Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 2 PBCP > Gastrointestinal Physiology and Metabolism > Flashcards

Gastrointestinal Physiology and Metabolism Flashcards

1
Q

describe the 4 different types of secretory glands associated with the gastrointestinal tract

A
  1. Single cell mucous glands – e.g. goblet cells. Produce mucous in response to epithelial irritation
  2. Pit glands – e.g. crypts of Lieberkuhn. contain both goblet cells and enterocytes, which are specialised secretory cells producing digestive enzymes such as sucrose, maltase and enteropeptidase.
  3. Tubular glands – e.g. oxyntic glands. These branched glands are found in the stomach and are composed of several different cells which produce multiple secretions in response to food
  4. Complex glands – e.g. salivary glands. These lie outside the walls of the gastrointestinal tract and are composed of both acinar and ductal epithelial cells. The acini are lined with 3 different types of glandular cells whose primary secretions are modified by the ductal epithelium en route to the gastrointestinal tract.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

describe the effect of increased parasympathetic activity on salivary gland function

A

increased acinar synthesis/secretion
increased ductal epithelial transport
increased blood flow via VIP, ACh
increased contraction of acinar myoepithelial cells

rapid flow of enzyme-rich saliva

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Outline bilirubin metabolism and excretion

A

it is a breakdown product of haemoglobin

transported in the blood bound to albumin

conjugated to glucuronic acid in liver to form bilirubin glucuronide which is excreted into bile canaliculi and ducts

Intestinal bacteria then convert conjugated bilirubin to urobilinogen

circulating urobilinogen = urobilin
intestinal urobilinogen = stercobilin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Outline how bile secretion is controlled

A

The mixture is secreted into the bile canaliculi to the common hepatic duct and then stored and concentrated in the gall bladder.
The presence of fatty acids in the duodenum after a meal stimulates CCK release from I cells which induces gall bladder contraction, relaxation of the sphincter of Oddi, and emptying of bile into the intestine via the common bile duct.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the functions of bile salts

A

bile salts act as a detergent to decrease surface tension and promote emulsification of fat particles, creating a large surface area for the action of lipases.

Bile salts then combine with lipid digestion products (monoglycerides, free fatty acids) to form micelles

Micelle formation is necessary for efficient fat absorption since it maintains a large surface area for lipid diffusion across the mucosal epithelium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is jaundice and describe the three forms of jaundice

A

Jaundice occurs due to elevated levels of plasma bilirubin leading to yellow discolouration of the eyes, skin and mucous membranes

  1. Pre-hepatic jaundice:
    - due to haemolysis
    - excess bilirubin production
    - increased levels of circulating bilirubin
    - e.g. sickle cell anaemia, haemolytic disease of the newborn
  2. Hepatic:
    - inability of liver to conjugate/excrete bilirubin
    - e.g. hepatitis, alcoholic liver disease
  3. Post-hepatic:
    - obstruction of bile duct
    - e.g. gallstones, pancreatic carcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Explain the role of epithelial digestive enzymes

A

The cells of the intestinal mucosa also play an important digestive function, particularly in relation to carbohydrates. Oligosaccharides and polypeptides are present in the small intestine as a result of carbohydrate digestion by pancreatic α-amylase and protein digestion by pepsin/proteases. However, the intestine is unable to absorb these and further digestion is necessary to produce monosaccharides and amino acids. This is mediated by oligosaccharidases and peptidases which are bound to enterocytes of the crypts of Lieberkuhn covering the epithelium of the intestinal brush border with their active sites exposed to the luminal contents.

oligosaccharidases digest monosaccharides;

peptidases digest amino acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe how the small intestine is specialised for absorption

A

The luminal surface of the small intestine is suitably adapted for absorption by possessing both specific transport mechanisms and a large surface area

Increase absorptive SA:

  • mucosa - into macroscopic folds which project up into lumen.
  • Microscopic mucosal projections, known as villi, which contain their own blood supply and lacteal.
  • Folding of the epithelial membrane produces numerous microvilli, giving rise to the term epithelial brush border
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Outline the absorption mechanisms for carbohydrates

A

Carbohydrates absorbed as monosaccharides (glucose, galactose, fructose)

Absorption of glucose and galactose occurs via secondary active transport, energy being provided by the Na+/K+ ATPase on the basolateral membrane. The process is Na+-dependent and relies on a Na+ co-transport carrier molecule in the luminal epithelial membrane to move monosaccharides against the concentration gradient.

In contrast, fructose absorption across the apical membrane occurs by facilitated diffusion. This requires a diffusion gradient from the intestinal lumen into the epithelium, the carrier molecule (GLUT5) simply acting to decrease the diffusion barrier created by the fatty cell membrane.

high intracellular concentrations of monosaccharides generated during absorption generate the concentration gradients required for these nutrients to diffuse across the basolateral membrane into the mucosal capillaries. For all monosaccharides, this process occurs via facilitated diffusion linked to a carrier protein (GLUT2) to increase the rate of transport through the lipid membrane.

see lecture 4 for diagram

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Outline the absorption mechanisms for proteins

A

Proteins absorbed as short peptides and amino acids via secondary active transport

using an H+ co-transport system

H+ gradient across the apical membrane is created by a luminal Na+/H+ exchanger, the energy for the process being provided by the Na+/K+ ATPase on the basolateral membrane

Several specific carrier molecules are required to link H+ movement to transport of different peptides and amino acids

Absorbed short peptides are then degraded by intracellular peptidases before transport of amino acids across the basolateral membrane into the mucosal capillaries occurs via facilitated diffusion.

see lecture 4 for diagram

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Outline the absorption mechanisms for lipids

A

see lecture 4 for diagram

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Outline the absorption mechanisms for sodium and water

A

see lecture 4 for diagram

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Outline the absorption mechanisms for lipids

A

see lecture 4 for diagram

Pancreatic lipase hydrolises triglycerides to form fatty acids and monoglycerides

these are Transported to epithelial border in micelles

Monoglycerides, FFAs enter the epithelial membrane by diffusion at the apical membrane

Monoglycerides and free fatty acids are then reconstituted into triglycerides by intracellular enzymes before being taken up by the endoplasmic reticulum and packaged within a lipoprotein coat to form chylomicrons

leave the mucosal epithelium through the basolateral lateral membrane via exocytosis, but as they are too large to enter the mucosal capillaries they pass into the intravillous lymphatics (lacteals).

then returned to the blood via the lymphatic system

Micelles recycled to ferry more lipid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Outline the absorption mechanisms for sodium and water

A

see lecture 4 for diagram

Water:

  • mostly osmosis
  • Dilute chyme which decreases intestinal osmolarity and therefore favours absorption of water

Sodium:

  • primary active transport of Na+ out of the epithelial cells (via a Na+/K+ ATPase on the basolateral membrane) into the paracellular space between adjacent cells is followed by electrostatic diffusion of Cl-
  • this creates an osmotic gradient in the paracellular space and therefore water moves in via osmosis
  • less Na+ in the cell so Na+ from intestine moves in via facilitated dissuasion
  • Movement of Na+ and H2O into the paracellular space elevates hydrostatic pressure and fluid is forced out into the interstitium
  • this helps absorption into mucosal cellsmutual dependence of Na+ and nutrient absorption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Outline the absorption mechanisms for vitamins

A

see lecture 4 for diagram

FAT-SOLUBLE VITAMINS (A, D, E & K):
- absorbed with fats in which they are dissolved

WATER-SOLUBLE VITAMINS (e.g. C, B2, Folic acid):
- generally diffuse across intestinal mucosa if taken in sufficiently high doses

VITAMIN B12:

  • needs intrinsic factor which comes from parietal cells
  • Intrinsic factor binds to vitamin B12 in the intestine
  • forms a dimer
  • protective against digestion and allows binding to the epithelial cell membrane receptor
  • Vitamin B12 dissociates from intrinsic factor within the cell and is carried in the blood bound to transcobalamin II
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Outline the absorption mechanisms for calcium

A

see lecture 4 for diagram

  • requires vitamin D - can get from diet and skin
  • regulated by parathyroid hormone
  • Parathyroid hormone promotes renal activation of vitamin D
  • increases levels of Ca2+ binding protein in the mucosal epithelium
  • increases activity of the Ca2+ ATPase in the basolateral membrane
  • increasing intestinal Ca2+ absorption
  • The activity of parathyroid hormone is inhibited by elevated plasma Ca 2+ levels thereby providing negative feedback regulation of intestinal Ca2+ absorption.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Outline the absorption mechanisms for iron

A

see lecture 4 for diagram

  • ferrous (Fe2+), rather than ferric (Fe3+), ions are absorbed
  • relies on binding to a transport protein, known as transferrin
  • Fe2+-transferrin complex then binds to an epithelial membrane receptor
  • passes into the cell by endocytosis
  • inside the mucosal epithelium, the Fe2+ is released from transferrin as is absorbed into the circulation, where it becomes bound to plasma transferrin.
  • In iron deficiency (e.g. following blood loss) the ability to absorb iron is increased, with an increased density of membrane receptors for the iron-transferrin complex.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what can deficiency in vitamin B12 cause

A

Deficiency of vitamin B12 most commonly results from pernicious anaemia, an autoimmune disease in which antibodies are produced against parietal cells leading to intrinsic factor deficiency and malabsorption of vitamin B12.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Define metabolism and metabolic rate

A

Metabolism = Sum of
CATABOLIC + ANABOLIC pathways

Sum of all chemical processes involved in:

  • Producing energy from exogenous (eg food) and endogenous (eg glycogen) sources
  • Synthesising and degrading structural and functional tissue components
  • Disposing of resultant waste products

Conversion of chemical energy to other forms of energy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Define energy balance and describe situations that affect it

A

In the steady state INPUT OF FOOD = OUTPUT OF WORK/HEAT

Input of food is balanced against the output of work and heat generated in support of key metabolic processes, such as:

(1) mechanical work of muscle contraction, cell movement
(2) synthetic reactions required for fuel storage, tissue building, generation of essential functional molecules;
(3) membrane transport - minerals, ions and amino acids;
(4) generation and conduction of electrical, chemical and mechanical signals;
(5) heat production for temperature regulation and as a result of inefficient chemical reactions; and
(6) detoxification and degradation

POSITIVE ENERGY BALANCE needed in childhood, pregnancy, post-illness/trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Describe mechanisms that influence energy intake

A

regulated by hypothalamus

  • lateral nuclei of the hypothalamus - house the main feeding centre, stimulation of which increases the desire for food
  • ventromedial nuclei serve as the satiety (feeling full) centre - if this stimulated - inhibits the feeding centre

two distinct types of neurons in the arcuate nuclei:

  1. proopiomelanocortin (POMC) neurons:
    - which secrete (alpha)-melanocyte-stimulating hormone ((alpha)-MSH) and cocaine- and amphetamine-related transcript (CART)
    - reduce food intake
  2. orexigenic neurons:
    - secrete neuropeptide Y (NPY) and agouti-related protein (AGRP)
    - increase food intake

Short term regulation:

  • nutrient related signals:
  • decreased glucose/FFAs = increased food intake
  • increased cholecystokinin (CCK) / glucagon-like peptide-1 (GLP-1) = decreased food intake
  • GI distension = vagal inhibitory signals = decreased desire for food

Long term regulation:

  • sensing of energy stores:
  • increased leptin/insulin = decreased food intake
  • Overfeeding = positive energy balance = less reward for food, increased satiety (fullness), decreased food intake
  • Energy deprivation = negative energy balance = more reward for food, decreased satiety, increased food intake
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is the equation for BMI, and what are healthy, overweight and obese values

A

weight in kg divided by height in m2

  • BMI between 20 and 25 = healthy
  • clinical terms a BMI of 25-30 = overweight
  • > 30 = obese
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is the equation for BMI, and what are healthy, overweight and obese values

A

weight in kg divided by height in m2

  • BMI between 20 and 25 = healthy
  • clinical terms a BMI of 25-30 = overweight
  • > 30 = obese
  • not a direct measure adiposity and does take in to account increased muscle mass
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what % body fat is considered obese in men and women

A

% body fat – obesity defined as >25% in men and >35% in women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Explain the central role of glucose in carbohydrate metabolism

A
  • Carbs absorbed as monosaccharides - glucose, galactose, fructose
  • Monosaccharides undergo enzymatic hepatic interconversion to glucose
  • large amounts of glucose phosphatase in liver cells - this converts glucose-6-phosphate to glucose
  • glucose is final common pathway for transport of carbs to tissue cells
  • glucose high molecular weight so needs facilitated diffusion
  • glucose transporters
  • from high to low conc
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Show how insulin secretion is regulated

A

insulin secretion turned off by reduced circulating glucose levels

amino acids:

  • mainly arginine and lysine
  • stimulate insulin secretion - promotes efficient protein metabolism

gastrointestinal hormones:

  • eg gastrin CCK, GIP and GLP-1
  • promote secretion
  • as an anticipatory response

Autonomic nervous system:
- secretion reduced by sympathetic and increased by parasympathetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

describe the metabolic actions of insulin

A

in adipose tissue:

  • increase glucose uptake
  • increase lipogenesis
  • decrease lipolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

describe the effects of insulin on glucose metabolism

A

Insulin increases facilitated diffusion of glucose

Insulin promotes hepatic glucose metabolism:
- increase in insulin:
> increase in glucokinase - increase glucose uptake
> increase glycogen synthetase - increase glycogen storage
- decrease in insulin:
> increased activity of liver phosphorylase - increased glycogen breakdown
> increase activity of phosphatase - increased glucose release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

describe the effects of insulin on glucose metabolism

A

Insulin increases facilitated diffusion of glucose

Insulin promotes hepatic glucose metabolism:
- increase in insulin:
> increase in glucokinase - increase glucose uptake
> increase glycogen synthetase - increase glycogen storage
- decrease in insulin:
> increased activity of liver phosphorylase - increased glycogen breakdown
> increase activity of phosphatase - increased glucose release

Insulin does not influence glucose metabolism in the brain:
- Brain cells freely permeable to glucose and utilise glucose as major energy substrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

describe glucagon and its action

A

Produced by pancreatic a-cells in islets of Langerhans

Secretion mainly stimulated by decrease in blood glucose

Counter-regulatory to the metabolic actions of insulin

it promotes hepatic glucose release:
- promotes glycogenolysis and gluconeogenesis

potent activation via cascade amplification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

how is glucagon secretion regulated

A

secretion stimulated by:

  • decrease blood glucose
  • increase circulating amino acids
  • exercise

secretion inhibited by:
- somatostatin - this has a general suppressive action on metabolism - extends period over which nutrients may be utilised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

describe how hormones other than glucagon regulate carb metabolism

A

adrenaline/moradrenaline:

  • α-adrenergic activation - increase glycogenolysis - increase blood glucose
  • β-adrenergic activation - increase lipolysis by adipose tissue - more free fatty acids

cortisol:

  • stimulation go hepatic gluconeogenesis - mobilisation of extra hepatic AAs
  • decrease in glucose uptake in muscle and adipose tissue
  • increase lipolysis by adipose tissue

growth hormone:

  • increase hepatic gluconeogenesis
  • increased lipolysis and fattu acid utilisation
  • decrease tissue uptake of glucose
  • increased protein synthesis

they all protect against hypoglycaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what is the difference between type 1 and type 2 diabetes

A

Type 1 Diabetes (~10 % of cases):

  • insulin-dependent
  • b-cell dysfunction
  • viral infection, autoimmune, hereditary
  • juvenile onset typically ~14 years

Type 2 Diabetes (~90 % of cases):

  • non-insulin dependent
  • insulin resistance
  • obesity-related
  • adult onset typically >30 years
34
Q

name some adverse effects of hyperglycaemia

A
  • tiredness
  • frequent urination
  • sudden weight loss
  • wounds that won’t heal
  • always hungry
  • blurry vision
  • numb or time;ing hands or feet
  • always thirsty
35
Q

describe glycosuria

A

Normally all filtered glucose reabsorbed in proximal tubule via SGLT1/2 cotransporters and GLUT2 transporters - resulting in return of glucose to circulation

  • if renal threshold go approx 10mmol/L is reached then the proximal tubule is overwhelmed and excess glucose is excreted in the urine
  • gliflozins are a drug that decrease renal glucose reabsorption and therefore decrease blood glucose
36
Q

describe glucotoxicity

A

more glucose = more reactive oxygen speicies
- reacts with or alters proteins e.g. advanced glycation end-products (AGE), glycated haemoglobin (HbA1c)

  • aberrant cellular messaging
  • chronic inflammation
  • b-cell dysfunction
  • endothelial dysfunction
  • TISSUE DAMAGE
37
Q

describe the consequences of the switch to fat metabolism in uncontrolled diabetes

A
  • increased hormone-sensitive lipase (inhibited by insulin) causes increased lipolysis
  • this means more free fatty acids taken up bu the liver - this leads to B-oxidation to form ketone bodies (acetoacetate, β-hydroxybutyrate) both of these are acidic - decrease in blood pH and causes metabolic acidosis or diabetic ketoacidosis
  • build up of H ions compete for binding sites on proteins with potassium (K+) - this means potassium is displaced and leads to hyperkalaemia
38
Q

describe the effect on body protein in uncontrolled diabetes

A

less insulin means an increased utilisation of protein and fat for energy - this leads to a depletion of body protein

therefore untreated diabetes can lead to:
- rapid weight loss - asthenia (lack of energy) - polyphagia (increased appetite) - severe tissue wasting

39
Q

describe the diagnosis of diabetes mellitus

A

Urinary glucose:
If blood glucose > ~10 mmol/L, glucose as > renal capacity for reabsorption

Fasting blood glucose and plasma insulin:

  • Normal blood glucose: 3.4-6.2 mmol/L
  • Normal plasma insulin: ~10 mU/mL (if doing this you can tell T1 vs T2)

Glucose tolerance test:
Delayed decreased of blood glucose after oral bolus
- either decreased insulin or decreased insulin sensitivity

Ketoacidosis:
decreased insulin signalling - more FFAs - β-oxidation - acetoacetate - acetone

40
Q

Explain the role of amino acids in protein metabolism

A

Proteins largely absorbed as amino acids via 2o active transport
Only small quantities absorbed at any one time as slow digestion

Circulating amino acids are taken up by cells within 5-10 minutes

Low circulating concentrations; high protein turnover between cells/tissues

Amino acids actively reabsorbed in proximal tubules - normal conditions = no amino acid in urine - if protein in tubules exceeds amount then well start seeing protein in the urine

amino acids can be converted into a wide variety of proteins with diff functions

41
Q

describe the storage of amino acids

A

Free amino acids cannot be stored

need to be converted to peptides, poly peptides and then intracellular proteins

  • circulating amino acids usually v low
  • due to reverse equilibrium od proteins
  • amino acids stored in form of intracellular proteins - if needed there broken down by enzymes and go into the blood
  • maintains low levels of circulating AAs but also means there’s a constant availability

most is stored in the liver but also in kidney and intestinal mucosa

cell has limit to amount of protein stored
excess amino acids used immediately for energy to converted to fat/glycogen

42
Q

describe transamination

A

synthesis of non-essential AAs from essential AAs

Depends on formation of appropriate α-keto acids which act as precursors

Transamination – amino group transferred from amino acid to form α-keto acid

43
Q

describe the use of proteins as a source of energy

A

Limit to the amount of protein that can be stored by each cell

Excess amino acids immediately degraded by liver starting with deamination due to activation of aminotransferases

Refers to removal of amino groups from amino acids, occurs by transamination
involving reverse process to that related to synthesis of amino acids - deamination is essentially the reverse of transamination

44
Q

describe energetic utilisation of deaminated amino acids

A

Gluconeogenesis – some products of amino acid deamination (eg. α-ketoglutarate)
can enter TCA cycle and produce glucose

Ketogenesis forming acetyl CoA or acetoacetyl CoA which enters TCA cycle OR forms ketones

45
Q

describe briefly how urea is formed by the liver

A

Ammonia released during deamination highly toxic - readily ionises to NH4+
- converted to urea which may then be excreted by the kidneys

Urea contains two NH2 groups

  • one from NH4+ (carbamoyl phosphate)
  • one from aspartate
46
Q

Outline the hormonal control of protein metabolism

A

Growth hormone:

  • Promotes synthesis of cellular proteins
  • promotes AA membrane transport and RNA transcription/translation

Insulin:

  • Promotes cellular uptake of amino acids, inhibits protein catabolism
  • increases RNA transcription/translation, inhibits gluconeogenesis
  • Lack of insulin - increased plasma AAs - energy/gluconeogenesis - muscle wasting

Testosterone:

  • Growth hormone - continual muscle growth
  • Testosterone - transient muscle growth

Oestrogen:
- minor muscle growth but insignificant versus testosterone

Thyroxine:

  • increased cell metabolism - activation of anabolic/catabolic protein pathways
  • less CHO/fat - increased protein degradation, adequate CHO/fat - increased protein synthesis

Glucocorticoids:
- increase protein breakdown, increase circulating AAs, increase hepatic and plasma proteins - increase gluconeogenesis

47
Q

describe two in born errors of amino acid metabolism

A

Enzyme defects in the urea cycle

Deficiencies in enzymes involved in metabolism of AAs

48
Q

Indicate how nitrogen balance is measured and conditions which may lead to positive or negative nitrogen balance

A

NITROGEN RELEASED DURING PROTEIN METABOLISM = NITROGEN EXCRETION

N-intake > N-loss = +ve N-balance (anabolic state)

N-intake < N-loss = -ve N-balance (catabolic state)

Measurement:
- Estimated by measuring dietary protein intake and urinary nitrogen over 24 h

49
Q

List the types of lipids and their physiological importance

Outline the pathway of lipids from ingestion to utilisation in the tissues

Describe the types of lipoproteins and understand the differences between them

Understand the key factors in the regulation of blood lipid quantity

Understand what is dyslipidaemia and why it is a health risk

A

.

50
Q

List the types of lipids and their physiological importance

A

1) Triacylglycerol/Triglyceride/neutral fat:
- carbon that’s part of the carboxylate group at the start of a fatty acid is the alpha
- carbon at the end of the fatty acid - part of a methyl group - is called an omega
- saturated - only contains single c-c bonds - meat and dairy
- unsaturated - contains at lest one c=c bond - mono contains only one double bond - mono is the healthiest fatty acid for you - poly saturated are less healthy than mono but still better than saturated fatty acids
- carboxylate group at one end and methyl group bath the other

  1. Membrane lipids:
    - Phospholipids - 2 fatty acids bound to glycerol
    - Sphingolipids - one fatty acid tail bound to sphingosine
51
Q

List the types of lipids and their physiological importance

A

1) Triacylglycerol/Triglyceride/neutral fat:
- carbon that’s part of the carboxylate group at the start of a fatty acid is the alpha
- carbon at the end of the fatty acid - part of a methyl group - is called an omega
- saturated - only contains single c-c bonds - meat and dairy
- unsaturated - contains at lest one c=c bond - mono contains only one double bond - mono is the healthiest fatty acid for you - poly saturated are less healthy than mono but still better than saturated fatty acids
- carboxylate group at one end and methyl group bath the other

  1. Membrane lipids:
    - Phospholipids - 2 fatty acids bound to glycerol
    - Sphingolipids - one fatty acid tail bound to sphingosine

cholesterol:

  • Precursor for synthesis – acetyl co A
  • no fatty acids in cholesterol molecules - made up instead of parts of fatty acids so has similar properties
  • steroid nucleus - 4 carbon hydrogen ring structures
  • in the membrane - maintain fluidity of the membrane
  • consumed in diet
  • negative feedback to inhibit own synthesis
  • cholesterol is esterized - cholesterol esters are its most efficient transport form
52
Q

name some sources of fatty acids

A
  • dietary fatty acids
  • adipose tissue
  • endogenously synthesised fatty acids
53
Q

Outline the pathway of lipids from ingestion to utilisation in the tissues

A
  • emulsified by bile
  • degradation by lipases
  • absorption and conversion into triacylglycerols
  • incorporation into chylomicrons
54
Q

what are lipoproteins

A

lipoproteins:

  • Molecular complexes that consist of lipids and proteins. They function as transport vehicles for lipids in blood plasma.
  • Lipoproteins deliver the lipid components (cholesterol and triglyceride etc.) to various tissues for utilization.
  • Differ in the ratio of protein to lipids, & in the particular apolipoproteins & lipids that they contain
  • Vary in size & density - as density increases size decreases - as triglycerides are removed from a lipoprotein the density increases
55
Q

what are the functions of apolipoproteins

A
  • Structural component of lipoproteins
  • Enable transport of lipids
  • Interact with cell surface receptors
  • Activate/inhibit enzymes involved in lipoprotein metabolism
56
Q

describe the size, major core lipids, origin and mechanism of catabolism of chylomicrons

A

see lipid metabolism lecture slide 13

size:
up to 1 um

major core lipids:
dietary triglycerides (TGs)

origin:
intestine

mechanism of catabolism:
hydrolysis by LPL in tissues

57
Q

describe the size, major core lipids, origin and mechanism of catabolism of chylomicron remnants

A

see lipid metabolism lecture slide 13

size:
30-50nm

Major core lipids:
dietary cholesteryl esters (ChEs)

origin:
chylomicrons

mechanism of catabolism:
receptor-mediated endocytosis in liver

58
Q

describe the size, major core lipids, origin and mechanism of catabolism of very low density lipoproteins (VLDL)

A

see lipid metabolism lecture slide 13

size:
40-100nm

Major core lipids:
endogenous TGs

origin:
liver

mechanism of catabolism:
hydrolysis by LPL in tissues

59
Q

describe the size, major core lipids, origin and mechanism of catabolism of intermetiede density lipoproteins (IDL)

A

see lipid metabolism lecture slide 13

size:
25-35 nm

Major core lipids:
endogenous TGs and ChEs

origin:
VLDL

mechanism of catabolism:
~50% receptor-mediated endocytosis in liver;
~50% conversion to LDL

60
Q

describe the size, major core lipids, origin and mechanism of catabolism of Low density lipoproteins (LDL)

A

see lipid metabolism lecture slide 13

size:
18-28 nm

Major core lipids:
endogenous ChEs

origin:
IDL

mechanism of catabolism:
receptor-mediated endocytosis in liver or tissues

61
Q

describe the size, major core lipids, origin and mechanism of catabolism of high density lipoproteins (HDL)

A

see lipid metabolism lecture slide 13

size:
5-10 nm

Major core lipids:
endogenous ChEs

origin:
intestine, liver

mechanism of catabolism:
receptor-mediated endocytosis in liver

62
Q

describe the exogenous lipid pathway

A

see lipid metabolism lecture slides 15-17

Removal of chylomicrons from the blood - Plasma triacylglycerol and cholesterol transport

chylomicrons bind dietary triacyglycerols and cholesterol in the intestines

they are then transported in the blood

in the bloodstream chylomicrons bind to endothelium of capillaries of skeletal muscle and adipose tissue

enzyme lipoprotein lipase hydrolyses the triacylglycerols and free fatty acids are released into the tissues

what remains is a chylomicron remnant - containing mostly cholesterol - returns from the capillaries

chylomicron remnant makes its way to the liver and is taken up by liver by LDL receptors and dietary cholesterol is delivered

bile acids and cholesterol are delivered from the liver to the intestines

63
Q

describe the endogenous lipid pathway

A

see lipid metabolism lecture slides 18-21

manufacture of lipids within the body itself and how those lipids are transported to peripheral tissues

VLDL are synthesised in the liver and they deliver endogenous triglycerides and cholesterol to the tissues

VLDL delipidated in capillaries by lipoprotein lipase - releases free fatty acids - taken up by cells of muscle and adipose tissue

glycerol backbone delivered to liver or kidney cells - to be converted to dihydroxyacetone phosphate

dilapidated VLDL emerge from capillaries as intermediated density liporoteins (IDL)

after degradation to IDL or LDL, about half are taken up by the liver via receptor-mediated endocytosis

tissues other than the liver take up cholesterol from LDL via LDL receptors

cholesterol removed from cell surface membranes by HDL - this cholesterol delivered to liver

64
Q

describe reverse cholesterol transport

A

cholesterol removed from cell surface membranes by HDL - this cholesterol delivered to liver - process still poorly understood

65
Q

describe how blood lipid levels are regulated

A

regulated by hormones

see lipid metabolism lecture slide 25

Insulin – promotion of fat synthesis and storage

promote mobilisation of fatty acids and depletion of fat reserves by promoting hormone-sensitive lipase:
Stress hormones:
- Adrenaline and noradrenaline
- glucocorticoids (cortisol)
- growth hormone

Cause mobilisation of fatty acids and depletion of fat reserves by accelerating metabolic processes:
- thyroid hormone

66
Q

describe the use of triglycerides for energy

A
  • Fatty acids enter the mitochondria
    through carnitine cycle
  • Undergo b-oxidation
  • Eventually acetyl-CoA is formed
  • Glycerol is phosphorylated
    into glycerol-3-phosphate
  • Enters the glycolytic pathway
  • Eventually acetyl-CoA is formed

Almost all cells (exception: brain tissue and red blood cells) can use fatty acids for energy

67
Q

what is dyslipidemia

what are its primary and secondary causes

A 
Higher or lower than normal concentration of lipoproteins in the plasma specifically:
↑ Total Cholesterol (TC)
↑ LDL
↑ TG
↓ HDL

Causes:
Primary:
- genetic disorders

Secondary:

  • diabetes
  • nephrotic syndrome
  • hypothyroidism
  • drug induced
  • hypertension
68
Q

what are the main sites of calcium absorption, excretion and storage in the body

A

absorption: small intestine
excretion: kidneys
storage: bones

69
Q

what are the normal plasma calcium levels

A

Normal plasma calcium levels are 2.35-2.55 mmol/L

two types:
diffusible and non-diffusible protein bound

within diffusible:
ionised (free calcium) and bound to anions

within non-diffusible:
bound to albumin and bound to globulin

70
Q

what is the effect of pH on protein bound and free calcium

A

As pH decreases, H+ displaces Ca2+ from binding sites and the amount of iCa2+ increases.

Conversely, as the blood pH increases, albumin and the globulins become more negatively charged and bind more calcium, causing the amount of iCa2+ circulating to decrease.

71
Q

what are some of the physiological functions of Calcium

A

see calcium intro lecture slide 7

  • Bones and teeth
  • Glycogen metabolism
  • Protein secretion
  • Plasma membrane integrity
  • Coagulation
72
Q

what is the action of parathyroid hormone (PTH) on bone kidney and intestine

also what are its regulators

A

Bone:

  • Short-term: rapid exchange from bone pool to ECF
  • Long-term: resorption (osteoclasts)

Kidney:

  • reabsorption of Ca2+
  • excretion of PO43-
  • formation of 1,25-dihydroxycholecalciferol

Intestine:
- Ca2+ absorption

Regulators:

  • Low calcium (Ca2+)
  • High phosphate (PO43-)
73
Q

describe the action of vitamin D on the intestine kidneys and bone

what are its regulators

A

Actions
- Intestine: enhances Ca2+ absorption
(increases Ca2+ transport proteins – calbindin-D proteins)
- Kidneys: facilitates Ca2+ absorption
- Bone: increases calcification & mineralisation
(essential for normal osteoblast differentiation & function)

Regulators of active form:

  • PTH
  • Low PO43-
74
Q

what are the causes of Rickets & Osteomalacia

A

Osteomalacia - vit D deficiency in adults

Rickets - vit D deficiency in children

  • Lack of dietary vitamin D &/or sunlight (UV)
  • Malabsorption of fats
  • Failure to form calcitriol (active vitamin D)– can be due to chronic renal failure
75
Q

who are at risk of vitamin D deficiency

A

elderly and Those from minority ethnic groups with dark skin such as those of African, African-Caribbean and South Asian origin, because they require more sun exposure to make as much vitamin D

76
Q

what is the regulator for calcitonin and what are its actions on bone and kidneys

A

Regulator:
- High Ca2+

Actions

  • overall lowers blood calcium
  • Bone: inhibits resorption
  • Kidneys: increases Ca2+ excretion
77
Q

what hormones other than calcitonin, vitamin D and PTH act on bone

A

GH, IGFs:

  • Promotes positive Ca2+ balance
  • Excess - gigantism

Thyroid hormone:

  • Essential for normal bone maturation in utero
  • Excess - osteoporosis

Glucocorticoids:

  • Small amounts essential for normal bone development
  • Excess – osteoporosis

Oestrogen & Testosterone:
- Increase bone formation

Prolactin:
- increased calcium absorption

78
Q

what are the normal levels of calcium and the abnormal levels

A

Normal calcium ranges from 2.35-2.55 mmol/L

Abnormal calcium levels >3.5 mmol/L or < 1.9 mmol/L

79
Q

what is hypocalcaemia, what are its causes and what are the clinical signs

A

decrease in serum calcium levels

Causes:

  • Hypoparathyroidism - most caused by removal or accidental injury to parathyroid glands during surgery
  • Pseudohypoparathyroidism - post receptor resistance to parathyroid hormone - target cells resistant
  • Vitamin D deficiency - vit D needed for calcium absorption

Clinical signs:
- Hallmark is neuromuscular excitability followed by tetany - because calcium usually stabilises the RMP - can reach threshold more easily - involuntary skeletal muscle contraction which can be fatal

80
Q

what is chvostek’s sign, what is a positive response and what does this show

A

elicitation - tapping on the face at a point just anterior to the ear and just below the zygomatic bone

positive response - twitching of the ipsilateral facial muscles, suggestive of neuromuscular excitability caused by hypocalcemia

81
Q

what is trousseau’s sign, what is a positive response and what does this show

A

elicitation - inflating a sphygmomanometer cuff above systolic blood pressure for several minutes

positive response - muscular contraction including flexion of the wrist and metacarpophalangeal joints, hyperextension of the fingers, and flexion of the thumb on the palm, suggestive of neuromuscular excitability caused by hypocalcemia

82
Q

what is hyperparathyroidism what are its causes and what are the clinical signs

A

increased serum calcium

Causes:

  • Primary hyperparathyroidism - problem within parathyroid glands themselves
  • Secondary hyperparathyroidism - the stimulus is low Ca2+
  • Tertiary hyperparathyroidism - after long standing secondary hyperparathyroidism

Clinical signs:

  • ‘Bones’: Bone pain
  • ‘Stones’: Kidney stones
  • ‘Groans’: GI disruption e.g. abdominal pain, peptic ulcer, lack of appetite, constipation
  • ‘Moans’: CNS disturbance - depression of nerves, muscle weakness, lethargy, cardiac conduction abnormalities

Year 2 PBCP (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions