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B7PBL
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  1. What are the amino acid derived hormones?
    • complex glycopeptides: TSH, LH, FSH, hCG (common alpha, unique beta chains)
    • proteins: ACTH, GH, Prolactin
    • intermediate sized peptides: insulin, glucagon
    • small peptides: TRH
    • dipeptides: T4, T3
    • derivatives of single amino acids: catecholamines, serotonin (tyrosine)
  2. What are the steroid hormones (derivatives of cholesterol)?
    • intact steroid nucleus: testosterone, cortisol
    • cleaved B ring: vitamin D and metabolites
  3. What are the transporters of water-insoluble hormones?
    • Thyroid binding globulin
    • sex hormone binding globulin
    • corticosteroid binding globulin
    • -changes in binders cause change in total, not free
    • only the free fraction is biologically active!
    • free fraction regulated, not total!!!
  4. What's leptin?
    • -Regulates fat and thus weight
    • suppress appetite
    • increase energy expenditure
    • -Regulate reproduction (higher = earlier puberty)
    • -Modulate immune system (def = dec in CD4)
  5. What stimulates the growth of different pituitary cells?
    • NeuroD1: ACTH
    • GATA2, SF-1: LH/FSH
    • Pit-1: GH, PRL, TSH (and GATA2)
  6. How can you hurt the hypothalamus?
    • Injury: head trauma, surgery, radiation
    • Tumor
    • Infiltrative Disorders: Histiocytosis X, sarcoid
  7. Sellar Masses
    • -Pituitary Adenoma
    • -Non-pit causes
    • craniopharyngioma
    • cysts
    • arteriovenous malformations
    • lymphocytic hypophysitis
  8. Control of prolactin production?
    • Inhibitory control! = dopamine from hypothalamus
    • Stimulatory = TRH, prolactin stimulator hormone
    • Neuro-endocrine reflex arc = nipple stimulation inhibits dopa release from hypothalamus
  9. Growth Hormone regulation?
    • GHRH (stress, sleep, exercise) = stimulate
    • somatostatin, IGF-1 = inhibit
    • both regulated by CNS
    • GH secretion is pulsatile (6-12/day)
  10. Action of GH and IGF-1?
    • IGF-1:
    • liner growth in kids
    • increase protein synthesis
    • mobilize fats
    • decreases insulin resistance!!
    • GH:
    • increase hepatic glucose production and decrease glucose uptake into cells
  11. Treatment of acromegaly?
    • bromocriptine
    • somatostatin
    • pegvisomany (somavert): GH-R antagonist
  12. What happens when the beta cell senses high glucose?
    • GLUT 2 = transporter
    • hexokinase
    • more ATP=K channel closes...Insulin release!
    • insulin receptors on beta cells lead to upregulation of hexokinase
  13. What's the best marker for type I DM?
    antibodies to GAD

    extrusion of GAD is an apoptotic signal for beta cells, along with too much glucose, fats
  14. What are some useful markers for Dx of Type I DM?
    • insulin deficiency
    • serum C-peptide = best test of beta cell reserve
    • best tests for islet cell autoimmunity = anti-GAD65, anti-tyrosine phosphatase (15-20%)
  15. How does insulin therapy work?
    • Total Daily Dose = 0.5 units/kg/day
    • 50% of TDD = Basal insulin (glargine)
    • 50% of TDD = mealtime boluses (aspart)
  16. What are blood advanced glycosylation endproducts (AGEs)?
    • formed by Amadori reaction complexing glucose with amines, indicators of long-term extent of hyperglycemia
    • -HbA1c is a good example!
  17. Diabetic Nephropathy on LM?
    • mesangial expansion-->kimmelsteil-wilson nodular glomerulosclerosis
    • -correlates with GBM thickening and microalbuminuria
    • treat with ACEi or ARB
  18. What's diabetic cheiroarthopathy?
    What's Dupuytren's Contracture?
    • -stiff hand syndrome "prayer sign"
    • -trigger finger
  19. Dx of DM II
    • fasting ≥126
    • random ≥200 (with classic symptoms of DM)
    • OR
    • 2 hr postprandial ≥ 200 (OGTT)
    • OR
    • A1c ≥6.5%
  20. What are some post-receptor defects in DM II?
    • serine phosphorylation of insulin receptor
    • intracellular free fatty acids (nefas)
  21. Why does amylin matter in DM II?
    apoptotic signal (it's made with insulin)
  22. Metformin
    no hypoglycemia as monotherapy
  23. sulfonylureas and meglitinides
    • insulin secretagogues
    • -50% of dose gives you 80% response

    weight gain, hypoglycemia, inc risk CVD
  24. alpha-glucosidase inhibitors (acarbose)
    safe choice in the elderly; more postprandial hyperglycemia and less fasting
  25. What's Latent Autoimmune Diabetes of Adults (LADA)?
    • indolent loss of insulin secretory capability.
    • -anti-GADs are present
    • -progressive dec in c peptide
    • -NO ketoacidosis
    • Typical: middle aged, non-obese, no real Fam Hx
  26. What are the ADA guidelines for glycemic control?
    • A1c < 7%
    • fasting ~ 100
    • 2hr postpran <150
  27. What does cHG do?
    • produced early in pregnancy to stimulate corpus luteum to continue producing progesterone for the first 8 weeks
    • suppresses maternal immune function (rejection)
  28. What's human chorionic somammotropin (hCS)?
    • It's a placental lactogen/growth hormone
    • -Effects are opposite those of insulin
    • -mom can use fat for energy, glucose and protein go to fetus
  29. What's CRH's role in pregnancy?
    • Increases a lot throughout pregnancy.
    • may be important in the timing of parturition

    -cortisol has POSITIVE feedback to wake up axis in fetus-->increased prostaglandins and delivery
  30. Maternal Pituitary Changes?
    Postpartum?
    • Gland enlarges 2-3x (lactotrophs)
    • LH, FSH, GH are low
    • ACTH goes up (increase CRH)

    Sheehan's, lymphocytic hypophysitis
  31. maternal thyroid changes?
    disorders?
    total t3,4 increased d/t increase in TBG (synthesis, inhibition of breakdown by estrogen)

    grave's is most common - treat with PTU
  32. PCOS and pregnancy
    • increase fetal loss (30-40%)
    • insulin resistance--metformin can help
  33. What are some genes that play a role in early gonadal development?
    • WT1 --> urogenital ridge
    • SRY--> SOX9 is like it...DAX-1 blocks it to make girls
    • WNT-4: Meyer-Ritanski syndrome
    • DAX-1(anti-testis): blocked by SRY
    • double DAX = girl...careful when you look at karyotypes
  34. What's Congenital Adrenal Hyperplasia?
    • Classic: 21-Hydroxylase deficiency
    • -hyponatremia
    • -hypoglycemia (no cortisol)
    • -hyperkalemia (salt-wasting...don't lose K)

    Order that 17-hydroxyprogesterone
  35. What's ghrelin?
    Endogenous ligand of the Growth Hormone Secretogues-Receptor. GHS are man-made ligands capable of stimulating GH release.

    • found in stomach...and hypothalamus
    • stimulates food intake and obesity
  36. Actions of Growth Hormone?
    • -many are mediated by IGF-1
    • -pulsatile release. stages III, IV of sleep
  37. Growth Childhood-2 to Puberty
    • 2nd year > 10 cm/yr
    • 8cm 3rd year
    • 7cm 4th year
    • 4-6 cm/year from 4 to puberty
  38. How do you calculate Mid-Parental Height?
    males: ((mom's height + 13 cm) + (dad's height))/2

    females: ((dad's -13cm) + (mom's))/2

    • 13cm = 5 inches
    • SD=2.5 cm (6-10cm 95% of time)
  39. What's Laron Syndrome?
    IGF-1 deficiency d/t GH insensitivity
  40. What's the etiology of short stature in Turner's?
    • haploinsufficiency of short stature homeobox-containing (SHOX) gene
    • -found distal tip of X and Y
    • -doesn't get inactivated...need both copies
  41. What's the most common etiology of hypercalcemia?
    primary hyperparathyroidism
  42. what's the most common cuase of high calcium in hospital patients?
    it's that cancer
  43. What are two drugs you shouldn't take with primary hyperparathyroid?
    • lithium
    • thiazide diuretics
  44. What effect does Mg have on PTH function?
    low Mg impairs PT function...PTH synthesis and release and PTH resistance

    -Common: cis-platinum chemo and alcoholism
  45. what do you need to check before taking out the parathyroids?
    check that urinary Ca. could be the familial hypocalciuric hypercalcemia
  46. What do you get with that MEN II a and b?
    • RET gene mutation = test everyone
    • a.MTC
    • Pheo
    • Parathyroid
    • cutaneous lichen amyloidosis
    • Hirschsprung disease

    • b.MTC
    • Pheo
    • mucosal and GI (even mouth) neuromas...marfinoid habitus
  47. What do you get with that MEN I?
    • Parathyroid adenoma
    • Pancreatic (Z-E)
    • Pituitary (prolactinoma)

    MEN1 mutation = tumor suppressor
  48. What's the most common thyroid cancer?
    • Papillary.
    • females, 40s, juxtanodal invasion, 6% mortality
  49. What's Whipple's Triad?
    • hypoglycemia:
    • symptoms c/w neuroglycopenia AND
    • measured glucose < 55 (not fingerstick) AND
    • rapid resolution (5min) of sx w/ ingestion or IV admin of glucose
  50. What's Polyglandular Autoimmune Failure?
    Schmidt's Syndrome
    autoimmune thyroiditis and autoimmune adrenalitis

    -hypothyroid and ...
  51. What's pituitary apoplexy?
    • worst HA of life, sudden onset, holocranial 10/10 pain
    • -hemorrhagic or edematous infarction of pituitary tumor
    • -Tx: steroids, surgical decompression
  52. What are Chvostek and Trousseau signs?
    • C: hypocalcemia: facial muscle spasm upon tapping.
    • T: hypocalcemia: occlusion of brachial artery with BP cuff-->carpal spasm
  53. What is "Hungry Bone" syndrome?
    • -Cause of post-op hypocalcemia
    • low PO4
    • high alk phos
  54. What are the different names for Acute Renal Failure?
    • ARF
    • ATN: some say synonymous b/c it's the most common intrinsic cause
    • ARI
    • ARIRF: acute reversible intrinsic renal failure
  55. How do you get ATN?
    you need to have a hemodynamic change and(/or???) some nephrotoxin...

    toxins: sepsis, NSAIDs, epinephrine
  56. What do you get with AIN?
    eosinophils are seen on biopsy
  57. What's the BUN:creatinine for prerenal and intrinsic disease?
    • Prerenal azotemia: >40
    • Intrinsic: <20
  58. How do you calculate the fractional excretion of sodium (FEna)?
    = excreted solute/filtered solute

    = (UNa x V) / (GFR x PNa) = (UNa / PNa)/(UCr/PCr)

    • -Prerenal: <1%
    • -Renal: >2%
  59. What are some sx of CRF?
    • Azotemia >3 mo
    • uremia sx
    • small kidneys
    • edema, HTN, polyuria, nocturia
    • proteinuria, electrolyte disorders
    • broad, waxy casts in sediment
  60. What's the age progression for casts?
    • epithelial
    • mixed cell/ granular
    • coarse granular
    • fine granular
    • waxy
  61. What are two risk factors for focal glomerular sclerosis?
    • AIDS
    • IV drug use (heroin)
  62. What's a good indicator of glomerular disease?
    dysmorphic cells and RBC casts
  63. What % of stone formers are hypocitraturic?
    • 30
    • -Citrate complexes Ca and prevents CaOx crystallization
  64. What % of stone formers have hyperuricosuria?
    • 25-30
    • -Promotes CaOx crystallization
  65. Prostate Cancer death?
    • 2nd in US (10%)
    • -Age = risk factor
    • Beneficial?
    • fat
    • selenium
    • vitamin D
    • retinoids
    • lycopenes
  66. How do you diagnose prostate ca?
    transrectal us guided biopsy (TRUSP)
  67. What's the most common mass in the adult kidney?
    • simple cyst
    • -don't know the patho...cysts begin as dilatation of intact tubules in contact with nephrons...fill by filtration
  68. What are the PKD genes?
    -polycystin-1 and -2, found in renal tubular epithelium, hepatic bile ducts, pancreatic ducts

    • -over expressed in cysts
    • -involved in cell-cell and protein-protein interxn
    • -loss in ADPKD causes dec intracell Ca and inc cAMP leading to cell prolif and cysts
  69. What's ADPKD?
    • 4th commonest cause of ESRD
    • ADPKD1 most common. On Ch 16
    • ADPKD2 on 6
    • Dx: <30 = 2 cysts, 30-59 2 in each, <60 4 in each
    • Sx: HTN, hematuria, UTI, stone, failure, cysts outside kidney
    • CV: mitral prolapse in 25%
    • Intracranial aneurysms!!! (4-10%) screen CT or MRA (preferred). MCA most common. ACEi.
    • Thoracic and AAA
  70. What's Von-Hippel Lindau disease?
    • -AD
    • -Retinal angiomas, cerebellar and spinal hemangiomas and pheos
    • -70-80% have renal cysts
    • -40-60% RCC, bilateral, multicentric
  71. What's tuberous sclerosis?
    • -AD on 9 and 16 (close to ADPKD)
    • -angiomyopiomas of kidney are common
    • -renal failure = most common serious manifestation above 30
  72. What's PAF?
    • small protein
    • elemental zinc cofactor
    • diminished at time of UTI
  73. What's P-fimbriae?
    • pyelo in normal ut
    • colonizes vagina/foreskin
    • ascends tract
    • cell binding
  74. What about that Type 1 (mannose sensitive) fimbriae?
    • cystitis
    • binds to Tamm-Horsfall
    • binds latex caths
    • inhibited by mannose
  75. What's a complicated UTI? so what?
    • stones
    • catheter
    • DM
    • male
    • sepsis
    • old
    • obstruction

    upper tract eval, prolonged therapy, parenteral antibiotics?
  76. How do you dx UTI?
    • US = first imaging
    • CT most specific
    • UA is helpful
    • CandS critical
  77. What's xanthogranulomatous pyelonephritis?
    • complication of UTI
    • -triad: flank mass, nonfunction, ipsilateral stones
    • -foam cells in urine
    • -abnormal LFTs?
    • -relapsing UTI
  78. What's malakoplakia?
    bladder, renal, lung, and adrenal involvement
  79. What's Michaelis-Gutmann?
    • M-G bodies: basophilic inclusions
    • large mononuclear phagocytes
  80. What are the stages of kidney disease?
    • 1: <90 and persistent albuminuria
    • 2: 60-89 '' ''
    • 3: 30-59 ml/min per 1.73m2 (7.7%)
    • 4: 15-29 '' '' '' (0.21%)
    • 5: <15 or ESRD (2.4%)
  81. What's the target blood pressure for CKD with HTN?
    • <130/80
    • ACEi or ARB: reduce kidney damage in the long run, even if creatinine rises initially
  82. What's white coat HTN?
    • 2 reading <140/90 and 2 normals
    • -ambulatory pressure monitoring for eval
  83. What are some weird causes of HTN?
    • pain (180-200)
    • drug-induced : NSAID, oral contraceptives
  84. How do you treat HTN in a diabetic?
    lisinopril and HCTZ

    metoprolol and HCTZ are both diabetogenic...the ACEi is not!
  85. What's the PE finding for renal artery stenosis?
    bruit: systolic with a diastolic component
  86. How do you diagnose renal artery stenosis?
    intra-arterial digital subtraction angiography...b/c you can fix it at the same time.
  87. What's the workup for essential HTN?
    fasting glucose, lipid profile, and serum calcium

    other suggestions (JNC7): EKG, UA, Hct, K, Cr
  88. What do most people die from with ESRD?
    cardiovascular disease complications (half of mortality)
  89. Is urea responsible for all the ills of ESRD?
    Nope. beta-2 microglobulins and leptin do it too.
  90. What are the indications for urgent dialysis?
    • hyperkalemia
    • fluid overload, pulmonary edema
    • severe acidemia
    • pericarditis
    • encephalopathy
  91. How are compounds removed in dialysis?
    • small-->diffusion
    • big-->convection

    middle molecules are removed more efficiently
  92. What are some complications of dialysis?
    • HypoTn
    • bleeding
    • cramps
    • air embolism
    • Dialysis Dysequilibrium: high BUN-->fluid in brain
  93. How does water move in peritoneal dialysis?
    Where's the best cath site?
    How does it work?
    What's the big complication?
    • 1.Aquaporins! 5-10 angstroms. 50% of water removal.
    • 2. Parasternal
    • 3. negative pressure
    • 4. infection! multiple=non-functioning peritoneum
  94. What's the DDx for nephrotic syndrome in adults?kids?
    • Adults: Kids:
    • 1.Diabetes 1. Nil/FGS
    • 2.Membranous 2. MPGN
    • 3.Nil/FGS 3. IgA/H-SP
    • 4. Amyloidosis 4. Membranous
  95. What's focal segmental glomerulosclerosis?
    • segmental scars
    • foot effacement
    • no deposits
    • negative for IF or segmental IgM, C3
    • tends to begin at CMJ
    • -progresses to ESRD frequently!
    • -recurs in transplants!
    • *associated with AIDS, IVDuse
  96. What's membranous GN?
    • Immune complex-mediated - supEPIthelial - granular deposition of IgG and C3
    • Stages:
    • 1. looks normal
    • 2. fuzzy membranes
    • 3. domes
    • 4. very thick
    • -Secondary causes: NSAID, cancer, SLE, thyroiditis, infections
  97. What's MPGN?
    Type 1: more common, subENDOthelial, tram tracks. Classical complement pathway.

    Type 2: dense deposit disease. Purely alternate complement pathway: C3 only!!! muddy pink GBM on silver stain. recurrence in transplants.
  98. What's Berger's IgA nephropathy?
    • it's the most common form of GN. most frequent cause of ESRD (30%).
    • mesangial hypercellularity
    • mesangial immune deposits
    • mesangial IF with IgA and C3
  99. What's post-infectious GN?
    • acute diffuse proliferation-->exudative, lots of PMNs
    • -dec GFR, dark pee
    • -IF looks like MPGN
  100. What's crescentic GN?
    • not a dx
    • DDx: idiopathic, anti-GBM, Wegener, PAN, cryoglobulinemia, SLE, IgA Nephropathy, PSGN, HSP, MPGN, endocarditis, HepB, serum sickness, paraprotein-induced, membranous-associated
    • -ANCA: c=Weg, p=MPA, PAN
  101. What does lupus nephropathy look like?
    • I: normal
    • II: mesangial a. pos IF, EM b.hypercellular
    • III: Focal
    • IV: Diffuse (subendothelial deposits)
    • V: Membranous (subepithelial)
    • VI: Advanced Sclerosing GN

    watch out for small vessel thrombosis (anti-phospholipid antibodies)
  102. What does diabetic nephropathy look like?
    • nephrotic
    • mesangial expansion (NEGs)
    • mesangial nodules (Kimmelstien-Wilson)
    • EM shows GBM thickening
    • IF negative

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