PANCREAS- INSULIN/GLUCOSE RELATED DISORDERS Flashcards
GLC METABOLISM, DM 1 & 2
islets of langerhans cells
alpha- glucagon
beta- insulin
D- somatostatin
PP- pancreatic polypeptide
glucose metabolism
- insulin and glucagon function
insulin and gluc work antagonistically to keep plasma gluc conc in acceptable range
- insulin: when FED, moves ingested gluc into cells for energy production
- glucagon: when FASTING, gluc promotes glucose production from bodily stores
glucose metabolism
insulin
- storage/use where
- stored in
- excess glucose stored where
- what stim insulin release
- gluc driven intracellularly for storage/use in adipose tissue and skeletal muscle
- promotes storage as glycogen in liver and skeletal muscles
- excess glucose stored as glycogen or fat
- insulin release stim by plasma GLC >100
glucose metabolism
glucagon
- stim when
triggers liver and skeletal muscle to use glycogen and non glucose intermediates to synth glucsoe for release into bloodstream
- release stimulated by plasma GLC <100
glucose metabolism
glucose obtained from 3 sources
- intestinal absorp of food
- glycogenolysis (breakdown glycogen/ glucose store in storage form)
- gluconeogenesis (create gluc from precursors derived from carb, protein, fat metab)
gluc range high or low effects
low- sensitive tissue (ex: brain) will not function
high- cause lasting damage to cellular proteins
INSULIN
lipid v. protein metabolism
LIPID
- promotes fat storage within adipose tissue and liver
- controls storage and formation of TG
- inc cholesterol synth
PROTEIN
- stim uptake of AA into cells, promote protein synth
- inhibit protein breakdown
diabetes mellitus (DM)
- definition
- pathophys
PERSISTENT hyperglycemia
- defects in insulin secretion and/or insulin action
- results in exces of glucose in BLOODSTREAM, not enough in CELLS (starvation state)
DM1 v. DM2
DM1
- impaired insulin secretion 2/2 autoimmune destruction of pancreatic islet B cells
- dec/NO insulin production
DM2
- tissue resistance to insulin action
eventual impaired insulin production (if untreated)
DM1
- onset
- risk inc?
typical onset is ages <30
- rapid onset (weeks to months)
- 2-8x premature mortality risk compared to general population
DM1
- pathogenesis phases
1- B cell autoimmunity: islet related antibodies appear
2- asymptomatic loss of B cell secretory capacity due to inflamm
3- loss of B cell secretory function w/development of DM symptoms
DM1
- risk factors
- genetic predisposition (fam hx or autoimmune ds)
- viral trigger or pancreatic injury/trauma
- age <30
- linked to autoimmune ds and specific assoc genes (HLA DR3 and DR4)
DM2
- onset
- assoc in what pts
- patho
tissue resistance to insulin
- onset >30 yo
- strong assoc w obesity
- may be present prior to dx
patho: body can create insulin, but cells dont transport glucose through membrane into cells
- obesity assoc w elevated free fatty acid levels in plasma–>contributes to insulin resistance within skeletal muscles
DM2
pathogenesis steps
1- dec tissue sensitivity to insulin, stim B cells to produce MORE insulin
2- inc in insulin can make up for resistance temporarily
3- overworked B cells die off over time/fail to be stim by excess glucose–> lead to circ glucose and sx appear
DM2
- risk factors
- genetic predisposition (fam hx)
- age >45
- overweight
- sedentary lifestyle
- hx of gestational DM (or deliv baby >9lbs)
- african american, latino, american indian, alsak native descent
- non alc fatty liver ds
DM
- common symptoms
- polyuria/nocturia
- polydipsia
- polyphagia
- wt loss
- fatigue, blurry vision
- freq candidal infx
- numbness/tingling of extremities
3 P’s!!!!
DM
- common signs (skin, vasc)
skin changes
- acanthosis nigricans (DM2): thick velvety hyperpigmented skin in folds
- necrobiosis lipoidica diabeticorum: demarctated yellow-brown atrophic plaques (can be telangiectatic)
vascular
- eyes: cotton wool spots, flam hemorrhages, neovasc
- PV: lower ext dec pulse, ulcers
- neuro: dec vibratory/sensation, dec monifilament testing
DM SYMPTOMS
polyuria/nocturia
- serum glucose conc >180
- exceeds renal threshold for gluc reabsorption–> inc urinary glucose excretion
- prompts kidneys to make more urine (osmotic diuresis)—urinate more freq at night
DM SYMPTOMS
polydipsia
- glycosuria causes osmotic diuresis (polyuria)—> hypovolemia
- leads to polydipsia as body attempts to make up fluid losses
sugar juice exacerbates issue
DM SYMPTOMS
blurry vision
inc serum glucose levels cause fluid to move in and out of parts of eye (osmotic pressure)
- leads to lens changing shape, ability to refract light, and see clearly
diabetic retinopathy complication
DM SYMPTOMS
polyphagia + wt loss
- wt loss CAN be a presenting symptom
- glucose stays in bloodstream, rather than moving into cells—-> body thinks its starving–>prompts you to eat more and break down fat and muscle to compensate
DM SYMPTOMS
frequent candidal infections
inc blood sugar glucose levels also means inc gluc in sweat, saliva, and urine
- fungus loves sugar–> encouraged to grow under these conditions
DM SYMPTOMS
numbness/tingling extremities
secondary to neuropathy likely due to microscopic vasculitis
- causes ischemia to capillaries supply nerves (cause nerve damage)
DM SIGNS
DM2- acanthosis nigricans
assoc w significant insulin resistance
- causes cells to reproduce at more rapid rate
- hyperpigmented/thick velvety skin axilla, groin, back of neck