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IMMS > week 3 recap- water, membranes, glycolysis and kerbs and diet > Flashcards

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

1
Q

names of vitamins:

A

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

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2
Q

to work out base metabolic rate

A

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

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3
Q

rate limiting step in Krebs cycle

A

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

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4
Q

rate limiting enzyme in glycolysis

A

PFK-1

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5
Q

what is a kinase

A

enzyme that move phopshate groups

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6
Q

components of sucrose and lactose

A

sucrose- fructose, glucose

lactose- glucose and galactose

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7
Q

protein requirment

A

protein requirement: 0.8g/kg a day

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8
Q

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

A
  • 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
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9
Q

values of kcal/g for each

A

values for typical 70kg man:

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

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10
Q

what increases BMR

A

basal metabolic rate lowers:

  • age
  • sex
  • dieting/starvation
  • hypothyroidism
  • decreased muscle mass (less of you so need less energy needed)
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11
Q

What increases BMR

A

basal metabolic rate increases:

  • high BMI (more of you so more energy needed)
  • hyperthyroidism
  • low ambient temperature
  • fever/infection/chronic disease
  • caffeione (stimulant)
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12
Q

is spleen endocrineis skin endocrine?

A

yes, produces vitamin D (is a hormone)

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13
Q

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

A

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

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14
Q

vitamnin C- scientififc names, where found and uses

A

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

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15
Q

vitamin B12- scientififc names, where found and uses

A

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

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16
Q

vitamin K scientific names

A

Vit K- (phylloquinone, menaphthone

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17
Q

what vitamins are fat soluble

A

A, E, D ,K

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18
Q

what happens during starvation

A
  • 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)
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19
Q

Draw glycolysis chain

A

did you do it ;)

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20
Q

regulation of glycolysis

A

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

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21
Q

draw krebbs cycle

A

did you do it ;)

22
Q

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

A

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

23
Q

use of pyruvate after glycolysis (aerobic and anaerobic)

A
  • 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
24
Q

oxidatave phosphorylation

A

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
25
Q

lipid absorption and transport process, 8 step

A
  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)
26
Q

draw fatty acid beta-oxidation chain

A

in hand written notes or ppt

27
Q

draw fatty acid activation chain

A

in hand written notes or ppt

28
Q

draw ketogenesis chain

A

in hand written notes or ppt

29
Q

regukation of ketogenesis

A

-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)

30
Q

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

A

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.

31
Q

what casues acetyl CoA to be converted into ketone bodies

A

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.

32
Q

types of communication in and between cells

A
  • 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)
33
Q

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

A

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

34
Q

extra-cellular fluid components

A

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

35
Q

intra-cellular fluid

A

main cations presnt is potassium

36
Q

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

A

causes haemolysis of cells

37
Q

dehydration:

A

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

38
Q

types of membrane proteins

A

peripheral- loose attachment
integral- sits within membrane

39
Q
A

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

40
Q

body weight distrubutions of water in 70kg male

A

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

41
Q

how to estimate plasma osmality

A

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

42
Q

normal plasma osmolality

A

Normal plasma osmolality 275-295 mmol/kg

43
Q

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

A
  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
44
Q

excess water- poetential risks

A

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

45
Q

Types of oedema:

A

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)

46
Q

what is a pleural vs serous effusion

A

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

47
Q

transudate vs exudate

A

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)

48
Q

normal sodium levels

A

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

49
Q

hypernatreamia vs hyponatraemia
example of when conditions may cause this

A

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.

50
Q

percentages of body, constituents

A

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)

IMMS (6 decks)

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