Term
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Definition
Same as left and righ gonadal veins.
Left adrenal → left adrenal vein → left renal vein → IVC.
Right adrenal → right adrenal vein → IVC. |
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Term
| Which anterior pituitary hormones are acidophilic |
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Definition
|
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Term
| Which anterior pituitary hormones are basophilic |
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Definition
| B-FLAT - Basophils, FSH, LH, ACTH and TSH |
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Term
| Which pituitary hormones share a common subunit? Which subunit? |
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Definition
α subunit––common subunit to TSH, LH, FSH, and hCG.
β subunit––determines hormone specificity. |
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Term
| Effects of Somatostatin on Anterior pituitary secretion |
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Definition
| Somatostatin— decreases release of GH, and TSH. |
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Term
| 17a-hydroxylase deficiency |
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Definition
↓ sex hormones, ↓ cortisol, ↑ mineralocorticoids. Cx = HYPERtension, hypokalemia; phenotypically female but no maturation.
directly before block: pregnenolone and progesterone |
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Term
| 21a-hydroxylase deficiency. |
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Definition
Most common form. ↓ cortisol (increased ACTH), ↓ mineralocorticoids, ↑ sex hormones. Cx = masculinization, female pseudohermaphroditism, HYPOtension, hyperkalemia, ↑ plasma renin activity, and volume depletion. Salt wasting can lead to hypovolemic shock in the newborn.
Directly before block: Progesterone and 17hydroxyprogesterone |
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Term
| 11ß-hydroxylase deficiency |
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Definition
↓ cortisol, ↓ aldosterone and corticosterone, ↑ sex hormones. Cx = masculinization, HYPERtension (11-deoxycorticosterone is a mineralocorticoid and is secreted in excess).
Directly before block 11-deoxycorticosterone and 11-deoxycortisol |
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Term
| Which endocrine hormones act through the cAMP pathway |
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Definition
| ACTH, LH, FSH, TSH, ADH (V2), hCG, MSH, CRH, PTH, calcitonin, glucagon. |
|
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Term
| Which endocrine hormones act through the cGMP pathway |
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Definition
|
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Term
| Which endocrine hormones act through the IP3 pathway |
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Definition
| GnRH, TRH, GHRH, ADH (V1), Oxytocin |
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Term
| Which endocrine hormones act via tyrosine kinase |
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Definition
|
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Term
| Inheritance of MEN syndromes |
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Definition
| Autosomal Dominant. Associated with ret gene in MEN types II and III. |
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Term
| Drugs that can cause nephrogenic diabetes insipidus |
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Definition
|
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Term
| Treatments fo Diabetes Insipidus |
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Definition
| Adequate fluid intake. For central DI––intranasal desmopressin (ADH analog). For nephrogenic DI––hydrochlorothiazide, indomethacin, or amiloride. |
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Term
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Definition
Mechanism: Sympathomimetic serotonin and norepinephrine reuptake inhibitor. Supresses appetite.
Clinical use: Short-term and long-term obesity management.
Toxicity: Hypertension and tachycardia. |
|
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Term
| Propylthiouracil, methimazole |
|
Definition
Mechanism: Inhibit organification and coupling of thyroid hormone synthesis. Propylthiouracil also ↓ peripheral conversion of T4 to T3.
Clinical use: Hyperthyroidism.
Toxicity: Skin rash, agranulocytosis (rare), aplastic anemia. |
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Term
|
Definition
characterized by a replacement of the normal thyroid parenchyma by a dense fibrosis that invades adjacent structures of the neck and extends beyond the thyroid capsule. This makes the thyroid gland stone-hard and fixed to adjacent structures. The inflammatory process infiltrates muscles and causes symptoms of tracheal compression. Surgical treatment is required to relieve tracheal or esophageal obstruction.
A shared mechanism with retroperitoneal fibrosis and sclerosing cholangitis has been suggested |
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Term
|
Definition
| Alot of different functions, relaxes smooth muscle and leads to intestinal secretions. VIPoma results in diffuse wateri diarrhea. |
|
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Term
|
Definition
| follicular and undifferentiated lymphomas |
|
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Term
|
Definition
|
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Term
|
Definition
| Breast, Ovarian and gastric carcinoma. |
|
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Term
|
Definition
| small cell carcinoma of the lung |
|
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Term
| Family history of premature coronary artery disease, yellow tonsils, enlarged lymph nodes and hepatomegaly with weak hands. What disease and what's the pathophysiology? |
|
Definition
| Tangiers disease. Deficiency in cholesterol transporter ABCA1. Macrophages can't transfer cholesterol to HDL and become Foam cells. Often presents with low total cholesterol. Causes sensory neuropathies and muscle wasting of the hands. |
|
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Term
|
Definition
| major protein component of high density lipoprotein (HDL) in plasma. The protein promotes cholesterol efflux from tissues to the liver for excretion. It is a cofactor for lecithin cholesterolacyltransferase (LCAT) which is responsible for the formation of most plasma cholesteryl esters. |
|
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Term
|
Definition
| responsible for the activation of lipoprotein lipase (LPL) in capillaries[1] and thus begins the catabolism of the chylomicrons and VLDL. It is also found in HDL. Deficits of this apoprotein C2 present with grave hypertriglyceridemia and hyperchylomicronemia during fasting |
|
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Term
| Cholesteryl ester transfer protein (CETP) |
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Definition
| also called plasma lipid transfer protein, is a plasma protein that facilitates the transport of cholesteryl esters and triglycerides between the lipoproteins. It collects triglycerides from very-low-density (VLDL) or low-density lipoproteins (LDL) and exchanges them for cholesteryl esters from high-density lipoproteins (HDL), and vice versa. Deficiency elevates HDL-cholesterol but it can't function normally. |
|
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Term
|
Definition
TcH2O = Urine flow rate - (Urine Flow Rate X Urine Osm)/Plasma Osm
With ADH the # is -
Without it is +
isotonic = 0 |
|
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Term
|
Definition
potassium channel activator, which causes local relaxation in smooth muscle by increasing membrane permeability to potassium ions. This switches off voltage-gated calcium ion channels which inhibits the generation of an action potential.
It is used as a vasodilator in the treatment of acute hypertension or malignant hypertension.[1]
It is also used to decrease hypoglycemia due to the secretion of insulin in disease states such as insulinoma |
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Term
| Medications commonly associated with hyperprolactinemia |
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Definition
| Anything that blocks dopamine, tricyclics, tranquilizers, methyldopa, opiates and phenothiazines such as chlorpromazine. |
|
|
Term
| 3-beta-hydroxysteroid dehydrogenase |
|
Definition
| Enzyme that converts pregnenolone to progesterone. It is lacking in the fetal adrenal cortex so steroid synthesis is shunted away from mineral and glucocorticoids and toward DHEAwhich is then metabolized to androgens and estrogens by placental tissue |
|
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Term
|
Definition
| catalyzes conversion of cholesterol to pregnenolone in the adrenal cortex. Activated by ACTH and inhibited by ketocanazole. |
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Term
| Which hypothalamic nuclei regulates circadian rythms |
|
Definition
| Supreachiasmatic, also regulates ACTH secretion via CRH |
|
|
Term
| Which hypothalamic nuclei synthesizes ADH and oxytocin |
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Definition
| Supraoptic and paraventricular, regulates water balance |
|
|
Term
| Which hypothalamic nuclei regulates dopamine that inhibits prolactin |
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Definition
|
|
Term
| Aspiration of thyroid mass shows "solid balls" of neoplastic follicular cells, blood vessels and fibrous stroma in the center of the balls. Diagnosis? |
|
Definition
| Papillary carcinoma of the thyroid |
|
|
Term
| Name the two long acting insulin drugs |
|
Definition
|
|
Term
| Name the short acting insulion drugs |
|
Definition
| Lispro, Aspart, glulisine |
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Term
| Rate limiting step for fatty acid synthesis, regulation and disease association. |
|
Definition
| Acetyl-CoA carboxylase, requires biotin. Increased by insulin and citrate, inhibited glucagon and palmitoyl-CoA. Associated with myopathic CAT-2/CPT-2 deficiency which manifest by muscle weakness/aches and myoglobinuria provoked by prolonged exercise. Increase in muscle triacylglycerols. |
|
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Term
| Rate limiting step for fatty acid oxidation, regulation and disease association. |
|
Definition
Carnitine acyltransferase-1 (CAT-1). Inhibited by malonyl-CoA(product of Acetyl CoA carboxylase).
Medium chain Acyl-dehydrogenase deficiency |
|
|
Term
| Contraindications of biguanides, sulfonylureas and thiazolidinediones. |
|
Definition
Biguanides - Cac cause lactic acidosis, don't use in renal failure or electrolyte disturbances.
Sulfonylureas - hepatic clearance, don't use in hepatic failure.
thiazolidinediones - exacerbate CHF and periperal edema |
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Term
|
Definition
| analogue of amylin, a small peptide hormone that is released into the bloodstream by the β-cells of the pancreas along with insulin, after a meal. aids in the absorption of glucose by slowing gastric emptying, promoting satiety via hypothalamic receptors (different receptors than for GLP-1), and inhibiting inappropriate secretion of glucagon |
|
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Term
| Glucagon-like peptide-1 analogs |
|
Definition
| exenatide, liraglutide. Don't cause hypoglycemia. Augment pancreatic response, decrease glucagon release, slow gastric emptying and increase satiety. |
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Term
|
Definition
High in hyperthyroid, low in hypothyroid, assuming normal TBG levels.
The patient's serum is mixed with the labeled thyroid hormone; then, the resin is added to the whole mixture to measure the amount of free labeled thyroid hormone. So, for instance, if the patient is truly hypothyroid, and TBG levels are normal, then there are many sites open for binding on the TBG, since the total thyroid hormone level is low. Therefore, when the labeled hormone is added, it will bind mostly to the TBG, leaving little of it left for binding to the resin. In contrast, however, if the patient is truly hyperthyroid, and TBG levels are normal, the patient's endogenous hormone will saturate the TBG binding sites more, leaving less room for the labeled hormone, which allows greater binding to the resin. |
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Term
|
Definition
| rT3, unlike T3, does not stimulate thyroid hormone receptors. However, rT3 nonetheless binds to these receptors, thereby blocking the action of T3. Under stress conditions, the adrenal glands produce excess amounts of cortisol. Cortisol inhibits the conversion of T4 to T3, thus shunting T4 conversion from T3 towards rT3. Consequently, there is a widespread shutdown in T3 binding across the body. This condition is termed Reverse T3 Dominance. It results in reduced body temperature, which slows the action of many enzymes, leading to a clinical syndrome, Multiple Enzyme Dysfunction, which produces the effects seen in hypothyroidism. Effects include fatigue, headache, migraine, PMS, irritability, fluid retention, anxiety and panic |
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