Endo-Diabetes Flashcards
Differentiate Type 1a and Type 1b diabetes
Type 1a: autoimmune destruction of beta cells
Type 1b: Non-autoimmune destruction of beta cells
Most reliable and convenient tests for identifying DM in asymptomatic individuals
HbA1c or FPG
Key regulator in insulin secretion
Glucose
Glucose level that stimulates insulin synthesis
> 70mg/dL
Rate limiting step that controls glucose-regulated insulin secretion
Glucokinase (liver)
Hexokinase(everywhere else)
Most potent incretin
Glucagon-like peptide 1(GLP-1)
Major portion of postprandial glucose utilized by
Skeletal muscle
Features of diabetes do not become evident until how much beta cells are destroyed?
70-80%
Major susceptibility gene in T1DM
HLA region on chromosome 6
Central to the development of T2DM
Insulin resistance and abnormal insulin secretion
Predominantly accounts for increased FPG levels
Increased hepatic glucose output
Results in postprandial hyperglycemia
Decreased peripheral glucose usage
Honeymoon phase
Time when glycemic control is achieved with modest doses of insulin
Ketone bodies
Acetoacetate(excreted in the urine)
B-hydroxybutyrate
Acetone(not used as source of energy)
Preferred method for detecting ketones that more accurately reflect the true ketone level
Serum or plasma assays for B hydroxybutyrate
Preferentially detected by a commonly used ketosis detection reagent (nitroprusside)
Acetoacetate
Consistent finding in DKA and distinguishes it from simple hyperglycemia
Ketonemia
Etiology of hyperglycemic hyperosmotic state(HHS)
Relative insulin deficiency & inadequate fluid intake
Prominent features of both HHS and DKA
Volume depletion and hyperglycemia
Confirm a patient’s need for insulin
Low c-peptide level
Symptoms of diabetes usually resolve when glucose is
<200mg/dl
Standard of care in diabetes management
Self monitoring of blood glucose
Standard method for long term glycemic control
Measurement of Hba1c
Most serious complication of therapy of DM
Hypoglycemia
Microvascular manifestations of DM
Retinopathy, neuropathy, nephropathy
Macrovascular manifestations of DM
CAD, PAD, CVD
Leading cause of blindness between ages 20 and 74
DM retinopthy
Non-proliferative DM retinopathy
Retinal vascular microaneuryms, blot hemorrhages, and cotton wool spots
Hallmark of proliferative DM retinopathy
Neovascularization in response to retinal hypoxia
Most effective therapy for DM retinopathy
Prevention
Treatment of proliferative retinopathy
Panretinal laser photocoagulation
Treatment of macular edema
Focal laser photocoagulation
Optimal therapy for DM nephropathy
Prevention by control of glycemia
Preferred therapy for DM nephropathy
Renal transplantation from a living related donor
Most common site of foot ulcers
Great toe or metatarsophalangeal(MTP) areas
Optimal therapy for foot ulcers and amputation
Prevention
Most common site of ulceration
Plantar surface of foot
Most common form of diabetic neuropathy
Distal symmetric polyneuropathy(commonly sensory)
Most commonly involved nerve in mononeuropathy
CN III(heralded by diplopia)
Most prominent GI symptoms in DM
Delayed gastric emptying and altered small- and large-bowel motility
Most common pattern of DM dyslipidemia
Hypertryglyceridemia and reduced HDL
Type 1 DM
usually <30 yo autoimmune cause DKA is the most common complication HLA-DR3, -DR4 Depleted beta cells Islet leukocytic infiltrate
Type 2 DM
Strong polygenic genetic predisposition
Islet amyloid deposit
Defense against hypoglycemia
1st line: decreased insulin
2nd line: increased glucagon
3rd line: increased epinephrine
Compromises physiologic defense against hypoglycemia
Defective glucose counterregulation
Compromises behavioral defense against hypoglycemia
Hypoglycemia unawareness
Hypoglycemia in non-beta cell tumors is due to
Overproduction of insulin like growth factor II
Prototypical cause of endogenous hyperinsulinism
Insulinoma
Ingestion of an insulin secretagogue
Hypoglycemia with increased C-peptide levels
Exogenous insulin
Causes hypoglycemia with low C-peptide levels
Hormones derived from proopiomelanocortin(POMC)
MSH, ACTH, B-lipoprotein, B-endorphin
Main site of ADH/Vasopressin synthesis
Supraoptic nuclei of the anterior hypothalamus
Main site of oxytocin synthesis
Paraventricular nuclei of the anterior hypothalamus
Site of oxytocin and ADH/vasopressin storage and secretion
Posterior pituitary
3 parts of the adrenal cortex
From outer to inner: (GFR) Zona glomerulosa(aldosterone secretion) Zona fasciculata(cortisol secretion) Zona reticularis(weak androgen secretion)
2 products of the adrenal medulla
Epinephrine (80%)
Norepinephrine (20%)
Decreases Ca2+ & phosphate excretion but increases urinary Ca2+; increases intestinal Ca2+ absorption
Vitamin D
Stimulated by LH, releases the “libido” hormone testosterone
Leydig cells
Mnemonic: LLL: LH, Leydig, Libido Hormone
Stimulated by FSH, nurse cell for sperm
Sertoli cells
Mnemonic: SSS: FSH, Sertoli cells, Sperm
Increases blood glucose, has direct and indirect effects (via IGF-1)
GH
GHRH -> GH -> IGF-1
CRH -> ACTH ->
Cortisol
ZF (largest area in the AC)
Weak androgens
DHEA, androstenedione (ZR, AC): significantly only in females