• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/17

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

17 Cards in this Set

  • Front
  • Back

Lifestyle measures to reduce BP

Weight reduction


Less salt


Less alcohol


Less fat and sat fat


Increased exercise


Increased fruit and veg



Lifestyle measures to reduce CV risk

Stop smoking


Reduce fat and sat fat


Replace sat fat with mono-unsat


Increase oily fish consumption

Metabolic disease

Combination of disorders


Increase risk of CV disease and diabetes




Fasting hyperglycemia


High BP


Midriff fat


Decreased HDL


High TG

Pancreatic cells


What do they secrete

Beta - insulin


Alpha - glucagon


Delta - somatostatin

Diabetes

Hyperglycemia


Polyuria


Macrovascular disease (atherosclerosis)


Microvascular disease (retinopathy, neuropathy)

Type 1 Diabetes

Insulin dependent


Early onset


Auto immune destruction of islet cells, no insulin production


Muscle cramps, faintness, cardiac arrhythmias, infections

Type 2 Diabetes

Non-insulin dependent


Late onset


Impaired secretion, only get second phase secretion


Insulin resistance, impaired receptor functioning


Overweight, obese, physically inactive, family history

What does diabetes treatment aim for?

Achieve glucose homeostasis between 4-8mmol/L


Relieve symptoms and prevent acute complications: polyuria, blurred vision, weakness


Reduce long term complications: micro and macrovascular disease


Restore metabolism and metabolic disease

Treatment for diabetes



Targeting glucose absorption: alpha-glucosidase inhibitors (acarbose)


Target insulin secretion: meglitinides (repaglinide)


Targeting insulin actions: biguanides (metformin), dipeptidyl peptidase-4 inhibitors (sitagliptin), glucagon like polypeptide antagonists (exenatide)



Acarbose

alpha-glucosidase inhibitors


block enzymes that digest and absorb starches in small intestine


SE: flatulence, abdominal discomfort, loose stools, contraindicated in patients with IBS or cirrhosis

Repaglinide

meglitinides


stimulate insulin secretion rapidly for short duration


inhibit Katp channels on beta cells


depolarises islet cells, causing calcium influx


calcium stimulates exocytotic release of insulin granules


SE: less risk of hypoglycemia and weight gain than sulphonylureas

Metformin

Biguanides


increase peripheral glucose utilisation and decrease hepatic glucose production


decrease LDL and TG


activates AMPK


SE: GIT disturbances, possible weightloss, lactic acidosis. contraindicated in renal impairment because excretion unchanged in urine

Sitagliptin

dipeptidyl peptidase-4 inhibitors DPP-4


increase native GLP-1 levels by inhibiting their metabolism


increases insulin and decreases glucagon


GLP-1 are incretins released from GIT after food, increase insulin and decrease glucagon


SE: upper respiratory tract infections, headaches, pancreatitis, potential hypoglycemia in combination

Exenatide

Glucagon like polypeptide 1 (GLP1) receptor agonist


potentiate glucose mediated insulin secretion


suppress glucagon release


slow gastric emptying


reduce appetite


SE: nausea, vomiting, diahhorea, weight loss, immune reactions, endocrine neoplasias in pituitary

How is insulin stimulated for release

1. GLUT2 transporters on islet cells, uptake glucose


2. Glucose moves through Glucose-6-phosphate pathway to make ATP


3. ATP inhibits ATP sensitive K+ channels on islet cells


4. Depolarisation, calcium influx to cell


5. Calcium stimulates exocytotic release of insulin granules

How does insulin work?

1. Binding of insulin to TyrK insulin receptor


2. Switch on intracellular phosphorylation cascades via PI3K


3. Activation of mitogenesis, protein synthesis, glycogen synthesis and glucose transport


4. GLUT4 on subcellular vesicles to translocate to membrane


5. Uptake of glucose into cell and utilisation

How do incretins work?

Released from GIT after food intake


Increase insulin and reduce glucagon


Incretins deactivated by DPP-4