Hypothalamus Anatomy and Hypothalamic Nuclei
• Anterior hypothalamic nucleus - Body temperature, thermal regulation (heat dissipation), stimulates parasympathetic ns, destruction results in hyperthermia.
• Paraventricular nucleus - Water balance & stress, produces ADH & oxytocin, destruction causes diabetes insipidus
• Dorsal & lateral hypothalamic area - Water balance & stress, produces ADH & oxytocin
• Posterior hypothalamic area - Shivering, thermal regulation, destruction causes inability to thermoregulate, stimulates the sympathetic CNS
• Dorsomedial nucleus - GI tract, stimulation results in obesity and savage behavior
• Lateral & medial preoptic nucleus - Blood pressure, contains sexually dimorphic nucleus, regulates release of gonadotropic hormones
• Supraoptic nucleus - Water Balance
• Ventromedial nucleus - Satiety center, destruction results in obesity & savage behavior
By @rev.med
#Hypothalamus #Anatomy #Nuclei #neurology #neuroanatomy #nucleus
Pituitary Mass Effects - Pathogenesis and Clinical Findings
• Pituitary turnors are almost always a benign adenoma. Pituitary adenomas are very common - approximately 1 in 6 individuals. These are usually asymptomatic and are found incidentally. Symptomatic pituitary adenomas that require treatment are much less common and affect approximately I in 1000 individuals.
• For pituitary masses of all sizes, it is important to determine whether the pituitary tumor is secreting (70%) or non-secreting (30%) as secreting tumors can be targeted with medication. The most common secreting tumors secrete prolactin (most common), growth hormone, and ACTH.
• Typically (but not always) the anterior hormones will be lost in the following order; GH, LH, FSH, TSH, ACTH, PRL. This order (with the exception of prolactin) is the order of least-essential to most essential hormones needed for survival. A good mnemonic to remember the order the hormones are is, "Go Look For The Adenoma Please".
Signs / Symptoms / Complications:
• Hyperprolactinemia
• Diabetes insipidus
• Loss of pituitary hormones
• Headaches
• Nausea and vomiting
• Hypothalamic dysfunction
• Bitemporal hemianopsia
• Hydrocephalus
• Diplopia
• Post-nasal drip
• Meningitis
#Pituitary #MassEffects #Macroadenoma #SideEffects #endocrinology #mnemonic #GLFTAP #pathophysiology
Glucocorticoid-Induced Osteoporosis: Pathogenesis and Clinical Findings
• Negative feedback on hypothalamus/pituitary, Decreasing ACTH -> Decr Sex Hormones (LH, FSH, Testosterone, Estrogen)
• Inhibit production of osteoblasts and GF's -> Osteoblasts and Growth Factors (GF's)
• Decrease Vit-D (1-25-OH2) synthesis and action -> Decr Ca2+ Absorption, Incr Ca2+ Excretion
• Upregulate gene expression of osteoclasts -> Incr Osteoclasts
• Inhibit production of osteocytes -> Decr Osteocytes
• Increase Marrow Fat -> Fat emboli
-> Reduced Bone Formation, Increased Bone Resorption, Decreased Blood Supply
#Glucocorticoids #steroids #Osteoporosis #pathophysiology #signs #symptoms #diagnosis
Acromegaly - Diagnosis and Management Summary - GrepMed Handbook
Clinical Presentation:
• Classic Acromegaly: frontal bossing, enlarged jaw (macrognathia), ↑ hand + feet size, coarsening facial features, soft tissue swelling and organomegaly
- c/f ring tightening, ↑ glove & shoe size, ↑ heel-pad thickness, paresthesias (carpal tunnel) and OSA
- Arthralgias, hypertrophic arthropathy
• Insidious onset, often undiagnosed for 10+ years.
- Usually presents ~5th decade → peripheral/acral enlargement
- If GH excess occurs before epiphyseal fusion (children) → Gigantism
• Organomegaly: Visceral organs, macroglossia, goiter, LV hypertrophy, colon (↑polyps & malignancy)
• Cutaneous: hyperhidrosis, hair growth, skin tags, skin thickening, acanthosis nigricans, cutis verticis gyrata.
• Macroadenoma direct effects: Headache (60%), Vision Δs (bitemp hemianopia 10%), HyperPRL (30%), Hypogonad (50%)
• Metabolic: Insulin resist + DM, Hyperphosphatemia (70%)
• ↑Mortality due to CVD & colon malignancy
Pathophysiology:
• Acromegaly occurs secondary to GH hypersecretion.
• GH stimulates liver IGF-1 (somatomedin C) secretion. GH + IGF-1 → multisystemic anabolic effects with acromegaly and organomegaly.
• ~98% - GH-secreting pituitary adenoma (Up to 30% of pituitary adenomas are mixed GH & PRL)
• ~2% - Extrapituitary secretion: pancreatic islet cell tumor, excess GHRH release, central (hypothalamic hamartoma) or peripheral (bronchial/abdominal carcinoid or SCLC).
Differential Diagnosis (Pseudoacromegaly/Acromegaloid): insulin resistance pseudo-acromegaly, obesity, hypothyroidism, pachydermoperiostosis, drugs (phenytoin, minoxidil), genetic (Beckwith Wiedemann syndrome)
Diagnosis and Workup:
• Serum IGF-1 level (↑Sens) - GH levels not useful as levels are variable
- If IGF-1 equivocal: Oral glucose suppression test → ⨁ if failure to suppress GH levels to <1ng/mL.
• Pituitary testing: ↑PRL in mixed adenoma, ↓(TFT, LH, FSH & ACTH) 2/2 adenoma mass effect
• Pituitary MRI+contrast
Management:
• 1st line - Transsphenoidal surgical resection for adenoma
• Medical Tx (non-surgical candidates, adjuvant Tx, or post-op residual dz): Somatostatin analogues (Lanreotide) ± GH receptor antagonist (Pegvisomant) ± D2 agonist (Carbergoline)
• Radiotherapy: Relapse or refractory cases
By Dr. Anuj Thakre (@thakre_anuj)
#Acromegaly #Diagnosis #Management #Endocrinology #Treatment #Pathophysiology
Menstrual Cycle Physiology: Correlating the Ovarian and Uterine Cycles
Note: Some charts show different relative levels of the gonadotropins (LH and FSH) to estrogen and progesterone, but the key is
to compare the relative levels of estrogen with progesterone, and to observe how they change compared to the gonadotropins.
Ovarian Cycle
1. Follicular phase (around 10-14 days long)
• Starts at puberty (unclear mechanisms), 6-20 follicles re-activated per month.
• One follicle outpaces the others, continues to develop into the mature follicle (others degenerate).
• The process also involves hormones released by theca and granulosa cells (activin and inhibin) that affect follicle development as well. See also "Follicular Phase Explained" slide.
2. Ovulation
• Release of secondary oocyte around day 14 (can vary)
• Triggered mostly by LH surge. See also "Ovulation Explained" slide.
3. Luteal phase (always 14 days long)
• Follows release of oocyte
• Transformation of granulosa and theca cells of the follicle into the corpus luteum, which secretes progesterone and a bit of estrogen to negatively feed back on the anterior pituitary and inhibit the growth of new follicles.
• Corpus luteum degenerates in 14 days if no fertilization (thus, luteal phase is always 14 days long). See also "Luteal Phase Explained" slide.
Uterine Cycle:
1. Menses (menstrual bleeding)
• Occurs during the first part of the follicular phase of the ovarian cycle due to the sharp decline in progesterone
2. Proliferative phase
• Before and up to ovulation, the endometrium adds new cell layers, especially due to estrogen
• During late proliferative phase: estrogen makes cervical mucous thinner, more abundant, and stringier, which allows it to be penetrated by sperm.
3. Secretory phase
• Corpus luteum hormones, mostly progesterone, limit endometrial growth while endometrial secretions.
• After ovulation, progesterone causes mucus to become thick and tacky, less likely to be penetrated by sperm.
#UterineCycle #MenstrualCycle #OvarianCycle #pathophysiology #comparison #endocrinology