
  • which extends into the submucosa to innervate a neuron of the submucosal plexus,
  • which then innervates the muscular layer of the mucosa to activate or inhibit GI motility.



  • Acetylcholine INcreases GI motility (it’s the major parasympathetic neurotransmitter – the “D” in the “SLUDS” acronym stands for defecation or diarrhea.
  • Norepinephrine DEcreases GI motility (it’s the major postganglionic sympathetic neurotransmitter).
  • Opioid peptides DEcrease GI motility.
  • Serotonin INcreases GI motility – serotonin syndrome causes diarrhea.


  • Amitriptyline decreases circulating acetylcholine, so it decreases GI motility.
  • Donepezil increases circulating acetylcholine, so it increases GI motility.
  • Beta-blockers decrease circulating norepinephrine, so they increase GI motility.
  • Venlafaxine increases circulating norepinephrine, so it decreases GI motility.
  • Morphine is an opioid agonist, so it decreases GI motility.
  • Naltrexone is an opioid antagonist, so it increases GI motility.
  • Quetiapine decreases circulating serotonin, so it decreases GI motility.
  • Citalopram increases circulating serotonin, so it increases GI motility.

Protection in the Digestive Tract


Digestive tract utilizes various mechanisms to protect the body (internal environment) from the external environment.
It specifically protects against:

  • Chemical damage
  • Exposure to toxins
  • Microorganism entry


(found throughout the entire GI tract)

1. Tight junctions

  • Dense network of claudins and other proteins just below the apical surface of the GI epithelium.
  • Intrinsic barrier of the digestive tract. They form a nearly impermeable barrier that prevents GI tract luminal contents from freely leaking through the mucosal layer.
Tight junctions prevent entry of microorganisms and other potentially harmful substances or toxins (such as HCl produced in the stomach) into the digestive tract wall.

2. Mucus lining

  • Feature of all mucous membranes (mucosa).
  • Mucus = alkaline (bicarbonate) secretion that protects against shear stress and chemical damage throughout the digestive tract.
    Secreted by:

1. Mucous cells in oral cavity

  • Forms mucus lining
  • Secreted as a component of saliva to primarily aid food bolus formation.
  • Minor protective role in the oral cavity (protects the mouth from acidic food and pathogens)

2. Mucous neck cell in stomach.

  • Mucus lining provides a chemical barrier between the stomach lumen and its epithelium
  • Neutralizes acidic secretions during a meal (with its bicarbonate component), and
  • Prevents autodigestion of the mucosa by proteases.

3. Goblet cells in small intestine.

  • Mucus lining continues as a chemical barrier between the acidic chyme present in the intestines and the intestinal mucosa.

Unique protective features in these three GI organs.


Secretes saliva, which contains:

  • Lysozymes, which lyse bacteria.
  • IgA antibodies, which maintain mucosal immunity, and
  • Defensins, which are host defense antimicrobial peptides of innate immunity.


Parietal cells

(in the epithelium of the mucosal layer, which lines the lumen of the stomach)

  • Secrete HCl, which primarily digests protein; however,
  • HCl creates a harsh environment, which kills many microorganisms. The gastric mucosa is largely protected from this harsh environment by the alkaline mucus lining.

Clinical Correlate: Gastric Ulcers

  • Breaks in the mucosal barrier exposes the GI wall to corrosive HCl and proteases
  • Causes gastric wall erosion and inflammation
  • Common cause: H. pylori (bacteria) is a common cause of gastric ulcers, which erodes the epithelial barrier.
  • Ulcers can also occur in lower esophagus and in the small intestine (specifically, the duodenum).

High Cellular Turnover Rate

  • GI epithelium sheds frequently as it becomes damaged from continued exposure to its lumen’s harsh chemical environment and continuous shear stress gastric motility.
  • Regeneration: epithelial stem cells replenish damaged or dead epithelial cells.
  • The GI epithelium divides, or turns over, almost constantly to replace damaged cells with new, mature ones – unlike the heart, which almost never replaces its cardiac cells.

Stem cells

  • Located at the top of gastric glands
  • Replenish gastric secretory and mucous cells that protect the stomach surface.


Paneth cells

  • Found in its villi crypts
  • Contain secretory granules filled antimicrobial peptides, which are secreted into the GI lumen.
  • Provide another layer of host defense in the small intestine.

Stem cells

  • Replenish damaged, or dead, absorptive and goblet cells that are shed from villi; they reside adjacent to paneth cells in villi crypts.

Paneth cells = “protectors of stem cells”

  • Secrete factors to maintain these stem cells to promote cellular renewal.
Note: Although the digestive tract relies on high rates of cellular division to replace old, damaged cells – this also corresponds to higher rates of mutations and, thus, increased incidence of cancer in GI epithelium (carcinoma).

Liver and Gallbladder Physiology


Digestive function

  • Bile synthesis and secretion

Other functions

  • Nutrient metabolism
  • Synthesis of plasma proteins
  • Secretion and modification of hormones
  • Storage of essential molecules
  • Removal of aged blood cells
  • Detoxification


  • Muscular sac
  • Stores and concentrates bile (which is synthesized in the liver)


  • Cholesterol-derived and alkaline
  • Secreted by the liver
  • Stored in the gallbladder.
  • Released into the digestive tract postprandially (following ingestion of a meal) upon sphincter of Oddi opening.

Bile Secretion

Regulated by secretin and CCK


  • Secreted from the duodenum in response to acidic chime in the duodenum
  • Acts on the liver to stimulates bile secretion.
  • Bile (which contains bicarbonate) neutralizes the acidic chyme.


  • Secreted from duodenum in response to fatty acids present in the chyme
  • Acts on the gallbladder – produces gallbladder contraction
  • Acts on sphincter of Oddi to promote its relaxation
  • Thus, stimulates bile flow into the duodenum – the bile salts (another major component of bile) can emulsify fats (like a detergent) for their digestion and subsequent absorption in the small intestine.
Note: bile also contains cholesterol, lecithin (phospholipids), bile pigments, and trace metals.

Bile Salt Recycling in Enterohepatic Circulation

  • Bile salts pass down the length of the small intestine to the ileum
  • Reabsorbed into circulation at the ileum (they the enter recycling pathway: enterohepatic circulation).
  • Travel through the hepatic portal vein back to the liver where they are recycled and re-secreted into newly formed bile.
Note: The hepatic portal vein drains nutrient-rich blood from the small intestine to the liver for metabolic processing.
  • Small amount of bile salts continues through the rest of the digestive tract; approximately 5% of bile salts are eliminated in feces (along with other bile components).
Note: The liver synthesizes more bile salt from cholesterol to account for its loss.

Bile Salt Structure

Bile Salts = Amphipathic molecules, meaning they have hydrophobic and hydrophilic sides.

  1. Cholesterol precursor = hydrophobic portion, the cholesterol precursor,
  • Composed mainly of non-polar hydrocarbons, which interact with the lipid droplets.
  1. Polar hydroxyl and carboxyl groups = hydrophilic portion, polar hydroxyl and carboxyl groups
  • Exposed to the surrounded aqueous solution.

Fat Emulsification

Bile salt’s amphipathic nature aids in fat digestion.

  • Bile salts and phospholipids (another amphipathic molecule and emulsifying agent) increase the surface area of large fat globules
  • Aid in their breakdown into smaller emulsification droplets and prevent their reaggregation.
    Lipid droplets comprise triglycerides.
    Lipase, with the help of colipase, digest triglycerides into their simpler components:

Monoglyceride (glycerol), and

[Two] fatty acids.

which are absorbed by the small intestine.

  • Bile salts arrange the monoglyceride, fatty acids, and phospholipids to form spherically-arranged micelles.
  • Promoted by amphipathic nature of fatty acids and phospholipids promotes this spherical formation
  • Micelles continuously form and breakdown.

Micelles = Holding stations for digested fats

  • Continuously exchange lipids with the surrounding solution.
  • Form to keep otherwise insoluble fats in small, soluble aggregates.
  • Break down to replenish digested fat products that are absorbed.