week 3 recap- water, membranes, glycolysis and kerbs and diet

Question 1

names of vitamins:

Answer 1

vitamin a- retinol
vitamin B2 - riboflavin
vitamin C- ascorbic acid
vitamin D- calciferol
vitamin E- tocopherol
omega 3- alpha-linolenic acid

link to nhs websoite with more vitamins- expected to know

Question 2

to work out base metabolic rate

Answer 2

1 kcal/kg/hour (times weight by hours by 1)

Question 3

rate limiting step in Krebs cycle

Answer 3

from isocitrate to alpha-ketoglutarate is rate limiting (isocitrate dehydrogenase)

Question 4

rate limiting enzyme in glycolysis

Answer 4

PFK-1

Question 5

what is a kinase

Answer 5

enzyme that move phopshate groups

Question 6

components of sucrose and lactose

Answer 6

sucrose- fructose, glucose

lactose- glucose and galactose

Question 7

protein requirment

Answer 7

protein requirement: 0.8g/kg a day

Question 8

mass of storage of excess energy e.g. fat, carbihydrate and protein and where they’re stored

Answer 8

• fat- adipose (only 15% water), 15kg of triglycerides
• carbohydrate- as glycogen in liver and muscle, can store 200g in liver, can store 150g muscle
• protein- muscle (80% water), 6kg in muscle

Question 9

values of kcal/g for each

Answer 9

values for typical 70kg man:

carbohydrate- 4kcal/g
protein- 4kcal/g
alcohol- 7kcal/g (8g in 1 unit of alcohol)
lipids- 9 kcal/g

Question 10

what increases BMR

Answer 10

basal metabolic rate lowers:

• age
• sex
• dieting/starvation
• hypothyroidism
• decreased muscle mass (less of you so need less energy needed)

Question 11

What increases BMR

Answer 11

basal metabolic rate increases:

• high BMI (more of you so more energy needed)
• hyperthyroidism
• low ambient temperature
• fever/infection/chronic disease
• caffeione (stimulant)

Question 12

is spleen endocrineis skin endocrine?

Answer 12

yes, produces vitamin D (is a hormone)

Question 13

name the endocrine organs and other organs that have endocrine function?

Answer 13

hypothalamus, pituitary, thyroid, parathyroid, pancreas, adrenal, ovary, testis
endrocrine funtion: skin, heart, gut

Question 14

vitamnin C- scientififc names, where found and uses

Answer 14

vit C (ascorbic acid) found in fresh (not cooked) fruit and veg, used in collagen syntheiss, improves iron absorption, antioxidant, water soluble - creates expensive urine

Question 15

vitamin B12- scientififc names, where found and uses

Answer 15

Vit b12: (cobalamin) meat, dairy eggs etc., helps with protein synthesis, DNA syntheiss, regenerate folate, fatty acid synthesis, energy production

Question 16

vitamin K scientific names

Answer 16

Vit K- (phylloquinone, menaphthone

Question 17

what vitamins are fat soluble

Answer 17

A, E, D ,K

Question 18

what happens during starvation

Answer 18

• reduced insulin secretion
• glycogenolysis (gkycogen stored in liver broken down)
• brain requires 150g glucose/day
• longer fasts need glucogenesis (makes glucise from non-lipid sources)

Question 19

Draw glycolysis chain

Answer 19

did you do it ;)

Question 20

regulation of glycolysis

Answer 20

PFK1 affected by many moelcules:
ATP- inhibitor (stop)
citrate- inhibitor, accumilation (stops)
AMP (adensosine monophosphate)- activator (go)
fructose 2,6 bisphosphate - regulator (go)

Question 21

draw krebbs cycle

Answer 21

did you do it ;)

Question 22

krebs cycle regulation of diffrent hormones:
pyruvate dehydrogenase
citrate synthase
isocitrate dehydrogenase
alpha- ketoglutarate

Answer 22

pyruvate dehydrogenase - activated by ADP, inhibited by ATP, NADH, Acetyl CoA
citrate synthase- activated by ATP, NADH, citrate
- isocitrate dehydrogenase- activated by ACP, inhibited by ATP, NADH
- alpha-ketoglutarate dehydrogenase- activated by Ca, inhibited hy ATP, NADH, Succinyl Co2, GTP

Question 23

use of pyruvate after glycolysis (aerobic and anaerobic)

Answer 23

• anaerobin conditions:
  lacatate formation is catalysed by lactate dehydrogenase, regeneration of NAD
• aerobic conditions:
  eneters mitochondria converted to Acetyl Coa and CO2 by pyruvate dehydrogenase, acetyl CoA can enter kreb’s cycle for more energy production

Question 24

oxidatave phosphorylation

Answer 24

occurs in inner mitochondrial membrane in areobic conditions

release majority of energy during cellualr respirtation

reduced NADH or FADH2 from glycolysis or krebs’ cycle are oxidised and their elctrons passed through ETC. The final electron acceptor is O2.

energy relased by this process in firm of ATP

• NADH and FADH2 are oxidised and pass electrons to ETC. These carriers accept electrons and pass them on in redox reaction.
• electrons passed doen ETC to final elctron acceptor- oxygen (therefore water formed)
• The free energy is used to ‘power’ the movemnt of H+ ions accross the inner membrane creating a proton motive gradient
• ATP is then produced as protons pass back through ATP synthase

Question 25

lipid absorption and transport process, 8 step

Answer 25

1. bile salts emulsify fats in smalla intestine 2. intestinal lipases degrade triglycerides 3. breakdown products such as fatty acids are taken up by intestinal mucosa and converted to triacylglycerides 4. Triacylglyceride are then incorporated with cholesterol and approteins into chylomicrons 5. chylomicrons move through lymphatic system and bloodstream to tissue. 6. Lipoprotein lipases activated by ApoC-II in the capillary, release fatty acids and glycerol 7. fatty acid enters cell 8. fatty acids are oxidiesd as fuel or reseterfired as storage (myocytes or adipocytes)

Question 26

draw fatty acid beta-oxidation chain

Answer 26

in hand written notes or ppt

Question 27

draw fatty acid activation chain

Answer 27

in hand written notes or ppt

Question 28

draw ketogenesis chain

Answer 28

in hand written notes or ppt

Question 29

regukation of ketogenesis

Answer 29

-release of free fatty acids, increases ketogensis (more acetyle CoA produced) -high concentartion of glycerol-3-phosphate in liver incraeses triglyceride production, reducing fatty acids reducing acetyl CoA production -high ATP demand, acetyl CoA is used in krebs -dependent on presnt of glucagon (activation) or insulin (inhibition)

Question 30

clinical significance of ketogenesis - presenting symptoms, groups that may present, why symptoms present

Answer 30

Ketoacidosis: - presnting symptoms: hyperventilation and vommitting Insulin deficiency: (when inadequate insulin or increased requiremnt e.g. infection, trauma hyperglycaemia (high blood glucose) and production of ketone bodies Alcoholic: high blood ethanol, and likely depleted proetin and carb stores (tend to eat less) impaired gluconeogenesis, decreased inslulin and increased glucagon, as well as high ethanol levels itself: all increase lipolysis (free fatty acids) therefore increased ketone production. acidic blood- impairs imbility of haemoglobin- analysis of blood gases, low pH, pO2 is high body is hyperventilating to remove CO2 (which is acidic), causes hyperventilating and high pO2 HCO3 is used to incraese pH of blood (mop up acidity) so levels are low as lots being used.

Question 31

what casues acetyl CoA to be converted into ketone bodies

Answer 31

shortages of cabohydrates, happens very very low levels in mormal physiology, The heart and skeletal muscles preferentially utilise ketone bodies for energy preserving glucose for the brain.

Question 32

types of communication in and between cells

Answer 32

- autocrine (cells talking to itself, signal molecule relased by cell and bing to receptor on same cell) - paracrine (signal between neighbouring cells, short distances, signal that's easily inactivated e.g. interleukins in immune system, Platelet derived growth factor PDGF and regulates cell growth) - endocrine (cell talks to other cells elsehwere in body by release of hormones into blood)

Question 33

3 types of hormones, description, properties and speed of response, example

Answer 33

Amino acid derivative hormones: - very small, often made from tyrosine e.g. adrenaline, quick response Peptide hormones: - made of amino acids, vary in size, some carbohydrate side chain (glycoprotein) , hydrophillic, quick response e.g. insulin, stored in secretory granules (therefore can be quickly released) Steroid hormone: - derived from cholesterol, differnet enzymes modify cholsetrol to produce variety of hormones, hydrophobic therefore must move in blood within transport protein, can dissolve in lipids, slower response as it affects DNA e.g. testosterone in puberty

Question 34

extra-cellular fluid components

Answer 34

cations- sodium, main contributor anions- chloride and bicarbonbate glucose and urea proteins= produce coloid oncotic pressure

Question 35

intra-cellular fluid

Answer 35

main cations presnt is potassium

Question 36

why is water with no salts etc. not given to patients

Answer 36

causes haemolysis of cells

Question 37

dehydration:

Answer 37

movement of water from ICF to ECF (instatitial fluid and plasma) which stimulates osmoreceptors to cause thirst, posterior piruitary releases ADH which affects PT and DT in kidney, this increases water intake, restore ECF osmolarity

Question 38

types of membrane proteins

Answer 38

peripheral- loose attachment integral- sits within membrane

Answer 39

One of either… Serine (PS - phosphatidyl-serine) Choline (PC - phosphatidyl-choline) Inositol (PI - phosphatidyl-inositol) Ethanolamine - PE (phosphatidyl-ethanolamine) Sphingomyelin - SM SM and PC found on outer PS, PI, PE found on inner

Question 40

body weight distrubutions of water in 70kg male

Answer 40

60% of body weight is water 42l- 40% intracellular 28l, 20% extracellular 14l (of this 3l intravascular and 11l interstitial)

Question 41

how to estimate plasma osmality

Answer 41

Estimated plasma osmolality = 2[Na] + 2[K] + urea + glucose mmol/L

Question 42

normal plasma osmolality

Answer 42

Normal plasma osmolality 275-295 mmol/kg

Question 43

changes in ECF volume, renin-angiotensisn-aldosterone system response:

Answer 43

1. hormone regulated, kidney detects lower pressure due to fall in ECF, causes renin to be produced by granules in Renal juxtaplomerluls appuratus, rudes Na to DCT 2. renin cleave angiotenesin from liver converting it into angiotensin I which is converted to angiotensisn II by ACE, 3. adrenal gland detects this and secreted aldosterone (causes kidneys to Na, Cl reabsoprtion and K excretion, H2O retention) causing increase in sympathetic activity (increase noradrenaline and therefore vasoconstriction and increase bp) - this is badly explained, need to know more level of detail

Question 44

excess water- poetential risks

Answer 44

Hyponatraemia (blood sodium too low), low ECF osmolality, flow from ECF to ICF, increases pressure on organs Cerebral overhydration -Headache -Confusion -Convulsions

Question 45

Types of oedema:

Answer 45

inflammatory oedema (vasodilation occured so more gaps in endothelium incraes permeablity, leakage of albumin and fluid less oncotic pressure pulling it back) venous oedema (venous end dilates due to gravitational forces, increased water leaving even in venous end due to high pressure) lymphatic oedema (issues in lymphatic system or too much fluid within lymphatic system) hypoalbuminaemic oedema (reduced albumin so reduced coloid pressure bringing water back in at venous end)

Question 46

what is a pleural vs serous effusion

Answer 46

pleural- between pleura surounding lung should normally have little liquid in and effusion is when too much fluid gathers (lymphatic drainage issues or inbalance in osmotic pressures) serous- excess water in body cavity

Question 47

transudate vs exudate

Answer 47

transudate- fluid pushed through capillary due to high pressure (low protein content) exudate- fluid leaks around cells due to inflammation and incraesed permeability of membranes (high protein content could also contains other cells)

Question 48

normal sodium levels

Answer 48

135-146 mmol/L are normal sodium levels (this is a ration), more commonly affected by changes in water not sodium

Question 49

hypernatreamia vs hyponatraemia example of when conditions may cause this

Answer 49

hypernatreamia- high sodium levels - mineralcorticoid, slat poisoning hyponatraemia- low sodium lvels- diuretics, addisons's disease, SIADH clinical effects of rapid change or extremes in sodium levels- brain damage etc.

Question 50

percentages of body, constituents

Answer 50

60% of body is water- 42L of water Of this: 28L (66%) is intracellular fluid 14l (33%) is extracellular fluid (made up of 3L of plasma, 11L of interstitial fluid)