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173 Cards in this Set

  • Front
  • Back
Where are three possible receptor locations on which a hormone acts?
Cell membrane; Cytoplasm; Nuclear membrane
What two factors affect the strength of an endocrine response at the cellular level?
Receptor density & Length of binding time
What are three examples of hormones which bind to receptors on the cell surface?
Insulin; Growth hormone; Catecholamines (Epinephrine, norepinephrine, dopamine); Histamine
What are two classes of hormones that are capable of diffusing through the cell wall? Why are they able to diffuse passively?
Thyroid and Steroid hormones. These hormones are fat-soluble, and can thus pass easily through the lipid bilayer
Testosterone production in the Leydig cells of the testicles having an effect on testicular development in nearby cells is an example of what type of signalling?
Paracrine signalling
Malignant self-stimulation by hormonal release is what type of signalling?
Growth hormone, ACTH & Thyroxine are all part of what class of hormones?
Cholesterol derivatives are part of what class of hormones? What are some examples?
Steroid hormones (Sex hormones, Glucocorticoids, Mineralocorticoids, Vitamin D & derivatives)
What is testosterone converted to (by 5a-reductase), which can lead to androgenization in older women?
Will cutting the hypophyseal stalk cause a deficiency in Oxytocin or Vasopressin?
No. Although the anterior pituitary hormones will be affected due to their precursors' secretion into the bloodstream in the hypothalamus, posterior pituitary hormone precursors are not released into the bloodstream until they have reached the pituitary gland. (Something like that...)
Congenital hypothyroidism is termed what?
Which two hormones play the largest role in electrolyte and water homeostasis?
Vasopressin & Aldosterone
What are the two metabolic goals of energy homeostasis?
1. Provide sufficient energy to each tissue in the form that is required in different metabolic states
2. Prevent high concentrations of glucose, fatty acids and fat in the circulation
Shortly after a meal, what happens to your insulin and glucagon levels?
An increase in blood glucose levels will cause an increase in insulin levels, and a decrease in glucagon.
What three liver processes does insulin increase? What three does it decrease?
Increase: Glucose stored as glycogen, TG synthesis, glycolysis
Decrease: Glycogenolysis, ketogenesis, gluconeogenesis
True or false: Glucagon causes increased lipolysis?
True. Glucagon is trying to mobilize energy stores in the body.
What effect does glucagon have on the muscles?
No effect! There are no glucagon receptors in muscle tissue.
Triglycerides absorbed through the small intestine are stored primarily where?
Adipose tissue
In the postabsorptive state, where does muscle tissue get fatty acids from?
Triglycerides stored in adipose tissue are broken down into fatty acids and glycerol. Fatty acids then travel to the muscles for conversion to Acetyl CoA.
True or false: In a state of prolonged fasting, the brain is able to make use of ketone bodies for energy?
True, though typically only when there is a serious deficiency in glucose availability
What is an example of a short-term effect by signal transduction? What about a long-term effect?
Short: Regulation of enzyme activity
Long: Regulation of gene expression
Which molecule triggers insulin secretion? What inhibits insulin secretion?
Trigger: Glucose
Inhibition: Epinephrine
Which glucose transporter is upregulated by insulin?
What fasting blood glucose level (in mM) is diagnostic for diabetes mellitus? What random plasma glucose level is diagnostic?
Fasting: 7.0 mM
Random: 11.1 mM
In pre-diabetes, how is insulin secretion affected?
Insulin secretion is increased in pre-diabetes, as it has a more difficult time regulating blood sugar.
What are three sources of hyperglycemia in diabetes (Type I or II)?
Decreased glucose uptake into muscle and adipocytes; Ongoing gluconeogenesis; Glycogen breakdown in liver
What metabolic changes in untreated diabetes can affect amino acids?
Amino acid uptake and protein synthesis is not stimulated (due to a problem with insulin signalling). These free amino acids are also gluconeogenic precursors, so an excess will cause excess glucose production by the liver.
How are ketone bodies formed in type I diabetes?
Breakdown of TG into fatty acids (+glycerol) => FA are absorbed by the liver, converted to Acetyl CoA, which can be ketogenic in the absence of insulin regulation.
Leptin is secreted by which type of tissue? What is it released in response to?
Secreted by adipose tissue, it is released in response to adequate adiposity and energy storage. It then signals the brain to reduce further food intake.
Type 1 diabetes represents about what percentage of total diabetes?
HLA DR3 & DR4 is a risk factor for which condition?
Diabetes mellitus type I
What is the only confirmed virus known to be a risk factor for DM1?
Congenital rubella
What immune marker is present in 80-90% of new DM1 patients? Is it specific?
Islet cell antibodies. It is a non-specific marker for immune reactivity.
Why is screening for diabetes-associated antibodies not done in clinical practice?
There is no therapeutic intervention available to prevent the disease course.
Approximately how many beta cells are left by the time DM1 becomes symptomatic? (5%, 15%, 30%, 50%)
Why does the "honeymoon" period occur following diagnosis and initial treatment of DM1?
Exhaustion of functional beta cells prevents proper functioning. Relief from exhaustion by treatment with insulin allows these non-destroyed cells to retain normal function, for a short time until they are eliminated by the immune process.
True or false: Oral glucose tolerance tests are often done for diagnosis of type 1 diabetes.
False. Patients typically present with clear symptoms, and their blood glucose levels are through the roof, thus an OGTT is not needed.
C-peptide tends to be _____ in type 2 diabetes, and ______ in type 1. (high, low)
Type 2: High
Type 1: Low
C-peptide is cleaved when insulin is produced by the body. In type I, there is no insulin being produced, so no C-peptide is cleaved.
Why does high sodium occur in diabetic ketoacidosis?
DKA is associated with high glucose levels in the blood (besides ketones). Water is osmotically drawn into the bloodstream due to the hypertonic glucose concentration. When water flows, so does sodium.
In patients with DM1, what are two factors which reduce blood glucose levels? What are two that increase it?
Decrease: Insulin & Activity
Increase: Carbohydrates & Stressors (exams, illness)
What are the two broad categories of long-term complications of diabetes?
Microvascular & Macrovascular
What are three microvascular complications of diabetes?
Retionpathy; Nephropathy; Neuropathy
Hemoglobin A1c reflects glycemic control over what timeframe?
2-3 months (RBCs live ~120 days; A1c reflects the average glucose level exposure over that time)
True or false: Diabetic retinopathy affects the blood vessels of the retina.
True. Increased permeability with exudates can occur, as well as neovascularization.
What are the 4 stages of diabetic nephropathy?
1. Normoalbuminuria (+hyperfiltration)
2. Microalbuminuria (Small amounts of protein in urine, possibly reversible)
3. Macroalbuminuria (Lots of protein in the urine, not reversible)
4. End-stage renal disease
Why does diabetic neuropathy affect the feet early on?
The nerves supplying the feet are the longest in the body, thus have the largest amount of surface area to be affected.
The DCCT demonstrated that good glycemic control can prevent what?
Microvascular complications of diabetes. (The extension study has demonstrated a reduction in macrovascular complications as well)
Is visceral or subcutaneous fat more problematic in DM2?
Visceral fat is more toxic.
What are the three core defects in DM2?
Insulin resistance; Glucagon dysregulation; Beta-cell dysfunction
Annual fundoscopy should be done how long following diagnosis of type 1 diabetes? Does this change in type 2?
Type 1: 5 years after diagnosis
Type 2: immediately after diagnosis, due to more subtle clinical presentation
What is the A1c target for most diabetic patients (DM2)
< 7.0%
What is the class of drugs involved in insulin sensitization (besides metformin), which is also implicated in fluid retention side effects (e.g. CHF)?
Thiazolidinediones (TZD's)
What is metformin's main function? What are two other, lesser effects?
Main: Decreased gluconeogenesis in liver
Lesser: Increased insulin secretion, increased insulin sensitivity
With slightly elevated A1c, what is the main source of glucose which is contributing to the elevation?
When A1c is slightly elevated, it is postprandial (after-meal) glucose that is the main contributor to the elevation of A1c. In more elevated A1c state, it is the tonic, basal glucose which is the major contributor of excess.
What are the two main incretin-based diabetic therapeutic approaches?
- Mimic endogenous incretin action (GLP-1 analogues, which are not broken down by DPP-IV)
- Prevent incretin degredation (enzyme inhibitor; DPP-IV inhibitor)
What are four physiologic roles of (endogenous) incretins?
Helps the pancreas secrete more insulin; Suppresses glucagon; Is more active when sugars are high; Less active when sugars are low to avoid hypoglycemia
Between apolipoprotein A and apolipoprotein B, which is associated with HDL, and which with LDL?
HDL: apoA
LDL: apoB
Target LDL is partially based on risk for what?
Coronary artery disease
Are dietary complex carbohydrates or simple sugars worse for you in terms of high cholesterol?
Simple sugars should be reduced. Complex carbohydrates, such as soluble fibre, are actually beneficial to LDL reduction.
How do plant sterols work to reduce LDL?
Plant sterols compete with cholesterol for absorption through the intestines, thus less bile is reabsorbed, and the liver is forced to upregulate LDL receptors to steal cholesterol from the blood to synthesize more bile.
HMG-CoA reductase inhibitors are more commonly known as what?
What is the primary mechanism of action of statins?
They reduce hepatic cholesterol synthesis, causing upregulation of LDL receptors to pull cholesterol out of the bloodstream
What class of drugs are useful for lowering TG's and raising HDL? Are they good for preventing coronary artery disease?
Fibrates. There is very little evidence to suggest they reduce CAD.
What is the mechanism of Nicotinic Acid? (we probably don't need to know this, but it can't hurt)
Decreases hepatic production of vLDL and apoB
Flushing and potential hepatotoxicity are side effects of what LDL-lowering medication?
Niacin (& derivatives)
What are five classes of drugs used for treatment of dyslipidemia?
Statins, Fibrates, Niacin, Bile acid binding resins, Cholesterol absorption inhibitors
What is the bony cavity in which the pituitary gland sits?
Sella turcica
What are the six primary hormones which are released by the anterior pituitary lobe?
Growth Hormone; Adrenocorticotrophic releasing hormone; Thyroid-stimulating hormone; Follicle-stimulating hormone; Luteinizing hormone; Prolactin
Which two hormones are released by the posterior pituitary lobe?
Oxytocin & Vasopressin (ADH)
LH/FSH given in a pulsatile fashion will ___________ sex hormone production, while giving LH/FSH tonically will ___________ sex hormone production.
Pulsatile: Increase/stimulate
Tonic: Decrease/inhibit
The variation in cortisol production during 24 hours is called what type of rhythm?
Diurnal rhythm
What are two broad categories of actively testing for hormone abnormalities?
Suppression & Stimulation tests
What are three general pituitary disease patterns?
Reduced production of hormones; Excessive production of hormones; Effects of tumour compression on adjacent structures
What are the two most important hormones released by the anterior pituitary? (Produced in the core of the AP, according to pituitary lecture)
Polyuria and polydipsia can result from a deficiency in which pituitary hormone?
ADH (Vasopressin)
What are three questions to ask when confronted with a pituitary tumour?
- Is it a functioning or a non-functioning tumour?
- Is there an associated pituitary insufficiency?
- Is the tumour causing any compressive features?
Nerve entrapment and snoring may be signs of a functioning pituitary tumour releasing which hormone?
Growth Hormone
Pituitary adenomas initially cause what type of vision loss?
Superior bitemporal quadrantinopia (leading to bitemporal hemianopia)
A low urine concentration in a water deprivation test is indicative of what condition?
Diabetes insipidus
Purple striae are common in which endocrine condition?
Cushing's syndrome/disease
From outer to inner, what are the three zones of the adrenal cortex?
Glomerulosa; Fasciculata; Reticularis (GFR)
Which two adrenal cortex zones does ACTH stimulate? What compounds do these zones produce?
Fasciculata (Cortisol) & Reticularis (Adrenal androgens)
What benefit is there to having CRH controlled by neural systems?
It is able to respond in times of stress, stimulating ACTH => Cortisol
What protein does cortisol bind mainly to in the blood stream? What about testosterone & estradiol?
- Cortisol: Corticosteroid binding globulin (75%). Only 15% is bound to albumin.
- T/E: Sex hormone binding globulin (60%)
Metabolization of adrenal steroids occurs primarily in which organ?
What is the most common cause of Cushing's syndrome?
Exogenous glucocorticoids (e.g. prednisone)
What are some clinical presentation signs of Cushing's? (There are a TON)
Central obesity; Moon facies; Supraclavicular & dorsal fat pads; Plethora; Purple striae; Thin skin; Easy bruising; Hirsutism; Acne; Telengectasia; Psychosis; Depression; Hypertension; CV disease; Myopathy; Osteopenia; Osteoporosis; Infections; Poor wound healing; Menstural disorders; Decreased libido; Glucose intolerance/diabetes; Hyperlipidemia; Kidney stones
What are the three steps in diagnosis of an endocrine disease (e.g. Cushing's)?
Clinical suspicion; Biochemical confirmation; Anatomical localization (CBA)
What other measure might you want to check in a 24 hour urine free cortisol test to ensure an adequate collection volume?
Urinary creatinine
Why is the 2mg/48h dexamethosone suppression test better than the 1mg/overnight test?
It is more specific
If Cushing's syndrome is suspected, which two (or three) tests should be done, and in which order? (This is to confirm the presence of Cushing's, not the anatomical location)
1 mg overnight dexamethasone suppression test; then 24 hour urine free cortisol or 2 mg DST
Which two tests can be used in tandem to pinpoint the anatomical location of Cushing's syndrome?
ACTH (Radioimmunoassay) & High dose (8 mg) Dex suppression test.
What is the condition "Addison's disease" specific to?
Primary adrenal insufficiency
What is the most common cause of Addison's disease?
Autoimmune process (adrenalitis)
Hyperpigmentation occurs due to extremely high levels of what hormone?
ACTH. Melanocyte-stimulating hormone is created as a byproduct of ACTH synthesis, and increases melanin production in cells, causing hyperpigmentation
Is 24-hour urine free cortisol a useful test for diagnosis of Addison's disease? What are some passive testing alternatives?
Nope, it's not very sensitive at low levels. Alternatively, a high random serum cortisol virtually excludes insufficiency, and a low serum cortisol associated despite physiological stress is good evidence of adrenal insufficiency
What does an lack of cortisol response to an ACTH stimulation test indicate? What does it not allow you to distinguish?
Adrenal insufficiency, but that test alone can't determine if it's primary or secondary. You might think it's secondary, but the cortisol-releasing cells of the adrenal gland may atrophy in response to chronically low ACTH, thus they cannot be stimulated by exogenous ACTH.
If there is a normal response to ACTH stimulation test in suspected adrenal insufficiency, what test should be ordered next?
Insulin tolerance test. A normal response to ACTH stimulation excludes primary adrenal insufficiency, so to test for secondary adrenal insufficiency, you need to give insulin to test the entire H-P-A axis. Insulin should cause hypoglycemic-induced cortisol release - if it does not, then secondary adrenal insufficiency (i.e. pituitary) is likely.
Following an decreased (abnormal) response to an ACTH stimulation test in suspected adrenal insufficiency, what test should be done next to identify the anatomical location? How would you interpret the results?
Plasma ACTH levels should be measured. If they are elevated, then it is primary adrenal insufficiency. If it is not elevated, than it is likely secondary adrenal insufficiency.
In acute adrenal crisis, what is the first line treatment (along with volume replacement)?
Steroids! (Hydrocortisone)
In which direction does the thyroid gland typically enlarge?
Inferiorly, behind the clavicle
Thyroglobulin is produced in which cells?
Thyroid follicles
Which residues of thyroglobulin are iodinated to form mono- and diiodothyroinine?
Tyrosine/Tyrosyl (Depending on the lecture...)
What is the most common measure of thyroid function?
Which thyroid hormone is biologically active?
T3 (Converted from T4 in peripheral tissues)
Which enzyme catalyzes the coupling of MIT and DIT to form T3/T4?
Thyroid peroxidase/Thyroperoxidase (Depending on the lecture...)
Which organ is the major extrathyroidal T4 conversion site for production of T3?
What three factors can affect carrier protein number/function?
Physiologic changes; Drugs; Disease
Mental retardation and incomplete development can result from a congenital lack of what hormone?
Thyroid hormone
What is the most important test after clinical history and physical exam in the evaluation of thyroid masses?
Fine needle aspiration biopsy
Is a thyroid lump more at risk for malignancy in men or women?
Men. A large percentage of women actually have a innocuous lump in their thyroid gland.
90-95% of thyroid cancers arise from which type of cell?
Follicular cell
What is the most common type of thyroid cancer?
Papillary thyroid carcinoma
Following synthesis, where is thyroglobulin stored?
The colloid
Which ion is exchanged for iodide during uptake into the follicular cells of the thyroid gland?
What are the six major steps in the synthesis of thyroid hormone?
1. Thyroglobulin synthesis
2. Iodide trapping
3. Oxidation and organic binding of iodide
4. Coupling (of MIT/DIT)
5. Proteolysis and release
6. Intrathyroidal deiodination (of unused DIT/MIT)
Aside from T3, what other compound can be synthesized by deiodination of T4?
Reverse T3 (rT3), which is not biologically active.
Does GI motility increase or decrease in response to thyroid hormone?
What is the clinical syndrome that results when tissues are exposed to high levels of circulating thyroid hormone?
Lid lag and lid retraction are common signs in what condition?
Hyperthyroidism (Graves' disease)
What are the three most common causes of hyperthyroidism?
Graves' disease; Toxic adenoma/multinodular goiter; Thyroiditis
What are four symptoms associated with Graves' disease?
Thyrotoxicosis; Goiter; Ophthalmopathy; Dermopathy
Why does ophthalmopathy occur in Graves' disease?
Cytotoxic T-lymphocytes respond to thyroid autoantibodies, which are also present in orbital tissue. Extraocular muscles then become infiltrated with lymphocytes and edema, causing swelling of the eye muscles.
Pretibial myxedema is a symptom found in which condition?
Graves' disease
What is the most common imaging technique for investigation of Graves' disease? How would this change in thyroiditis, or nodules?
- Radioactive iodine uptake and scan - should have high uptake and homogenous involvement of gland.
- In thyroiditis, hormone is being spilled out, and iodine uptake is low
- In nodules, uptake is not homogenous
What are the two initial drug therapies for treating Graves' disease?
Beta-blocker (propanolol) & Anti-thyroid drug (Anti-TPO)
What are two treatment options of Graves' disease if initial drug therapy fails?
Radioactive iodine therapy & Thyroidectomy (has many side effects & risks)
What are five causes of primary hypothyroidism?
Hashimoto's thyroiditis; Subacute thyroiditis; Iatrogenic; Drugs; Iodine deficiency or excess
How do Graves' and Hashimoto's thyroiditis differ pathophysiologically?
Both are immune-mediated, however Graves' autoantibodies stimulate chronic production of thyroid hormone (bind and stimulate TSH receptor), while in Hashimoto's, the autoantibodies bind and block the TSH receptor (Also, lymphocytes infiltrate the thyroid and destroy the normal architecture)
What is the normal treatment of Hashimoto's thyroiditis?
Synthetic human T4 (Levo-thyroxine) replacement. (If someone is missing the conversion enzyme for T4=>T3, you may consider giving them T3)
In males, what function does LH serve? What about FSH?
LH: Testosterone production in Leydig cells of testes
FSH: Testicular growth & spermatogenesis
What is the term for onset of female breast tissue development?
What are the absolute physical markers of puberty onset for boys & girls?
Boys: Testicular enlargement (Testosterone-dependent)
Girls: Breast development (Estrogen-dependent)
What is the staging system for pubertal development in adolescents?
Tanner system
What would an unresponsive GnRH stimulation test indicate when assessing adolescents?
An unresponsive test (i.e. no LH/FSH rise) would indicate either a pre-pubertal or hypergonadal state.
What are the two broad categories for causes of non-constitutionally delayed puberty? What does each indicate?
Hypogonadotropic hypogonadism (Problem with pituitary/hypothalamus) & Hypergonadotropic hypogonadism (Problem with gonad)
Why is bone age investigation useful in assessing hypogonadism?
Looking at the hand/wrist growth plates can determine what the person's physiologic age is (to see if it is a constitutional delay)
With what therapeutic intervention might you consider treating a 15-year old boy who has constitutionally delayed puberty?
A short course of low dose testosterone - to "kick-start" puberty.
What four components are necessary for a normal menstrual cycle?
Normal pulsatile secretion of GnRH, LH & FSH; Normal pituitary gland; Normal ovaries; Normal outflow tract
Insulin resistance and ovarian hyperandrogenism are pathogenic for which condition?
Polycystic Ovarian Syndrome
PCOS Amenorrhea can lead to uterine cancer through what mechanism?
Buildup of endometrium through chronic hormonal stimulation can lead to endometrial hyperplasia, which can become dysplastic and possibly malignant.
What ages are considered precocious puberty in boys and girls?
Boys: < 9; Girls: < 8
Why is treatment for central precocious puberty important? What is the treatment?
Psychosocial issues + Growth spurt problems - if the child starts puberty too early, she will end up being short (What's wrong with being short!). Treatment is typically GnRH agonist IM every 3-4 weeks - this is a tonic administration, and suppresses the natural pulsatile release to prevent puberty.
What medication may be administered to decrease insulin resistance in PCOS?
True or false: The vast majority of cases of hypertension have no identifiable cause?
True - 95% of hypertension cases are "essential hypertension" have have no identifiable cause.
What are the two hormones secreted in the largest amounts in the adrenal medulla?
Epinephrine (80-85%) & Norepinephrine (15-20%)
What is the basic definition of a pheochromocytoma?
Catcholamine-secreting tumour arising from chromaffin cells of the adrenal medulla (usually)
Which type of hormone is secreted in excess from a pheochromocytoma?
Catecholamines (Norepinephrine, Epinephrine)
Which of the following is not one of the 6 P's in Pheochromocytoma? (Paroxysms, Palpitations, Perspiration, Paresthesia, Pallor)
Paresthesia. The other two are Pain (headache) and Pressure (Hypertension)
Norepinephrine is metabolized to what compound? What about epinephrine?
Nor => Normetanephrine
Epi => Metanephrine
What is typically measured in a 24-hour urine sample with suspect pheochromocytoma?
Epinephrine, Norepinephrine, Normetaneprhine, Metanephrine (VMA may still be measured, but not very useful)
What three pre-operative preparation strategies are used in pheochromocytoma, and in what order?
Alpha-adrenergic blocker; Volume expansion; Beta-adrenergic blocker.
Always do an alpha block first, as beta blockers alone can make the hypertension worse (vasodilatory peripheral beta-adrenergic receptors)
Laprascopic adrenalectomy is always done for treatment of what condition?
What is produced in the zona glomerulosa?
Mineralocorticoids (Aldosterone)
How does hypertension occur in Cushing's?
The cortisol-inactivation enzyme (found only in the kidney) is overwhelmed by excess cortisol, and it can activate the aldosterone receptor to raise blood pressure
What is the physiological action of renin?
Renin converts angiotensiongen to angiotensin I
What two physiological properties does angiotensin II have?
Vasoconstriction (increases blood pressure directly) & stimulates aldosterone release from the adrenal cortex (causes salt retention)
What hormone abnormality might you wonder about with spontaneous hypokalemia?
Hyperaldosteronism (Increased sodium retention, increased potassium secretion in urine)
What two compounds are measured for screening of suspect hyperaldosteronism?
Aldosterone & Renin (measure ratio)
What type of loading test can be used to diagnose hyperaldosteronism?
Saline loading test (promote volume expansion, if aldosterone does not go down, it is pathogenic)
What procedure should be done before surgery to ensure localization of hyperaldosteronism?
Selective adrenal vein sampling (In case the "mass" on CT is actually an incidentaloma/red herring)
What is the primary medical therapy for treating hyperaldosteronism? (Bonus: what is a side effect of the older drug?)
Aldosterone receptor blocker/antagonists (Spironolactone & Eplerenone) Spironolactone also blocks testosterone receptors, so gynecomastia is problematic in men
What food has been known to inhibit 11BHSD2 (Cortisol => Cortisone conversion enzyme in kidney)?
What is the Friedewald equation used for?
For approximation of LDL levels given other lipid values (HDL = totChol - LDL - TG*k)
What 5 symptoms/signs are diagnostic for metabolic syndrome (in general, not specific numbers)? How many are required for diagnosis?
High BP (>130/85); High fasting blood glucose; Elevated waist circumference; Low HDL cholesterol; High Triglycerides. Three are required for diagnosis (according to AHA and NHLBI)
What is the nature of a fatty liver in metabolic syndrome?
Insulin resistance leads to the accumulation of excess TGs in the liver, and subsequent development of hepatic steatosis. This can be exacerbated by additional oxidative injury, required to manifest the necro-inflammatory component seen in steatohepatitis.
TNF-alpha and other inflammatory cytokines are released from which endocrine tissue?
Adipose tissue. Also released are Plasma-activating factor I (pro-thrombotic); Adoiponectin (glucose regulation & fatty acid catabolism) & resistin (pro-inflammatory)
Why is it important to ask about polyuria and polydipsia in an amennorheic woman with breast discharge?
It could be indicative of a compressive prolactinoma preventing ADH release from the posterior pituitary, leading to diabetes insipidus.
At what time of day should serum cortisol be checked?
In a normal person, in the morning (8 am) - the cortisol levels are highest at this time
Explain how excess prolactin prevents proper menstruation or pregnancy.
Prolactin inhibits GnRH production, which suppresses LH/FSH production, required for menstruation
What is the first-line treatment for a symptomatic prolactinoma in a woman who wishes to become pregnant?
Dopamine agonist (Dopamine is an inhibitor of prolactin synthesis and release). Also, because this woman wishes to become pregnant, you wouldn't want to give her a combined oral contraceptive.
In suspected Cushing's, if serum ACTH levels are normal or elevated, and no cortisol suppression occurs with high-dose Dexamethasone administration, what is the most likely cause of the hypercortisolism?
It is likely there is an ectopic tumour secreting ACTH. Such a tumour would not respond to negative feedback by high cortisol (Dex suppression); ACTH would be high as the tumour is actively secreting ACTH (the pituitary is likely not secreting any ACTH due to feedback).
In suspected Cushing's, if serum ACTH levels are undetectable, and no cortisol suppression occurs with high-dose Dexamethasone administration, what is the most likely cause of the hypercortisolism?
It is likely that the adrenal glands are overproducing cortisol. The feedback pathway is working (low ACTH), but suppression by dexamethasone would have no effect on the adrenal gland, as it does not respond to the 'reduced' ACTH which occurs with the Dex suppression test.