Which corticosteroid do you use for dangerous aldosterone deficiency?
Fludrocortisone: lots of mineralocorticoid activity
cAMP pathway
FLAT ChAMP
FSH
LH
ACTH
TSH
CRH
hCG
ADH (V2 receptor)
MSH
PTH
Also: calcitonin, GHRH, glucagon
cGMP pathway
Think vasodilators
ANP, BNP, NO (EDRF)
IP3 pathway
GOAT HAG
GnRH
Oxytocin
ADH (V1 receptor)
TRH
Histamine (H1 receptor)
Angiotensin II
Gastrin
Intracellular receptor pathway
VETTT CAP
Vitamin D
Estrogen
Testosterone
T3/T4
Cortisol
Aldosterone
Progesterone
Intrinsic tyrosine kinase pathway
MAP kinase pathway, think growth factors
Insulin, IGF-1, FGF, PDGF, EGF
Recetor-associated tyrosine kinase pathway
JAK/STAT pathway, think acidophils and cytokines
PIGGlET
Prolactin
Immunomodulators (cytokines IL2, IL6, IFN)
GH
G-CSF
Erythropoietin
Thrombopoietin
VIPoma
WDHA syndrome: watery diarrhea, hypokalemia, achlorhydria
Somatostatinoma
d-cell, a/w DM, steatorrhea, cholelithiasis, hypochlorhydria
Blocks insulin, gastrin, secretin, CCK, and GI motility
Basophilic and Acidiphilic anterior pit hormones
Basophils: B-FLAT–FSH, LH, ACTH, TSH
Acidophils: GP–GH, prolactin
Ghrelin
Stimulates hunter (orexigenic effect) and GH release (via GH secretagog receptor). Produced by stomach. Increase with sleep loss and Prader-Willi syndrome.
*Ghrelin make you hunghre.
Leptin
Satiety hormone, made by adipose tissue, decreased in starvation. Mutation of leptin gene –> congenital obesity. Sleep deprivation decreases production.
*Letin keeps you thin.
Endocannabinoids
Stimulate coritcal reward centers– Increase desire for high fat foods.
Cortisol functions
BIG FIB
1. Blood pressure: upreg a1 receptor on arterioles (more senstive to NE and E)
2. Insulin resistance
3. Gluconeogenesis, lipolysis, proteolysis
4. Fibroblast (decrease)
5. Inflammatory and Immune: inhibit PLA2, WBC adhesion, histamine release, eosinophils, IL2 production
6. Bone (decrease osteoblast)
***Exogenous cortisol can cause reactivation of TB and candidiasis (blocks IL2)
SHBG in M and W
Men: increased SHBG lowers free T –> gynecomastia
Women: decreased SHBG raises free T –> hirsutism
***OCPs, pregnancy both increase SHBG (free E remains same)
T3 functions
4B’s: Brain maturation, Bone growth, B-adrenergic effects, BMR increase (incr Na/K ATPase –> increase O2 consumption, RR, body temp)
Wolff-Chaikoff effect
Excess iodine blocks thyroid peroxidase (temp)–decreased iodine organification and decreased T3/T4.
Neuroblastoma
Children, Homer-Wright rosettes, neural crest,
Opsoclonus-myoclonus syndrome (dancing eyes-dancing feet)
HVA (dopamine breakdown) and VMA (NE breakdown) in urine
Bombesin and neuron-specific enolase +
N-myc oncogene
Hashimoto
Anti-thyroid peroxidase, antimicrosomal, antithyroglobulin abs
HLA-DR5 + HLA-B5
Increased risk of B cell marginal zone lymphoma
Hurthle cells (enlarged epithelial cell with abundant eosinophilic granular cytoplasm), lymphoid aggregate with germinal centers.
Type 4 hypersensitivity.
Congential hypothyroidism (cretinism)
D/t maternal hypothyroidism, thyroid agenesis, thyroid dysgenesis (MCC), iodine deficiency, dyshormonnogenetic goiter.
6 Ps: Pot-bellied, Pale, Puffy-faced, Protruding umbilicus, Protuberant tongue, Poor brain development.
Subacute thyroiditis de Quervain
After viral flu infection. Transient hyperthyroid first.
Granulomatous inflammation. Increased ESR, jaw pain, early inflammation, TENDER. HLA-B35
Reidel thyroiditis
Thyroid replaced by fibrous tissue that can extend into local structures–like anaplastic carcinoma!
IgG4-related systemic disease (autoimmune pancreatitis, retoperitoneal fibrosis)
Hard rock like painless goiter
Graves
IgG stimulate TSH receptors, retro-orbital fibroblasts, and dermal fibroblasts. Can present during stress (childbirth).
HLA-DR3 and HLA-B8
Scalloped colloids
Tx = b-blocker, thiomide, radioiodine ablation
Toxic multinodular goiter
Focal patches of hyperfunctioning follicular cells working independently of TSH due to mutation on TSH receptor. Increases release of T3/T4. Hot nodules rarely malignant!
