Diabetes Flashcards
Symptoms
Polyphagia - cells are starved so adipocytes begin to break down fat + muscle cells begin to break down protein. Get very hungry
Polydypsia - wee a lot so thirsty
Polyuria - glucose is osmotically active so need to wee more as more h2o drawn out
Glycouria - lots of glucose so spills into urine
T1D
Autoimmune - type 4 hypersensitivity (cell mediated) reaction to beta cells. Get destroyed as lost T cell self tolerance so T cells destroy + recruit other inflammatory cells to do so
Usually occurs in early life
May have HLA-DR3 or DR4
T2D
Produce less insulin or body cells can’t respond to insulin (cells don’t move glucose transporters to the plasma membrane)
Risk factors: HTN, obesity, genetics, lack of exercise
DKA
When cells are starved of energy, fats broken down into FFAs - made into ketones by liver which cause blood to become acidotic. Symptoms:
Kusmaul respiration = deep laboured breathing to try blow off co2
Hyperkalemia - H is taken into cell in exchange for K. Insulin also makes Na-K pump work harder so without this, even more K out of cell
High anion gap
Nausea/vomiting
Acute cerebral oedema
Pear drop breath as ketone bodies converted to acetone which is volatile + blown off
HHS
Hyperosmolar hyperglycaemic state
Glucose is osmotically active + if stuck in BVs - pulls h2o out so cells shrivel + h2o moves into BVs - lots urine produced
Can affect mental state
Complications of diabetes
Peripheral neuropathy
Lack of blood/nerves to periphery - ulcers
Retinopathy
Nephrotic syndrome as damage to aff/eff arterioles
Arterioles get hyaline deposits so harden
Metformin
Reduces weight
Decreases ATP in cell - increases AMPK (sends glut4 to PM for glucose uptake): decreased glucose output from liver, decreased intestinal absorption of glucose, increased glucose uptake by peripheral cells so helps resistance
SE = can cause lactic acidosis
Sulphonylureas
e.g. gliclazide
Blocks SUR1 K-ATP channel on cell - cell depolarises - Ca influx - insulin release
SE = GI disturbances
Thiazolidinediones
e.g. pioglitazone
PPARG agonist at cells such as liver, skeletal, adipose + increases txn of different genes. At liver - can cause reduced release of glucose. At skeletal - can cause increased uptake of glucose
SE = Water retention
GLP-1 analogues
Mimic incretin in the body, injected, degraded by DDP4
Incretin:
Slow glucose absorption into blood as decrease gastric emptying so feel fuller for longer
Stimulate insulin release from pancreas
Inhibit glucagon release from pancreas
SE = GI disturbances
DDP4 inhibitors
e.g. sitagliptin
Inhibit DDP4 so incretin stays around for longer
SE = GI disturbances
SGLT2 inhibitors
Prevent kidney from reabsorbing any glucose by blocking SGLT2
SE = UTI
