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83 Cards in this Set
- Front
- Back
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what does insulin do to
1) glycogenolysis 2) gluconeogenesis 3) glucose uptake and use |
1) decreases
2) decreases 3) increases |
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what does glucagon do to
1) glycogenolysis 2) gluconeogenesis 3) glucose uptake and use |
1) increases
2) increases 3) no effect |
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what does adrenaline do to
1) glycogenolysis 2) gluconeogenesis 3) glucose uptake and use |
1) increases by a1, B2 receptorss
2) increases indirectly 3) decreases |
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what does growth hormone do to
1) glycogenolysis 2) gluconeogenesis 3) glucose uptake and use |
1) no effect
2) increases 3) decreases |
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what does cortisol do to
1) glycogenolysis 2) gluconeogenesis 3) glucose uptake and use |
1) no effect
2) increases 3) decreases |
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what are the effect of insulin and glucagon on ketogenesis?
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insulin inhibitss
glucagon increases |
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what are the 3 ketone bodies and which provide energy?
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acetoacetate
B hydroxybutyrate (provide energyy) acetone |
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what are the tissues which don't require insulin for glucose uptake?
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BRICK
Beta cells of pancreas Red blood cells Intestinal cellls Central nervous system Kidney tubule |
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describe what happens to metabolism, in terms of liver, fat, muscle if there is a lack of insulin?
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reduced glucose uptake my muscle and tissue
causes blood glucose to rise causes fat lypolysis and protein breakdown fatty acids and amino acids to liver ketogenesis from fatty acids gluconeogenesis from amino acids increased glucose in blood increased ketones in blood |
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what are the short term effects of loss of insulin?
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osmodiuresis:
thirst dehydration polyuria Ketosis; abdominal pain nausea, vomiting, breathlessness |
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what are the long term effects of insulin loss?
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ketosis:
CNS depression coma osmodiuresis: decreased circulating volume decreased renal perfusion decreased cerebral blood flow decreased peripheral blood flow |
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in which type of diabetes does ketosis occur?
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type 1
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what proportion of people have type 1 / type 2 diabetes?
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15% / 85%
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what are the symptoms of diabetes shared by type 1 and 2?
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thirst
polyuria dehyrdation infections: candidiasis blurred vision |
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what are the symptoms specific to type 1?
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weight loss, ketoacidsosi
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what are the symptoms specific to type 2?
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2ndary compllications
altered mental status |
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what are the diagnositic criteria for diabetes
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symptoms +
fasting >7mmol random or OGTT > 11.1mmol (2hrs after 75 g glucose) |
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what are the two prediabetic conditions?
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fasting hyperglycaemia
impaired glucose tolerance |
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what is the diagnositic criteria if nos ymptoms of diabetes but impaired fasting glucose + random?
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test on a different day
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what are the diagnostic criteria for fasting hyperglycaemia?
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fasting >6.1, < 7
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what are the diagnostic criteria for impaired glucose tolerance?
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random or OGTT >7.8 <11.1
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what are the causes of type 1 diabetes?
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unknown
suscpetibility genes environmental triggers eg virus, toxin |
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what are the endocrine causes of DM?
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acromegaly
cortisol phaeochromocytoma all increase counterregulatroy hormones |
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which drugs can induce diabetes?
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B blockers
steroids Thiazide diuretics |
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what is the mechanism of action for metformin?
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activate AMP kinase
decrearses gluconeogenesis increases glucose uptake / use |
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what are the side effects and contraindicationf for metformin
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not in renal impairment
GI side effects |
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what is the MOA of sulphonylureas
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blockade ATP dependant K channels
increase insulin release |
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what is the MOA of prandial glucose regulators?
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blockade ATP dependant K channels, increase insulin release
short acting |
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what is the MOA for incretin mimetics?
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eg GLP1 mimetic
mimick affects of incretins potentiate insulin slow gastric emptying, increase satiety |
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what is the MOA for incretin enhancers
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inhibit DPP4 enzyme
degrades incretins enhances effects of incretins slow gastric emptying, increase satiety |
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what is the MOA for acarbose?
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inhibits glucosidase enzymje
inhibits carbohydrate and sucrose digestion |
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what is the MOA of thiazolidenione?
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actiavates PPAR-Y
intracellular transcription factor makes cells more sensitive to insulin |
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what is the strategy of treatment for T2DM
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1) treat with diet and excersise
2) 1 of metformin or sulphonurea 3) 2 of Metformin, sulphonurea, TZD, incretin enhancer / mimetic 4) 3 drugs or 2 drugs + insulin 5) insulin therapy / increase insulin dose |
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what is the side effects of sulphonylureas?
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hypoglycaemia
weight gain |
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what are the different types of insulin in order of action length?
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short acting analogues
short acting soluble intermediate acting long acting analogue long acting ultralente |
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what is the basobolus treatment plan?
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1 long acting insulin injection per day
3 short acting insulin injection at meal times |
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what is the 2 injections per day treatment plan
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2 injections
both have intermeiate and short acting inslin in them |
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what are the 2 treatment plans available for diabetes with insulin?
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basobolus
twice daily injectinos |
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what are the problems with insulin therapy
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painful - compliance
lipohypertrophy at injection site high insulin levels: CV risk scarring |
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what is the anagram for rememberign how to educate diabetic patients?
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Some Medics Don't Emphasize Importance So Get Crapped (on)
= support, medication, diet, exercise and smoking, importance of glycaemic control, special precautions, general health care, complications |
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discuss support provision in education of diabetics?
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emotional/psychological
inform social groups carry medical alert card |
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discuss how you would educate a diabetic patient about medication
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how they take it
what it all does how to store insulin how to inject insulin |
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discuss how you would educate a diabetic patient about diet
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high fibre
complex carbos with low GI low sugar, salt, fats alcohol = can mask hyper/hypo |
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discuss how you would educate a diabetic patient about exercise / smoking cessation
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exercise: reduce insulin resistance, weight loss
smoking cessation: reduce CV risk |
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discuss how you would educate a diabetic patient about special precautions
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what to do in illness
what to do in travel / time zone chanegs |
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discuss how you would educate a diabetic patient about general healthcare
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attend medical check ups
eye care foot care |
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what are the 3 acute complications of diabetes?
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hypoglyacemia
ketoacidosis hyperosmolar hyperglycaemic attack |
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what are the causes of hypoglycaemia?
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type 1: insluin overdoes, too much exercise, too little CHo
type 2; sulphonyureas renal and hepatic failure |
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how do you treat hypoglycaemia
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conciosu: sugary food then carb for sustained provision, glycogel
unconcious; IV glucose, or glucagon injectino but not after alcohol |
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what are the symptoms of hypoglyaceima
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counterregulatory / SNS; sweating, palpations, trmor, anxiety
neuroglycopaenia; loss of conciousness, slurred speech |
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what is the cause of diabetic ketoacidosis?
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in type 1 patients;
emotional disturbance missed insulin dose illnes mensutration / pregnancy |
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how do you treat DKA?
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give K+ nad HCO3-
give insulin |
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how do you treat HHA?
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same as DKA but with less insulin
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what are the two types and their subdivisions of chornic complications to diabetes?
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microvascular; nephropathy, neuropahty, retinopathy
macrovascular; cardiovascular, peripheral vascular, cerberovascular |
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how does microvascular complications occur
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capillary pathology
sorbitol/glucose metabolites glycosylate protein - advanced glycosylated end products |
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what are the stages of retinopathy
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background - aneurysm, haemorrhages
preproliferatibe: ischaemia, cotten wool spots proliferative, new blood vessels, vitroues haemmorhage, floaters maculopathy: from lipoprotein deposits advanced: retinal retractions |
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how many diabetics get retinopathy?
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95% after 20 years
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how many diabetics get neuropathy and nephropathy@:?
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15% eac
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describe diabetic nephropathy
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early: micoalbuminuria
then: protein uria, increase BP, decreased GFR later: end stage renal faiilure |
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describe diabetic neuropahty
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demyleniation
affects CNS, PNs, autonomic cramps, causalgia, loss of sensation, shooting pain, tingling especially in feet- causes foot ulcers |
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list the dietary factors which may cause cancer and explain why briefly
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obesity
animal fat and sat fats: may produce prostaglandins red / processed meat: react to form nitrous amines alcohol |
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list what dietary factors are protective againts cancer
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fruit and veg
fibre vit D and calcium phytochemicals |
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what diet and lifestyle advice do you give to someone to prevent cancer?
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exercise = 30min/day 5x a week
fruit and veg: varied, 400g/day increase consumption of complex, plant based carbs eg pulses, cereals reduce animal/sat fat intake. sat fat < 7% calories per day |
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how many cancer patients are undernourished at diagnosis?
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75%
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what causes undernutrition in cancer patients?
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increased BMR due to cancer
reduced appetite - anorexia dysphagia vomiting, diahhroea, nausea |
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describe the effects of cancer on metabolism?
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cancer produces inflammatory mediators - cytokines
cause protein degredation, lypolysis, catbolic state cause increased insulin resistance increased BMR |
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what are the consequences of cachexia on cancer patients?
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reduced response to therapy
increased hospitalisation reduced quality of life reduced dependance |
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define cachexia
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a hypermetabolic state characterised by anorexia and rapid weight loss
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what diseases can cause cachexia?
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cancer, infections eg HIV, TB, malaria, cystic fibrosis, chronic alcoholism
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how does cachexia differ from sarcopenia
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losss in protein and muscle mass
inflammation (more than in sarcopenia) increase in BMR |
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what are the main aims of enteral nutrition?
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reverse undernutriton
encourage weight further weight gain enhance immune fucntion reduce fatigue |
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how much protein should a cancer patient eat per day
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1.5g/kg
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when is enteral nutritional support provided/
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when patient is expected not eat proplerly for 7 days
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what is a peg tube?
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form of enteral nutrition
Percutanoeus endosopy tube goes into stomach through abdo wall |
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what is a nasogastric tube?
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form of enteral nutritions
goes through nose, eosophagus to stomach / jejunum |
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what is the energy density that most patients on nutritional support will tolerate?
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around 1kcal / ml
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how do you calculate the dose of nutritional support needed?
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schofield equation to get BMR
x stress factor 1.15 x refeeding factor - 0.25 (only give 25%) |
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what is parenteral nutritional support
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central (TPN) in jugular
or peripheral (PPN) in arm |
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when would you use parenteral nutritional support?
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when GI tract is not functinal, accesiible or safe to use eg colon cancer
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how are fats, carbohydrate and ptoetin provided?
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fat: triglyceride emulsions - lipases in circulation
carbs: as dextrose protein; as amino acids |
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what is the maximum dose of carbohydrate allowed in parenteral nutrition and why must it not be exceeded?
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4mg/kg/min
to prevent protein breakdown, hyperglycaemia, excessive CO2 production |
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what is the fat requirement for parenteral nutrition?
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0.7 - 1.2kg per day
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how do you calculate doses of protein, fat and carbs needed?
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fat: 0.7 - 1.3g / kg / day
proetin: 1.5g per kg per day CHO = EE - protein - fat |
