Please enable JavaScript.

Coggle requires JavaScript to display documents.

DIABETES (Rarer forms of Diabetes (Diabetes Insipidus (*DI) 2 subtypes…

- - - - Central DI
        
        centrally not producing ADH = vasopressin
        --> can't reabsorb water through Aquaporin-2 pores in the collecting duct of the kidney
        
        large amounts of NON concentrated urine (hypoosmolar)
        
        Central DI is further divided by timeframe
        --> transient Central DI = posterior pituitary
        --> chronic Central DI = hypothalamic
        
        Clinical Cases
        
        Clinical Case
        
        Notes:
        
        note that
        
        Clinical Case
      - Nephrogenic DI
        
        producing normal ADH, but not able to act on receptors at the CD of kidney = nephrogenic
        --> can't reabsorb water through Aquaporin-2 pores in the collecting duct of the kidney
- - - - Diabetic Gastroparesis Tx
        
        1st line = metaclopramide
        --> D2 dopamine receptor antagonist
        --> stops D2 inhibitory receptors in the stomach
        --> D2 inhibits myoenteric plexus for peristalsis
        
        2nd line = macrolides (erythromycin)
        --> primary Abx for 50s ribosome protein synthesis
        --> BUY AT 30, CELL AS 50
        --> secondary macrolide property = Motilin agonist in GI
        --> reason why main side effect of Macrolides is GI diarrhea and GI upset
        
        Diabetic Gastroparesis macrolide Tx
        
        2nd line = macrolides (erythromycin)
        --> primary Abx for 50s ribosome protein synthesis
        --> BUY AT 30, CELL AS 50
        --> secondary macrolide property = Motilin agonist in GI
        --> reason why main side effect of Macrolides is GI diarrhea and GI upset
        
        "MAC ACE for MOTILIN"
        --> macrolides have secondary motilin agonist
        --> ONLY used short term for gastroparesis
        --> < 4 weeks
  - - - Clinical Cases
        
        Clinical Case
        
        Notes:
        
        note that
        
        Clinical Case
        
        Diabetic case 1
      - Diabetic Nephropathy histology
        
        Diabetic Nephropathy (messangial expansion)
        
        Kimmelstiel-Wilson Nodule
        
        complication of diabetes CKD
      - PAthophys of DGN = Diabetic glomerulonephropathy
        
        3 distinct stages of DGN
        
        1 - DGN starts with glomerular hypertrophy due to the increase sugar levels and damage
        --> increase GFR in initial stage due to the extra Glomeruli
        --> with very LITTLE nephrotic albuminuria
        --> note this is like the compensated HF where at first seems good but then enters viscous cycle
        
        1 - DGN starts with increase GFR in initial stage
        --> with very LITTLE nephrotic albuminuria
- - - - Clinical Cases
        
        Clinical Case
        
        Clinical Case
        
        DKA presentation:
        
        hyperglycemia, glucosuria
        
        hyperketonemia, ketonuria
        
        polyuria
        --> due to high glycosuria
        --> creates osmotic gradient in the urine and draws in more water
        
        metabolic acidosis
        --> compensatory tachypnea
        --> trying to expel CO2 to compensate
        
        hyperkalemia
        --> due to high H+ in the blood
        --> H+ move into the cells and displace K+ that is normally high in cells
        --> even though you have hyperkalemia in DKA, your whole body K+ stores are actually low since you are excreting alot of K+ since your K+ blood levels appear high
        
        hyponatremia
        --> due to high glucose levels in the blood, also from high free water and sodium loss through polyuria
        
        DKA Treatment:
- - - - Clinical Cases
        
        Clinical Case
        
        Clinical Case
        
        Notes:
        
        note that
- - - - TZDs Mechanism of Action
        -
        
        Notes:
        -
      - Pioglitazone Clinical Case
        
        Notes
        
        Pioglitazone is a Thiazolidindione = TZD
        
        think Pioglitazone = TZD patients get "TEASED because they get fat"
        --> pioglitazone and other TZD's increase differentiation of preadipocytes into adipocytes and activity of PPAR-gamma
        --> this increases the uptake of FAs?
        
        TZDs also increase the expression of Glucose-type 4 receptors that increase glucose uptake in liver and muscle cells
  - - - Insulin resistance - higher baseline normal glucose response Case
        
        Notes
        
        note that in a glucose challenge you can have a normal glucose response even when there is insulin resistance
        --> normal glucose challenge meaning the levels don't rise above 140 mg/dL or 11 mmol/L
        
        but you must recognize signs of insulin resistance
        --> look at the baseline of the insulin before the challenge
        --> if baseline is raised, this means there is insulin restance since body needs higher levels to get a response