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Metabolism 2 PBL > PBL 1 > Flashcards

PBL 1 Flashcards

1
Q

define kwashiorkor

A

form of malnutrition caused by protein deficiency in the diet, this affects young children, the main sign is too much fluid in the bodies tissues which can cause swelling under the skin, could be due to a reduce plasma protein and electrolytes in the blood causing the fluid to enter the interstitial tissues

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2
Q

define marasmus

A

form of sever malnutrition usually occurs in children, loose a lot of muscle mass and subcutnaoues fat, it is characterstied by energy deficiency marasmums is inadequate energy intake in all forms including portien whereas Kwashiorkor is protein deficiency with adequate energy intake

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3
Q

define referring syndrome

A

this is a syndrome consisting of metabolic disturbances that occur as a result of reinstitution of nutrition to patients that are malnourished, this can trigger the synthesis of glycogen, fat and protein in the cells can cause the lower of phosphate, potassium and magnesium (as they are used in the synthesis of glycogen fat and proteins) in the blood causing cardiac symptoms

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4
Q

define pabrinex

A

this is an injection that contains vitamin B and C (thiamine, riboflavin, pyridoxine, nicotinamide and ascorbic acid)

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5
Q

define F75 diet

A

this is the diet that is used in the initial management of malnutrition beginning as soon as possible and continuing for 2-7 days, it is a diet that is low in protein or sodium and high in carbohydrate, they are also given vitamins but this does not include iron

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6
Q

define RUTF

A

– ready to use therapeutic food – it is a ready to use paste which does not need to be mixed with water thereby avoiding the risk of bacterial proliferation in the case of accidental contamination- product is peanut butter mixed with dried skim milk and vitamins and minerals

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7
Q

define a weight watchers program

A

assess each member by age, weight, height and gender and then determines how much food they need to lose at a safe rate, assigned a daily point target and spends those points on food

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8
Q

define a low glycemic index diet

A

this involves swapping high GI foods for low GI alternatives, has a number of potential health benefits including reducing blood sugar levels, aiding weight loss and lowering your risk of heart disease and type 2 diabetes

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9
Q

define an Atkins diet

A

this is a high fat high protein with low carb vegetables diet

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10
Q

what are the causes of kwashiorkor

A
  • Due to a lack of protein in the diet, need protein to make and repair new cells, protein is important for growth in childhood and pregnancy, lack of protein causes normal body functions to shut down
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11
Q

what is the treatment of kwashiorkor

A
  • F75 diet then an RUTF diet
  • Preventing low blood glucose
  • Treating infections with anitbitoics
  • Treat the dehydrogenation with formulated rehydration solution
  • Treating vitamin and mineral deficiencies, vitamin supplements are usually included in the special milk feeds and RUTF
  • Slowly introducing small amount of food and then gradually increasing it
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12
Q

what are the symptoms of kwashiorkor

A
  • Edema – this is not in marasumus
  • Change in skin and hair colour
  • Fatigue
  • Diahrroea
  • Loss of muscle mass
  • Damaged immune system
  • Irritability
  • Shock
  • Flaky rash
  • Stunted growth
  • Regular infection
  • cracked nails
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13
Q

what is the diagnosis of kwashiorkor

A
  • Checks for a enlarged liver and swelling
  • Check how well liver and kidneys are working by testing the urine and blood for anaemia
  • Measure the levels of vitamin and minerals in the body
  • Then blood and urine tests done to measure the level of protein and sugar in the blood
  • Arterial blood gas, blood urea nitrogen, blood levels of creatine, blood levels of potassium, urinalysis
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14
Q

what is the prognosis of kwashiorkor

A
  • Depends on how sever symptoms were when treatment began
  • If started early recover well
  • If treatment started in the later stages then they may be left with physical and intellectual disabilities
  • If treatment is significantly delayed can lead to death
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15
Q

what are the causes of marasmus

A
  • Nutrient deficiency is the main cause of marasmus, occurs in children that don’t ingest enough protein calories and carbohydrate, also have deficiens in iron, iodine, zinc, vitamin A
  • Viral and bacteria and parastitic infections can cause children to absorb fewer nutrients
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16
Q

what are the treatment of marasmus

A
  • F-75 or RUTF diet,
  • Interfusion of human albumin solution
  • May need oral rehydration
  • Initially F-75 – given dried skim milk that is mixed with boiled water and then once the children can tolerate this they are moved onto a RUTF diet which contains a vegetable mix
  • Has to be done slowly otherwise it can cause refeeding syndrome
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17
Q

what are the symptoms of marasmus

A
  • Underweight is the main symptom
  • Lost a lot of muscle mass and subcutaneous fat upper limb and buttocks tend to be more effected
  • Dry skin and brittle hair
  • Chronic diarrhoea
  • Respiratory infections
  • Intellectual disability
  • Stunted growth
  • Temperature unusual
  • Anaemia
  • Dehydration
  • Hypovolemic shock
  • Tachypena
  • Distention of the abdomen
18
Q

what are the diagnosis of marasmus

A
  • Physical examination through height and weight, lack of motion is malnourished child may help confirm a diagnosis of marasmus
19
Q

what are the prognosis of marasmus

A
  • Depends on how severe symptoms were when treatment began
  • If started early recover well
  • If treatment started in the later stages then they may be left with physical and intellectual disabilities
  • If treatment is significantly delayed can lead to death
20
Q

what is the role of liver in terms of glucose

A
  • Maintains an essential role in maintaining blood glucose levels
  • 100g of glycogen is stored in the liver and 300g is stored in skeletal muscle
  • Glycogen can then be degraded to release glucose in times of exercise or fasting
21
Q

what happens in glycogenolysis

A
  • One residue of glycogen is removed and converted to glucose-1-P by glycogen phosphorylase or de-branching enzyme
  • Glucose-1-P is converted to Glucose-6-P by phosphoglucomutase
  • Glucose-6-P is then converted to Glucose by glucose-6-phosphatase
  • This glucose then enters the bloodstream to be used throughout the body
  • This process is inhibited by insulin and triggered by glucagon
22
Q

describe what gluconeogensis is

A

Liver can convert amino acids, lactate, pyruvate, and glycerol into glucose too via gluconeogenesis – triggered via cortisol and glucagon, inhibiting by insulin

23
Q

describe what happens in lipogenesis is

A
  • Acetyl-CoA is converted to malonyl-CoA by acetyl carboxylase – this is allosterically activated by citrate and inhibited by AMP
  • Fatty acid synthase then adds 2 carbon molecules malonyl-CoA to a growing fatty chain
  • Fatty acid is then linked to a carrier protein
  • Lipogenesis is stimulated by the presence of insulin and inhibited by glucagon and adrenaline
24
Q

describe what happens in lipolysis

A
  • Fatty acids undergo beta-oxidation
  • This occurs in the mitochondria which produces acetyl-CoA which can enter the TCA cycle or be used to produce ketone bodies
  • Long chains of fatty acids are broken down into 2 carbon acetate units which are combined with Co-enzyme A to form acetyl CoA
  • The acetyl-CoA can then be combined with oxaloacetate to form citrate for the beginning of the TCA cycle
  • Glucagon and adrenaline stimulate the process of lipolysis whereas it is inhibited by insulin
25
Q

describe what happens in protein synthesis

A
  • Can be made in the liver using amino acids consumed in the diet
  • Stimulated by insulin and growth hormone
  • Proteins synthesised in the liver include – albumin, CRP, blood clotting factors, thrombopoietin, angiotensinogen
26
Q

what proteins are synthesised in the liver

A

albumin, CRP, blood clotting factors, thrombopoietin, angiotensinogen

27
Q

what are the two options for protein breakdown

A
  • transamination

- deamination

28
Q

what happens in transamination

A
  • One option is transamination where the amino acids group can be transferred to ketoacids through actions of alanine aminotransferase(ALT) and aspartate aminotransferase (AST)
  • The amino group can be added to alpha-ketoglutrate to form glutmate
  • Amino acid can be added to oxaloacetate to form asparate
29
Q

what happens in deamination

A
  • Amino group removed from amino acid to produce a ketoacid and ammonia via deamination
  • Uses glutaminase or low specificity L and D amino acid oxidase enzyme
  • Ammonia is converted to ammonium ion which must be removed via glutamine or the urea cycle
30
Q

how does weight watchers work

A
  • Point based system aimed at reducing overall calorie intake
  • Switches from glucose to fat metabolism but no significant ketogenesis
  • Main fat loss is from body fat
  • Group support
31
Q

what is a glycemic index

A

– this is a measure of how much food changes blood glucose level

32
Q

how does a low GI work

A
  • High GI – big rise in blood glucose level
  • Low GI – small rise in blood glucose level
  • Can be useful in diabetes management
  • Low GI often taken longer to digest, people feel less hungry and there is a reduce in the overall food intake, decrease in insulin secretion which can reduce fat storage
33
Q

how does an antkins diet work

A
  • Ketogenic diet – promotes use of ketone bodies
  • Carbohydrate restricted – low insulin levels prevents the fat storage
  • Slight intake – this prevents gluconeogenesis from body proteins
  • Maintains protein intake
  • Linked more closely to starvation – avoid complication because of proteins in the diet
34
Q

describe what refeeding syndrome is

A
  • Shifts in fluid and electorlytes that occur in patients that receive certain diets after being malnourished
  • Sever phosphate deficiency is a defining factor
  • Patient may also feature abdominal sodium and fluid balance, changes in glucose, protein and dat metabolism, hypokalaemia and low magensisum
  • Starvation results in a loss of intraceullar sotres of electrolytes such as phsopahte
35
Q

describe what happens in refeeding syndrome

A
  • Starvation results in a loss of intraceullar sotres of electrolytes such as phsopahte
  • Serum levels could appear normal despite changes and store depletion
  • Rising suagar blood glucose leads to increased insulin and decreased secretion of glucagon, insulin stimulates glycogen, fat and protein synthesis this requires phosphate, magnesium and thiamine which leads to depeletion
  • Insulin stimulates absorption of potassium via the sodium potassium ATPase symptoms which also transport glucose in the cell therefore magnesium and phopahte are taken up into the cell and water follows by osmosis
  • Leads to a decreae in serum levels of phosphate, potassium and magnesium
  • No potassium to slow the heart rate down increase cardiac output and arrthmias which leads to cardiac failure and death
36
Q

describe the medical aid in Yemen and the challenges that it faces

A
  • Outbreak of cholera in 2018
  • Supply and medical care is scarce and so is acess to drinking water and sanitation
  • Diphteria spread quickly
  • Diabetes causes a qauter of limb amutations – medical treatment when it is too late
  • Affects people with chronic illnesses
  • More than 80% of Yemens population lacks food, fuel drinking water and access to health care services
  • Lacks funding
  • Worst humanitarian crisis 24 million dependent on aid 80% of the population
  • Bottle neck at the ports – aid just comes through a few ports, contested much aid doesn’t make it into the country – country divided into different fractions so aid getting through these is affected
37
Q

describe what the blood results show

A
  • Thin BMI of less than 14 – this is because they are undernourished and malnourished therefore they have lost weight so there BMI drops as weight is decreased for their height
  • Oedema – this is due to the reduced albumin (plasma protein) and reduced sodium in the blood this means that due to the low plasma protein level more water has moved down the water potential gradient into the interstitial tissue and this has caused the oedema
  • Palpable enlarged liver – enlarged becase it is working more
  • Skin problems – inadequate amount of protein, the skin is made of collagen which is a polypeptide, therefore as there is not enough protiens and amino acid collagen synthesis is unaided
  • Hypochromic - haemoglobin is a polypeptide as well so less amino acid
  • Low range white blood cell – weakened immune system
  • Low platelet count
  • Low albumin – less protein in diet
  • Low sodium
  • Normal potassium - storage might be depleted even though it shows up as normal, if potassium becomes low it can cause the heart to speed up as potassium slows the heart
  • Low scale magnesium - regulating muscle and nerve function, blood sugar levels, and blood pressure and making protein, bone, and DNA. can lead to nausea vomitting seziures if it is low
  • Low scale phosphate - needed for the body to make protein for the growth, maintenance, and repair of cells and tissue
38
Q

what are the 4 main causes of oedema

A
  • Blocked lymphatic vessels
  • Decreased plasma proteins in the blood
  • Increased hydrostatic pressure pushing the blood out of the capillaries
  • Increased capillary permeability
39
Q

what can also cause oedema

A
  • DVT
  • PE
  • Pregnancy
  • Premenstrual signs and symtpoms
  • High blood pressure medications
  • NASIDs
  • Estrogens
  • Certain diabetes medication
  • Congestive heart failure
40
Q

what are the symptoms of oedema

A
  • Painful
  • Swelling
  • Heat
  • Shiny skin
  • Pitting oedema
  • Increased abdominal size
41
Q

what are the treatments

A
  • Lie down and use pillows to raise the swollen area
  • Gentile exercise to improve blood flow
  • Wash and dry and moisutrise feet to avoid infections
  • Don’t stand for long peroids of time
  • Don’t wear clothes or socks and shoes that are too tight
  • Depend on what causes it
  • Diuretics to remove the extra fluid such as loop diuretics perhaps
42
Q

what sources if glucose the complete source of metabolic energy

A

Glucose is often the complete source of metabolic energy in normal conditions in:
o The nervous system.
o Red Blood Cells.

Metabolism 2 PBL (9 decks)

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