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What is the basic organization of the endocrine pancreas?

clusters of cells termed islets of langerhans
single islet consist of multiple cell types, each producing one type of hormone
insulin secreted by beta cells and lie in the center of islets
glucugon by alpha cells


what does insulin do

incr. glut4 receptors on skelectal muscles and adipose tissues. glucose enters tissues. serum conc. decr.
incr. glycogen syntehsis and lipogenesis and incr protein synthesis


What is type 1 DM?

insulin deficiency leading to a metabolic disorder charachterized by hyperglycemia


What is the pathophysiology of type 1 DM? genetic associations?

autoimmune destruction of beta cells by t lymphocytes (type IV). inflammation of islets. associated with HLA-DR3 and DR4.
autoantibodies against insulin= may be there yrs before clinical disease


manifestations of type I dm

childhood with insulin deficiency
high serum glucose
weight loss and low muscle mass and polyphagia (they are breaking down fat, proteins)
polyuria, polydipsia, glycosuria.sugar in urine draws water in
tx: insulin


complications of type I DM

excessive serum ketoacidosis
often arises with stress (infection)
epinephrine increases glucagon= exacerbating lipolysis
incr. lipolysis = incr. free fatty acids. liver converts free fatty acids to ketones


clinical features of DKA

hyperglycemia, anion gap metabolic acidosis, hyperkalemia (K outside of cells, and a buffer for acid). much of K is lost in urine you are depleting K stores even though there is high K in the blood
Kussmaul respiration (rapid/deep breathing), dehydration, nausea, vomiting, mental status change, fruity smelling breath


tx of DKA

fluids, insulin, replacement of electrolytes, including K (which looks high in blood but is low in the body overall


type II DM: what is it, predisposition

end organ resistance to insulin leading to hyperglycemia
obesity: obesity leads to decr. number of insulin receptors.
very strong genetic predisposition


Insulin levels in type 2 DM

at first, insulin levels are increased- but later on, you see insulin deficiency d/t beta cell exhaustion


histo changes with type 2 DM

islets filled with amyloid


clinical features of DM type 2

polyuria, polydipsia, hyperglycemia. often clinically silent.


Dx of DM type 2

random glucose >200
fasting glucose >126
glucose tolerance test >200 mg/dL 2 hrs after glucose


tx of DM type 2

weight loss, drug therapy to counter insulin resistance, insulin


What is a main complications of type 2 DM

hyperosmolar non-ketotic coma
high glucose levels >500 mg/dL leads to life threatening diuresis.
hypotension and coma
ketones are abscent


What are the 2 major mechanisms for complications in type 2 DM?

non-enzymatic glycosylation of vascular basement membrane: stick sugar onto basement membrane (NEG) and osmotic damage


non-enzymatic complications

large and medium-sized vessels: leads to atherosclerosis, CV disease, amputations
NEG of small vessels leads to hyaline artherosclerosis, esp. in the kidney:
preferential involvement of efferent: hyperfiltration, then sclerosis of the mesangium, then kimmelstein-wilson syndrome, then nephrotic syndrome.
if you have afferent atherosclerosis- decr. blood supply,. and diffuse sclerosis of the glomerulus
NEG of hemoglobin leads to HbA1C.
MI is the most common cause of death.


What cells will take up sugar independent of insulin?

1. schwann cells: converts glucose to sorbitol, leads to osmotic damage. this causes neuropathy
2. pericytes of the the retinal blood cells. sugar in the pericytes goes to sorbitol, pericytes die, vessel wall is weakened and then you get aneurysms in the retina. if they rupture you can get blindness
3. lens can take up glucose. it goes to sorbitol (aldose reductase) and can cause cataracts


pancreatic endocrine tumors

tumors of islet cells. oftent a component of MEN1 (along with parathyroid hyperplasia and pituitary adenoma)



episodic hypoglycemia with mental status changes that are relieved by glucose. glucose down, insulin and C-peptide up- you are making the insulin within the body if you see a high C-peptide.


what is a gastrinoma?

tumor that produces gastrin. gastrin goes to paietal cells and makes them produce acid. treatment resistant peptic ulcers- zollinger ellison syndrome
may be multiple ulcers and can extend to jejunum


what is a somatostatinoma

tumor that makes somatostatin
inhibits gastrin- low acid production (achlorhydria)
also inhibits CCK, which is important for gall bladder contraction. incr. risk of gall stones and steatorrhea


What is a VIPoma

tumor makes vasoactive intestinal pepitde
causes watery diarrhea, hypokalemia, and achlorhydria (low acid production)

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