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Endocrinology
FA complete review
| Question | Answer |
|---|---|
| From which embryonic parts does the Thyroid diverticulum arise? | Floor of primitive pharynx and descends into neck |
| What is the normal remnant of the Thyroglossal duct? | Foramen cecum |
| What is the most common ectopic thyroid tissue site? | Tongue |
| What is a rare consequence of lingual thyroid removal? | Hypothyroidism |
| Where in the neck does a Thyroglossal duct cyst appear? | Anterior midline neck mass |
| What mass is located at the lateral neck? | Branchial cleft cyst |
| Persistent cervical sinus may lead to development of: | Branchial cleft cyst |
| Why neck mass moves with swallowing or protrusion of tongue? | Thyroglossal duct cyst |
| If the neck mass moves as the patient is asked to swallow, it most likely indicates? Where in the neck is it located MC? | Thyroglossal duct cyst; most commonly located anterior midline of neck |
| Thyroid follicular cells are derived from which embryonic tissue? | Endoderm |
| What tissue gives rise to Parafollicular cells? | Neural crest |
| What is another name used for Parafollicular cells? | C cells |
| What is produced by C cells? | Calcitonin |
| What are the 3 zones that make up the Cortex of the Adrenal gland? | Z. Glomerulosa, Z. Fasciculata, and Z. Reticularis |
| What is the main hormone produced by the Zona Glomerulosa? | Aldosterone |
| What is the primary regulation substance for the Z. Glomerulosa? | Angiotensin II |
| What class of hormone is Aldosterone considered? | Mineralocorticoids |
| What are regulatory hormones of the Z. Fasciculata? | ACTH and CRH |
| What hormone class is secreted by the Z. Fasciculata? | Glucocorticoids |
| What hormone is primarily secreted by Z. Fasciculata? | Cortisol |
| Which zona of the adrenal medulla secretes Androgens? | Zona Reticularis |
| What is the primary hormone produced by the Z. Reticularis? | DHEA |
| The adrenal cortex is derived from ____________________. | Mesoderm |
| The adrenal medulla is derived from _________________. | Neural crest |
| What are the main catecholamines secreted by the Adrenal medulla? | Epinephrine and Norepinephrine |
| What accounts for the regulation of catecholamine secretion in the adrenal medulla? | Preganglionic sympathetic fibers |
| What is another term used for Anterior Pituitary? | Adenohypophysis |
| What is another name used for the Posterior Pituitary? | Neurohypophysis |
| What hormones are secreted by the anterior pituitary gland? | FSH, LH, ACTH, TSH, prolactin, GH, and B-endorphin. |
| What area of the pituitary gland releases MSH? | Intermediate lobe of the pituitary (considered more anterior) |
| What is the name of the oral ectoderm that gives rise to the anterior pituitary? | Rathke's pouch |
| Which adenohypophysis hormones are considered Basophils? | FSH, LH, ACTH, TSH |
| What is the mnemonic used to remember Anterior pituitary basophil hormones? | B-FLAT |
| GH and PRL are ___________________________. | Acidophils |
| FLAT PiG | FSH, LH, TSH, PRL (prolactin), GH |
| What hormones are derivatives of Propiomelanocortin? | ACTH, MSH, and B-endorphin |
| Which subunit in the hormones secreted by the anterior pituitary determines hormone specificity? | Beta subunit |
| The alpha-subunit is shared by which anterior pituitary hormones? | TSH, LH, FSH, and hCG (not secreted by adenohypophysis) |
| Which hormone is shares the alpha subunit with TSH, LH, and FSH, but is not secreted by the anterior pituitary? | hCG |
| What hormones are stored and secreted in the Posterior Pituitary? | Vasopressin (ADH) and Oxytocin |
| Where are Oxytocin and Vasopressin, synthesized? | Hypothalamus |
| Which Hypothalamic nucleus make Vasopressin? | Supraoptic Nucleus |
| Which Hypothalamic nucleus synthesizes Oxytocin? | Paraventricular nucleus |
| What are the name for the carrier proteins used by Posterior Pituitary hormones? | Neurophysins |
| Which embryonic tissue layer gives rise to the Posterior Pituitary? | Neuroectoderm |
| What are the Pancreatic Islets of Langerhans? | Collections of alpha, beta and gamma endocrine cells |
| What are the Pancreatic peripheral endocrine cells? | Alpha cells |
| Pancreatic alpha cells secrete? | Glucagon |
| Where in the Islet of Langerhans are the Pancreatic Beta cells located? | Centrally |
| What is secreted by the Pancreatic Beta cells? | Insulin |
| Gamma cells of the pancreas are ___________________ in the Islet of Langerhans and secrete ____________________. | Interspersed; Somatostatin |
| Where is preproinsulin made? | Rough Endoplasmic Reticulum |
| Where is Proinsulin stored in the cell? | Secretory granules |
| How are the endogenous quantities of Insulin and C-peptide as they are naturally released? | Equal amounts |
| What two pathologic conditions yield high levels of Insulin and C-peptide? | Insulinoma and Sulfonylurea use |
| A patient with exogenous insulin therapy will yield a ________ level of C-peptide. | Low |
| What is the type of Insulin receptors? | Tyrosine kinase activity |
| What kind of transport is used to induce glucose uptake upon insulin stimulation? | Carrier-mediated transport |
| Insulin ____________ cross the placenta. | Cannot |
| What are some anabolic effects of insulin? | Increase: - glucose transport in skeletal muscle and adipose tissue - Glycogen synthesis and storage - Triglyceride synthesis Decrease: - Glucagon release - Lipolysis in adipose tissue |
| What are the anabolic effects of insulin in the kidneys? | Increase Sodium ion retention |
| Which pancreatic hormone can cause increase protein synthesis in muscles upon release? | Insulin |
| What is the main Insulin-dependent glucose transporter? | GLUT 4 |
| GLUT -4 is: | Insulin-dependent glucose transporter |
| What tissues and situations use or increase expression of GLUT4? | Adipose tissue, striated muscle. Exercise increases GLUT4 expression |
| Which are the Insulin- Independent transporters? | GLUT1, GLUT2, GLUT 3, GLUT 5, and SGLT1/SGLT2. |
| What mnemonic is used to remember the Insulin-independent glucose transporter tissues? | BRICK LIPS |
| What tissues use GLUT-1? | RBCs, brain, cornea, placenta |
| GLUT-2 is used by: | B-islet cells, liver, kidney, small intestine. |
| GLUT-2 is an Insulin - _______________________ glucose transporter, and it is also _________________. | Independent; Bidirectional |
| GLUT-3 receptors are seen in: | Brain and placenta |
| What kind of sugar is used by GLUT-5? | Fructose |
| GLUT-5 serves as receptor for which kind of tissues or organs? | Spermatocytes and GI tract |
| When can the brain start using ketone as source of energy? | Starvation |
| What organelle is lacking in RBCs? | Mitochondria |
| Why does RBCs are unable to use ketone for energy source at starvation times? | Lack of mitochondria |
| What is the major regulator of insulin release? | Glucose |
| What are the two major Incretins? | GLP-1 and GIP |
| How do incretins work? | Release after meals and Increase Beta cell sensitivity to glucose |
| The stimulation of alpha-2 receptors leads to a ______________ in insulin. | Decrease |
| Beta-2 receptor stimulation leads to an ______________ in insulin secretion. | Increase |
| What is the main function of Glucagon? | Elevate blood sugar levels to maintain homeostasis when concentration of bloodstream glucose falls too low. |
| Glucagon promotes: | 1. Glycogenolysis 2. Gluconeogenesis 3. Lipolysis 4. Ketone production |
| What 3 states or hormones inhibit glucagon release? | Insulin, hyperglycemia, and somatostatin |
| Glucagon is secreted by _______________________, in response to_____________________. | Alpha-cells of pancreas; Hypoglycemia |
| What is the function of ADH? | Increase water permeability of DCT and Collecting duct cells in kidney to increase water reabsorption. |
| What is the stimulus for ADH secretion? | Increase in plasma osmolality |
| How is the level of ADH in SIADH? | Inappropriately elevated despite low plasma osmolality |
| What is the function of CRH? | Increase release of ACTH, MSH, and B-endorphin. |
| What can lower the release of CRH? | Chronic exogenous steroid use |
| Increasing levels of prolactin lead to: | Decreased release of prolactin and TSH |
| Dopamine antagonist, such as antipsychotics may cause: | Galactorrhea due to hyperprolactinemia |
| GHRH works by increasing the release of: | GH |
| What is an GHRH analogue? | Tesamorelin |
| What is a common use for Tesamorelin? | HIV-associated lipodystrophy |
| What is the main function of GnRH? | Increase secretion of FSH and LH |
| Tonic GnRH: | Suppresses HPG axis |
| Pulsatile GnRH: | Leads to puberty and treatment of infertility |
| How is GnRH secretion inhibited? | By Hyperprolactinemia |
| What is the main function of Oxytocin? | 1. Causes uterine contractions during labor. 2. Milk letdown reflex in response to suckling |
| Increase levels of prolactin lead to a ________________ release of GnRH. | Decreased |
| What is a common malignancy that causes increased levels of Prolactin? | Pituitary adenoma |
| What are accompanying symptoms of Pituitary adenoma? | Amenorrhea, Osteoporosis, Hypogonadism, and Galactorrhea |
| Somatostatin analogs are used to treat? | Acromegaly |
| TRH stimulates the secretion of: | TSH and Prolactin |
| What is a common symptom seen with increased levels of TRH? | Galactorrhea |
| Prolactin is structurally homologous to _________. | Growth Hormone |
| Prolactin inhibits: | In females Ovulation and in males Spermatogenesis |
| What is associated with high levels of Prolactin? | Decreased libido |
| What pathway does Dopamine uses to inhibit Prolactin? | Tuberoinfundibular pathway of Hypothalamus |
| What is a common Dopamine agonist? | Bromocriptine |
| Bromocriptine is a ___________________ ____________________. | Dopamine agonist |
| Dopamine ANTAGONISTS: | Stimulate Prolactin secretion |
| Another name for Growth Hormone is: | Somatotropin |
| What are the 2 main functions of Growth hormone? | 1. Stimulates linear growth and muscle mass through IGF-1 secretion in liver. 2. Increase insulin resistance (diabetogenic) |
| What is the name often used for IGF-1? | Somatomedin C |
| What are some activities that stimulate the release of GH? | Exercise, deep sleep, puberty, hypoglycemia |
| Excess secretion of GH in adulthood leads to _______________. | Acromegaly |
| Excess secretion of GH in childhood leads to _________________. | Gigantism |
| What is the mco common cause of excess GH release? | Pituitary adenoma |
| Octreotide is an: | Somatostatin analog used in treatment of acromegaly |
| What hormone stimulates hunger? | Ghrelin |
| Where is Ghrelin produced? | Stomach |
| What condition stimulate the release of Ghrelin? | Sleep deprivation and Prader-Willi syndrome |
| Where in the Hypothalamus does Ghrelin act on? | Lateral area at the hunger center |
| What is the satiety hormone? | Leptin |
| Leptin is produced by: | Adipose tissue |
| A mutated leptin gene lead to ----> | Congenital obesity |
| Decreased levels of Leptin are seen with: | Sleep deprivation and Starvation |
| Leptin acts via: | Ventromedial area of the hypothalamus to decrease appetite |
| Where is the Satiety center in the Hypothalamus? | Ventromedial area |
| Where do Endocannabinoids work on? | Receptors in hypothalamus and Nucleus accumbens |
| Where in the Hypothalamus is ADH produced? | Supraoptic and Paraventricular nuclei |
| What is the function of ADH in V2-receptors? | Osmolality regulation |
| What is regulated by ADH at the V1-receptors? | Blood pressure |
| What is the primary function of ADH? | Serum osmolality regulation (ADH decreases serum osmolality, and Increase urine osmolality) |
| How is serum and urine osmolality regulated by ADH? | Regulation of aquaporin channel insertion in principal cells or renal collecting duct |
| How are ADH levels in Central Diabetes insipidus? | Low |
| Nephrogenic DI has ____________________ levels of ADH. | Normal to increased |
| What type of DI is developed in a mutated V-2 receptors? | Nephrogenic DI |
| What is a very common ADH analog? | Desmopressin |
| What are some common uses for Desmopressin? | 1. Central DI 2. Nocturnal enuresis |
| What are the two regulation actions of ADH? | 1. Osmoreceptors in hypothalamus 2. Hypovolemia |
| Which congenital adrenal hyperplasia is the ONLY one seen with Hypotension? | 21-hydroxylase deficiency |
| What is the significant lab seen in 17a-hydroxylase deficiency? | Decrease androstenedione |
| What is the male presentation of 17a-(OH) deficiency? | Ambiguous genitalia, undescended testitcles |
| What is the female presentation of 17a-(OH) deficiency? | Lack of Secondary sexual characteristics |
| 17a-hydroxylase deficiency is seen with excessive levels of: | Mineralocorticoids, which indicates Z. Glomerulosa hypertrophy |
| What type of adrenal cortex hormones are seen elevated in both congenital adrenal 21-(OH) and 11B-hydroxylase deficiencies? | Elevated Sex hormones (Androgens) |
| What is the difference in renin activity between 11B-(OH) and 21-(OH) deficiencies? | Renin activity is increased/elevated in 21-hydroxylase deficiency, and decreased n 11B-(OH) deficiency |
| Increased levels of 17-hydroxyprogesterone are seen in: | 21-hydroxylase deficiency |
| What is the MC congenital adrenal deficiency? | 21-hydroxylase deficiency |
| Presents in infancy with child wasting, or in childhood with precocious puberty. Dx? | 21-hydroxylase deficiency |
| 11B-hydroxylase deficiency is seen with key mineralocorticoid levels: | 1. Decreased Aldosterone 2. Elevated 11-deoxycorticosterone |
| Elevated levels of 11-deoxycorticosterone results in: | Elevated Blood pressure |
| How is the presentation the Female presentation of 21-hydroxylase deficiency? | Virilization |
| Decreased renin activity often indicates what congenital adrenal deficiency? | 11B-hydroxylase |
| What dermatologic condition is shared by all congenital adrenal enzyme deficiencies? | Skin hyperpigmentation |
| Why is there skin hyperpigmentation in all Congenital Adrenal enzyme deficiencies? | Increased MSH production, which is co-produced and secreted with ACTH. |
| Bilateral adrenal gland enlargement is seen all congenital adrenal enzyme deficiencies due to: | Increased ACTH stimulation |
| If the Congenital adrenal enzyme deficiency starts with 1 ---> | Hypertension |
| If the Congenital adrenal enzyme deficiency ends with 1 ----> | Virilization in females |
| Anastrozole and Exemestane work in the Z. _____________ of the adrenal cortex, and inhibit _____________. | Reticularis; Aromatase |
| Which enzyme is inhibited by Anastrozole? | Aromatase |
| Finasteride inhibits what Z. Reticularis enzyme? | 5a-reductase |
| The use of Finasteride prevents the formation of ________. | DHT |
| How is Cortisol most commonly found? | Bound to corticosteroid-binding globulin |
| Exogenous Corticosteroids can cause: | Reactivation of TB and candidiasis by blocking IL-2 production |
| How does cortisol affect Blood Pressure? | Increases BP: -- Upregulates a-1 receptors on arterioles --> increase sensitive to NE and Epi (permissive action) |
| How does Cortisol affects glucose levels? | Increases gluconeogenesis, lipolysis, and proteolysis |
| Why does high levels of Cortisol are seen with poor wound healing and decrease collagen synthesis? | Decreased fibroblast activity |
| What are the inflammatory and immune functions of Cortisol? | - Inhibits production of Leukotrienes and prostaglandins - Inhibits WBC adhesion ----> NEUTROPHILIA - Blocks histamine release from mast cells - Eosinopenia, lymphopenia -Blocks IL-2 production |
| How does Cortisol affect bone formation? | Decreases by decreasing osteoblast activity |
| Excess Cortisol often leads to: | Decreased CRH, ACTH, and cortisol secretion |
| What is the MC presentation Calcium in Plasma? | Ionized/free form which is the active form |
| How does an increase in pH affect Calcium homeostasis? | Increase affinity to albumin leading to ----> HYPOCALCEMIA |
| What are some signs and/or symptoms of hypocalcemia? | Cramps, pain, paresthesias, carpopedal spasm |
| What is the primary regulator of PTH? | Ionized/free Calcium |
| Changes in ____ affect PTH secretion. | pH |
| Changes in ________________ do not affect PTH secretion. | Albumin |
| Which cells in the Parathyroid gland secrete PTH? | Chief cells |
| What are the 4 main functions of PTH? | 1. Increase bone resorption of Ca2+ and phosphate. 2. Increase kidney reabsorption of Ca2+ in DCT 3. Decrease reabsorption of phosphate in PCT 4. Increase 1,25-(OH)2 production |
| Another name for 1, 25-(OH)2 D3? | Calcitriol |
| How is calcitriol production stimulated by PTH? | Stimulating kidney 1a-hydroxylase in PCT |
| What actions of PTH take place in the PCT? | Decrease reabsorption of phosphate and Increase production of calcitriol |
| Describe major anion and cation changes caused by PTH: | In serum: -- Increase Calcium concentration -- Decrease phosphate concentration In Urine: -- Increased phosphate and cAMP |
| RANK-L is secreted by: | Osteoblasts and Osteocytes |
| What hormone increases the expression (concentration) of RANK-L? | PTH |
| On which bone cell do RANK-L bind to RANK? | Osteoclasts |
| The formation of RANK-RANK-L complex on osteoclasts cause --> | Stimulate osteoclasts and increased serum Calcium --> bone resorption |
| How is PTH affected by a increases in serum Phosphate? | Increased PTH secretion |
| What are 3 common serum ionic changes that cause an increase in PTH release? | Decrease in serum Calcium and Mg2+, and an increase in serum Phosphate |
| Severe Mg2+ serum decrease causes a _______________ in PTH release. | Decrease |
| What are some common causes of Mg2+ loss? | Diarrhea, aminoglycosides, diuretics, and alcohol use |
| What is the function of Calcitonin? | Decrease bone resorption of Calcium |
| What happens to Calcitonin with an increase in serum Ca2+? | Increase Calcitonin secretion |
| Calcitonin opposes the actions of: | PTH |
| What is the main source of Thyroid hormones? | Follicles of Thyroid |
| What is the major Thyroid product? | T4 |
| What enzyme converts T4 into T3 in the Peripheral tissue? | 5'-deiodinase |
| What drugs can prevent the peripheral conversion of T4 into T3 int he peripheral tissue? | Glucocorticoids, Beta-blockers, and PTU |
| What are the important functions of Thyroid Peroxidase? | 1. Oxidation, organification of iodide 2. Coupling of MIT and DIT |
| What drugs inhibit thyroid peroxidase? | PTU and methimazole |
| DIT + DIT = | T4 |
| DIT + MIT = | T3 |
| What is the Wolff-Chaikoff effect? | Excess iodine temporary negatively inhibit thyroid peroxidase leading to decreased T3/T4 production. |
| What is the active form of thyroid hormone? | T3 |
| Which form of TH has greater affinity to nuclear receptors? | T3 |
| What are the Beta-adrenergic effects of T3? | Increase B1 receptors in heart ----> Increase in CO, HR, SV, and Contractility. |
| What drugs are used to treat the beta adrenergic effects of Thyrotoxicosis? | Beta blockers |
| How is Basal metabolic rate increased by T3? | Increase in NA+/K+-ATPase activity --> Increased Oxygen consumption, RR, and body temperature. |
| What blood sugar-related processes are stimulated by TH? | Glycogenolysis and Gluconeogenesis |
| What are the two main ways of Negative feedback of free T3/T4 release? | 1. Anterior pituitary ---> Decreased sensitivity to TRH 2. Hypothalamus ---> Decrease TRH secretion |
| Bound T3/T4 is -- | INACTIVE |
| What protein binds most of T3/T4 in blood? | Thyroxine-binding globulin (TBG) |
| What condition is seen with increased TBG? | Pregnancy and OCP use |
| What i the relation between TBG and Estrogen? | Elevated Estrogen (pregnancy) increased TBG, which leads to an increase in total T3/T4 |
| What kind of conditions lead to an overall increase in total T3/T4? | Conditions that increase Estrogen levels such as pregnancy and OCP use. |
| What are conditions that decrease levels of TBG? | Hepatic failure, steroids, and Nephrotic syndrome |
| TSI is positive in what thyroid pathological condition? | Graves disease |
| Steroid hormones are ____________________. | Lipophilic |
| How are most steroid hormones circulate in blood? | Bound to specific binding globulins |
| The binding of Steroid hormones to their specific blood binding globulin causes: | Increase their solubility |
| In men, an increase in sex hormone-binding globulin (SHBG) cause: | Lowers free testosterone ---> Gynecomastia |
| How is SHBG changed in concentration by use of OCPs and pregnancy? | Increased |
| In women a decrease in SHBG --> | Raises free testosterone leading to Hirsutism |
| Increased levels of cortisol result in development of what condition? | Cushing Syndrome |
| What is the MCC of Cushing Syndrome? | Exogenous corticosteroids, as these cause a decrease in ACTH, and bilateral adrenal atrophy. |
| What hormone level is measured to determine the cause of Cushing syndrome? | ACTH levels |
| In case of elevated Cortisol and ACTH, which then ACTH secretion is suppressed by Low dose Dexamethasone test, what are the most common causes of Cushing syndrome? | Exogenous glucocorticoids or adrenal tumor |
| What is the most common cause of No suppression of ACTH secretion with high dose dexamethasone test in screening for Cushing syndrome? | Ectopic ACTH secretion |
| Cushing disease is often referred as: | ACTH-secreting pituitary adenoma |
| What is responsible for majority of Endogenous cases of Cushing syndrome? | Cushing disease |
| What is the MC example of Ectopic ACTH secretion? | Small cell Lung cancer |
| What are the initial screening tests for Cushing syndrome? | 1. Increase free cortisol on 24 hour urine analysis 2. Increase midnight salivary cortisol 3. No suppression with overnight low-dose dexamethasone test |
| What is adrenal insufficiency? | Inability of adrenal glands to generate enough glucocorticoids and/or mineralocorticoids for the body's needs. |
| What are the general symptoms of adrenal insufficiency? | Weakness, fatigue, orthostatic hypotension, muscle aches, weight loss, GI disturbances, sugar and/ or salt cravings |
| What is the main lab measure disturbance in diagnosis adrenal insufficiency? | ACTH levels |
| Primary adrenal insufficiency is characterized by ______ cortisol and ______ ACTH. | Low cortisol; High ACTH |
| Low cortisol and ACTH levels indicate: | Secondary and Tertiary Adrenal Insufficiency |
| What type of adrenal insufficiency is seen with Pituitary/Hypothalamic disease? | Secondary and Tertiary Adrenal Insufficiency |
| Metyrapone is a drug used in diagnosis what disease? | Adrenal insufficiency |
| A Metyrapone Stimulation test in a patient with Primary adrenal insufficiency will yield ? | - Increase in ACTH - 11-deoxycortisol remains low |
| If ACTH and 11-deoxycortisol remain low after Metyrapone test, it indicates? | Secondary/Tertiary adrenal insufficiency |
| Addison's disease is? | Chronic Primary adrenal insufficiency |
| Primary adrenal insufficiency is: | Deficiency of aldosterone and cortisol production due to loss of adrenal gland |
| What are the clinical symptoms of Primary Adrenal insufficiency? | - Hypotension (due to hyponatremic volume contraction) - Hyperkalemia -Metabolic acidosis - Skin and mucosal hyperpigmentation |
| What is the most common cause of Acute Primary adrenal insufficiency? | Massive hemorrhage |
| What is Waterhouse-Friderichsen syndrome? | Acute primary adrenal insufficiency due to adrenal hemorrhage associated with septicemia, DIC, and endotoxic shock. |
| What is the most common organism the causes Septicemia leading to Waterhouse-Friderichsen syndrome? | Neisseria meningitidis |
| What is the MCC of Chronic Primary adrenal insufficiency? | Adrenal atrophy or destruction by disease |
| What are the most common causative disease of Addison disease in the Western world? | Autoimmune destruction of gland |
| TB is the most common cause of ______________ disease in the developing world. | Addison |
| What level of adrenal isnusfficity is seen with decreased pituitary ACTH production? | Secondary adrenal insufficiency |
| How is Secondary Adrenal insufficiency different from Primary, clinically? | Secondary Adrenal insufficiency does not present skin/mucosal hyperpigmentation and no Hyperkalemia |
| What is the term used for increased secretion of aldosterone form adrenal gland? | Hyperaldosteronism |
| What are the main clinical features of Hyperaldosteronism? | Hypertension, Low to normal K+, and metabolic Alkalosis |
| What is Conn Syndrome? | Primary Hyperaldosteronism due to adrenal adenoma |
| What are the causes of Primary Hyperaldosteronism? | Conn syndrome and bilateral adrenal hyperplasia |
| How are the levels of Primary Hyperaldosteronism of aldosterone and renin? | Increased Aldosterone and Decreased Renin |
| What kind of hypertension is seen with Conn Syndrome? | Resistant hypertension |
| What are some common causes of Secondary Hyperaldosteronism? | Renovascular hypertension, Juxtaglomerular cell tumor (renin-producing), and edema |
| What type of tumors arise from Neuroendocrine cells? | Neuroendocrine tumors |
| What enzyme is contained in Neuroendocrine cells? | Amine precursor uptake decarboxylase (APUD) |
| What are some hormones released by Neuroendocrine cells? | Serotonin, histamine, calcitonin, neuron-specific enolase [NSE], chromogranin A |
| Which are the two most common Neuroendocrine GI tumors? | Carcinoid and Gastrinoma |
| Which is a Neuroendocrine Lung tumor? | Small cell Carcinoma of the lung |
| Insulinoma and Glucagonoma are examples of: | Pancreatic Neuroendocrine tumors |
| Which kind of thyroid cancer is a neuroendocrine tumor? | Medullary carcinoma of the thyroid |
| Pheochromocytoma is an: | Adrenal gland neuroendocrine tumor |
| What is the MC adrenal gland tumor in children? | Neuroblastoma |
| Neuroblastoma originates from which kind of cell? | Neural crest cells |
| What is a common and key characteristic of Neuroblastoma? | Present with Opsoclonus-myoclonus syndrome |
| "dancing eyes-dancin feet" is a description of: | Opsoclonus-myoclonus syndrome seen in Neuroblastoma |
| Irregular abdominal mass in a 3 year old that crosses the midline. Patient present with uncontrollable feet movements and constant irregular blinking. Dx? | Neuroblastoma |
| What is a key histological findings in Neuroblastoma? | Homer-Wright rosettes |
| Neuroblastoma clinical labs: | Urine -- (+) for HVA and VMA (+) for Bombesin and NSE |
| N-myc oncogene + APUD tumor. Dx.? | Neuroblastoma |
| What is the most common adrenal gland tumor in adults? | Pheochromocytoma |
| What do most Pheochromocytomas secrete excess? | Epinephrine, NE, and dopamine |
| Which adrenal tumor causes symptoms in "spells"? | Pheochromocytoma |
| Besides catecholamines, what other hormone is secreted in Pheochromocytoma? | EPO |
| The excess EPO secretion in Pheochromocytoma results in : | Polycythemia |
| What are the five most common episodic hyperadrenergic symptoms of Pheochromocytoma? | Pressure (increased BP) Pain (headache) Perspiration Palpitations (tachycardia) Pallor |
| What is found in UA of a patient with Pheochromocytoma? | ELevated levels of catecholamines and catecholamine metabolites |
| What is the best treatment protocol for Pheochromocytoma, prior to surgery? | First irreversible a-antagonists (phenoxybenzamine), followed by beta-blockers |
| What is the most common alpha blocker used in tx of Pheochromocytoma? | Phenoxybenzamine |
| VIPoma is associated with with Autosomal dominant disorder? | MEN-1 |
| What is VIPoma's primary symptom? | Secretory diarrhea |
| VIPoma is associated with which syndrome? | WDHA syndrome |
| What does the WDHA syndrome consists of? | Watery diarrhea, Hypokalemia, Achlorhydria |
| What is achlorhydria? | Absence of hydrochloric acid in gastric secretions |
| What are the levels of K+ seen in WDHA syndrome? | Low |
| Hypothyroidism common symptoms include: | Cold intolerance Decreased sweating, weight gain, and hyponatremia Dry skin Periorbital edema Constipation |
| What are musculoskeletal findings of Hypothyroidism? | Hypothyroid myopathy (proximal muscle weakness, Increased CK) Carpal Tunnel syndrome, myoedema |
| Heat intolerance, profuse sweating, and unintentional weight loss are associated with which kind of thyroid condition? | Hyperthyroidism |
| Increased calorigenesis is an metabolic associated finding of: | Hyperthyroidism |
| Pretibial myxedema is associated with: | Graves disease |
| What are important and relevant ocular findings of Hyperthyroidism? | Ophthalmopathy in Graves disease including periorbital edema, and exophthalmos. |
| What is the difference in Thyrotoxic myopathy and Hypothyroid myopathy? | CK is elevated only in Hypothyroid myopathy |
| What are 5 most common presentations of Hypothyroidism? | 1. Hashimoto thyroiditis 2. Postpartum thyroiditis 3. Congenital hypothyroidism (Cretinism) 4. Subacute Granulomatous thyroiditis (de Quervain) 5. Riedel thyroiditis |
| What is another term used for Congenital hypothyroidism? | Cretinism |
| What is another term used for Subacute granulomatous thyroiditis? | de Quervain |
| What is the MCC of Hypothyroidism? | Hashimoto thyroiditis |
| Hashimoto thyroiditis is positive to which antibodies? | 1. Antithyroid peroxidase (anti-microsomal) 2. Antithyroglobulin |
| What is Hashimoto thyroiditis associated with? | - HLA-DR3 - Increased risk of non-Hodgkin lymphoma of B cell origin |
| What is the histology seen in Hashimoto thyroiditis? | Hurthle cells, lymphoid aggregates with germinal centers |
| What are the findings of the thyroid in Hashimoto thyroiditis? | Moderately enlarged, NON-tender thyroid |
| When is postpartum thyroiditis presented? | Self-limited throdoidid arising up to 1 year after delivery |
| What is the common histology seen in Postpartum thyroiditis? | Lymphocytic infiltrate with coaccional germinal center formation |
| What are the common findings of Cretinism? | Pot-bellied, Pale, Puffy face child with Protruding umbilicus, Protuberant tongue, and Poor brain development |
| What is an fetal form of hypothyroidism, due to antibody-mediated maternal hypothyroidism, thyroid agenesis, thyroid dysgenesis? | Cretinism |
| Which condition is associated with dyshormonogenetic goiter? | Cretinism |
| What is the most common cause of Cretinism in the USA? | Thyroid dysgenesis |
| What form of hypothyroidism often follows a flu-like illness? | de Quervain thyroiditis |
| Granulomatous inflammation is seen in the histology of which presentation of Hypothyroidism? | de Quervain thyroiditis |
| What are the clinical and lab findings of de Quervain thyroiditis? | Increased ESR, jaw pain, and very tender thyroid |
| Thyroid replaced by fibrous tissue with inflammatory infiltrate describes which type of Hypothyroidism? | Riedel thyroiditis |
| Riedel thyroiditis is considered a manifestation of: | IgG4-related systemic disease |
| What are some examples of a IgG4-related systemic disease? | Autoimmune pancreatitis, retroperitoneal fibrosis, non-infectious aortitis |
| Thyroid on physical exam is fixed, hard (rock-like), painless goiter | Riedel thyroiditis |
| What are some lesser causes of Hypothyroidism? | Iodine deficiency, goitrogens, Wolff-Chaikoff effect |
| What are some common goitrogens? | Amiodarone and Lithium |
| What is the most common cause of Hyperthyroidism? | Graves disease |
| What type of hypersensitivity is Graves disease considered? | Type II |
| The thyroid-stimulating immunoglobulin stimulates the TSH receptors on: | 1 Thyroid --> Hyperthyroidism, diffuse goiter 2. Dermal fibroblasts --> Pretibial myxedema |
| What HLA subtypes are associated with Graves disease? | HLA-DR3 and HLA-B8 |
| Inflammation and infiltration of retro-orbital space by activated T-cells in Hyperthyroidism lead to: | Exophthalmos |
| What is the described histology of Graves disease? | Tall, crowded follicular epithelial cells; scalloped colloid |
| What is the cause of Toxic Multinodular goiter? | Focal patches of hyperfunctioning follicular cells idistendenwith collid working independently of TSH |
| What type of nodules are rarely malignant? | Hot nodules |
| A mutated TSH receptor often lead to: | Toxic Multinodular goiter |
| How is A Thyroid storm treated? | 1. Beta blocker (Propranolol) 2. PTU 3. Prednisolone (corticosteroid) 4. Potassium iodide |
| What is a Thyroid storm? | Uncommon but serious complication that occurs when hyperthyroidism is incompletely treated/untreated and then significantly worsens in the setting of acute stress |
| What condition are common to precipitate a Thyroid storm? | Stress, infection, trauma, and surgery |
| What is a common activity that leads to Jod-Basedow phenomenon? | Previous Iodine IV contrast procedure |
| What is the opposite to Wolff-Chaikoff effect? | Jod-Basedow phenomenon |
| What is the Jod-Basedow phenomenon? | The consequences of administering iodine to a patient with iodine deficiency, to the point of making iodine replete. |
| What is the term used to describe a non-functional Thyroid adenoma? | "Cold" |
| The autonomous thyroid hormone production due to a Thyroid adenoma, is referred as: | "hot" or "toxic" |
| What is the histology seen in Thyroid adenoma? | Follicular; absence of capsular or vascular invasion |
| What are the most common complication of thyroidectomy to treat thyroid cancer? | Hoarseness of voice, hypocalcemia, and transection of recurrent and superior laryngeal nerves. |
| Reason for hoarseness complication after thyroidectomy? | Recurrent laryngeal nerve damage |
| What causes the hypocalcemia seen as adverse complications in thyroidectomy? | Removal of Parathyroid glands |
| What is a possible complication seen during ligation of the Recurrent and Superior Laryngeal nerves in a thyroidectomy? | Transection of the recurrent and superior laryngeal nerves |
| What is the most common type of Thyroid cancer? | Papillary carcinoma |
| What is the histologic description of Papillary thyroid cancer? | Empty-appearing nuclei with central clearing, psammoma bodies, and nuclear grooves. |
| What are some associated risk for the development of Papillary thyroid cancer? | 1. RET and BRAF mutations, 2. Childhood neck irradiation |
| Which thyroid cancer is associated with Psammoma bodies? | Papillary carcinoma |
| Which thyroid cancer is seen with "Orphan Annie eyes" and excellent prognosis? | Papillary carcinoma |
| Empty-appearing nuclei with central clearing | "Orphan Annie" eyes |
| Which thyroid cancer is associated with RAS mutation? | Follicular carcinoma |
| Thyroid cancer that invades thyroid capsule and vasculature; uniform follicles. | Follicular carcinoma |
| What kind of cells give rise to the Medullary Thyroid cancer? | Parafollicular "C cells" |
| Which thyroid cancer is seen with increased levels of Calcitonin release? | Medullary carcinoma |
| Which thyroid cancer is described as: sheets of cells in amyloid stroma (stains for Congo Red)? | Medullary carcinoma |
| What are the associated conditions with Medullary carcinoma? | MEN 2A and MEN 2B (RET mutations) |
| Which population is more often associated with Undifferentiated/anaplastic thyroid cancer? | Older |
| Which thyroid cancer has a very poor prognosis? | Anaplastic carcinoma |
| What kind of malignancy is associated with Hashimoto thyroiditis? | Lymphoma |
| Which are the MCC of Secondary Hyperparathyroidism? | Vitamin D deficiency, Decreased Calcium intake, and chronic renal failure. |
| What are the MCC of Primary Hyperparathyroidism? | PTH gland hyperplasia, adenoma, or carcinoma |
| Primary Hypothyroidism is mostly seen with? | Surgical resection of PTH glands and by autoimmune disease. |
| What are the levels of Calcium and PTH in PTH-independent hypercalcemia? | Decreased PTH and high Ca2+ |
| What are the MCC of PTH-independent hypercalcemia? | Excess Ca2+ intake, cancer, and Increased vitamin D |
| Increased PTH with low levels of Calcium, indicates which PTH condition? | Secondary hyperparathyroidism |
| What are the common findings of Hypoparathyroidism? | Tetany, hypocalcemia, and hyperphosphatemia |
| What are two common signs associated with Hypoparathyroidism? | Chvostek and Trousseau signs |
| What is Pseudohypoparathyroidism type 1A? | Unresponsiveness of kidney to PTH --> hypocalcemia despite increasing PTH levels |
| What is the name given to the constellation of physical findings in Pseudohypoparathyroidism type 1A? | Albright hereditary osteodystrophy |
| What are the findings that make up Albright hereditary osteodystrophy? | Shortened 4th/5th digits, short stature, obesity, developmental delay, and autosomal dominant heritage. |
| What is the genetic cause of Pseudohypoparathyroidism type 1A? | Defective Gs protein alpha-subunit causing end-organ resistance to PTH. |
| How is the inheritance of Pseudohypoparathyroidism type 1A? | AD; the defect must be inherited from mother due to imprinting |
| What is the difference in Pseudohypoparathyroidism type when the defective Gs protein alpha subunit comes from the father? | Same clinical presentation but there is no end-organ PTH resistance (PTH level normal). |
| What is osteitis fibrosa cystica? | Cystic bone spaces filled with brown fibrous tissue, known as "brown tumor". |
| What is the "brown tumor" seen in Osteitis fibrosa cystica? | Osteoclasts and deposited hemosiderin form hemorrhages --> bone pain. |
| Which type of HyperPTH are seen with Osteitis fibrosa cystica? | Mainly primary, but also seen in secondary hyperparathyroidism. |
| Primary hyperparathyroidism is seen clinically with: | Hypercalcemia, hypercalciuria, polyuria, hypophosphatemia, elevated PTH, elected ALP and cAMP in urine. |
| What are some secondary symptoms seen in Primary hyperparathyroidism? | Weakness and constipation, abdominal/flank pain, and neuropsychiatric disturbances. |
| Hypercalciuria seen in Primary hyperPTH causes ---> | Renal stones |
| Which renal condition is associated with secondary and tertiary hyperPTH? | Renal osteodystrophy |
| Renal osteodystrophy pathogenesis | Renal disease --> Secondary and Tertiary hyperparathyroidism ---> Bone lesions |
| What is commonly seen with Secondary Hyperparathyroidism? | Chronic renal disease |
| Decreased Ca2+ absorption and/or increased phosphate absorption , due to CKD, develops into ---> | Secondary hyperparathyroidism |
| How are the serum calcium levels different in Primary vs Secondary Hyperparathyroidism? | Primary Hyper PTH ----> Hypercalcemia Secondary Hyper PTH ---> Hypocalcemia |
| Which type of hyperparathyroidism is seen with hypocalcemia? | Secondary hyperparathyroidism |
| Which kind of hyperPTH is seen with extremely high PTH, hypercalcemia, and due to chronic renal disease? | Tertiary hyperparathyroidism |
| What is Nelson syndrome? | Enlargement of existing ACTH-secreting pituitary adenoma after bilateral adrenalectomy for refractory Cushing disease |
| What is the clinical presentation of Nelson syndrome? | Hyperpigmentation, headaches and bitemporal hemianopsia. |
| What is the cause of Familial hypocalciuric hypercalcemia? | Defective G-coupled Ca2+-sensing receptors in multiple tissues (Parathyroids, Kidneys). |
| What is the pathogenesis of Familial hypocalciuric hypercalcemia? | Higher than normal Calcium Levels required to suppress PTH. |
| What is the result of the excessive levels of renal calcium as consequence in Familial Hypocalciuric hypercalcemia? | Mild hypercalcemia and hypocalcemia with normal to elevated PTH levels |
| Elevated ALP is seen in ________ and _______ hyperparathyroidism. | Primary and Secondary |
| Excess GH in adults is: | Acromegaly |
| What is the MCC of acromegaly? | Pituitary adenoma |
| What does diaphoresis mean? | Excessive sweating |
| What is an associated increased in risk of developing in patients with Acromegaly? | Colorectal polyps and cancer |
| Increased GH in children causes: | Gigantism (increase linear bone growth) |
| What are non-surgical treatments of Acromegaly? | Octreotide (somatostatin analog) and Pegvisomant (GH receptor antagonists), dopamine agonists (cabergoline) |
| What are some clinical features of Acromegaly? | Large tongue with deep furrows, deep voice, large hands and feet, coarsening of facial features, frontal bossing, diaphoresis, impaired glucose tolerance (insulin resistance), and hypertension |
| What is Laron syndrome? | Defective growth hormone receptors --> decreased linear growth. |
| What is another term used for Laron syndrome? | Dwarfism |
| What are the clinical features of Dwarfism? | Short height, small head circumference, characteristic facies with saddle nose and prominent forehead, delayed skeletal maturation and small genitalia. |
| What are the main characteristics of Diabetes insipidus? | Intense thirst and polyuria with inability to concentrate urine due to lack of ADH (central) aor failure of response to circulating ADH (nephrogenic) |
| Which kind of DI is due to lack of ADH? | Central DI |
| Which kind of DI is due to failure of response to circulating ADH? | Nephrogenic DI |
| What are the MCC of Central DI? | Pituitary tumor, autoimmune, trauma, surgeny, ischemic encephalopathy, and idiopathic. |
| What are the MCC of Nephrogenic DI? | Hereditary (ADH receptor mutation, Secondary to hypercalcemia, hypokalemia, LITHIUM, demeclocycline (ADH antagonist) |
| What mood stabilizer is often a cause of Nephrogenic DI? | Lithium |
| Which kind of DI is seen with minimal change in urine osmolality, even after administration of ADH analog? | Nephrogenic DI |
| Increase of > 50% in urine osmolality after administration of ADH analog, is characteristic of ________ Diabetes insipidus. | Central |
| What are the treatments for Central DI? | Desmopressin and Hydration |
| What are some of the treatments used in Nephrogenic DI? | HCTZ, indomethacin, amiloride Hydration, dietary salt restriction, and avoidance of offending agent |
| How is the level of ADH in Central DI? | Low |
| How are the levels of ADH seen in Nephrogenic DI? | Normal to elevated |
| SIADH MCC by: | 1. Ectopic ADH (small cell lung cancer) 2. CNS disorders/head trauma 3. Pulmonary disease 4. Drugs (cyclophosphamide) |
| What are some of the most important features of SIADH? | - Excessive free water retention - Euvolemic hyponatremia with continued urinary Na+ secretion - Urine osmolality > Serum Osmolality |
| What is the first line of treatment for SIADH? | Fluid restriction |
| What are the secondary measures of treatment of SIADH? | Salt tablets, IV hypertonic saline, diuretics, conivaptan, tolvaptan, demeclocycline. |
| What test and result indicate Psychogenic polydipsia? | Increased urine osmolality during water deprivation test |
| How is the Euvolemic hyponatremia seen in SIADH causes? | Body responds to water retention by synthesizing more ANP and BNP --> increased Na+ secretion --> normalization of extracellular fluid volume ----> euvolemic hyponatremia |
| If the hyponatremia (low Na+ serum) is corrected to fast it may cause ----> | Osmotic Demyelination syndrome |
| What are some clinical signs seen in very low serum levels? | Cerebral edema and seizures. |
| Undersecretion of the pituitary hormones is known as: | Hypopituitarism |
| What is Sheehan syndrome? | Form of hypopituitarism. Ischemic infarct of pituitary following postpartum bleeding |
| Why does Sheehan syndrome occurs? | During pregnancy the pituitary gland experiences an induced growth leading to a increased susceptibility to hypoperfusion |
| What are the most common and characteristic features that indicated Sheehan syndrome? | Failure to lactate, absent menstruation, and cold intolerance. |
| Which are 3 very important and distinctive forms and causes of Hypopituitarism? | Sheehan syndrome, Empty sella syndrome, and Pituitary apoplexy. |
| What is the Empty sella syndrome? | Atrophy or compression of pituitary, often idiopathic. It is very commonly seen in obese women |
| What is a common morbidity of Empty sella syndrome? | Idiopathic intracranial hypertension |
| Where, anatomically, does the pituitary is located? | Lies in the Sella Turcica |
| What is Pituitary Apoplexy? | Sudden hemorrhage of pituitary gland, often in the presence of an existing pituitary adenoma. |
| How is the clinical view of a patient with Pituitary apoplexy? | Sudden onset severe headache, visual impairment, and features of hypopituitarism. |
| What are the ocular or vision deficits seen in Pituitary apoplexy? | Bitemporal hemianopia and Diplopia due to CN III palsy |
| What is a rare cause of Diabetes Mellitus? | Unopposed secretion of GH and Epinephrine |
| What are the main features of Diabetes mellitus? | Polydipsia, polyuria, polyphagia, weight loss, DKA (type 1), hyperosmolar hyperglycemic state (type 2). |
| DKA is seen in Diabetes mellitus type ____. | 1 |
| What are the two main categories of chronic DM complications? | 1. Nonenzymatic glycation 2. Osmotic damage |
| What are the Nonenzymatic glycation complications of DM? | 1. Small vessel disease (due to diffuse thickening of basement membrane). 2. Large vessel atherosclerosis, CAD, peripheral vascular occlusive disease, gangrene |
| What are the results of Small vessel disease seen in chronic DM? | Retinopathy, glaucoma, neuropathy, and nephropathy |
| What are the nephropathic features seen in a patient with Chronic Diabetes mellitus? | Nodular glomerulosclerosis, aka Kimmelstiel-Wilson nodules --> progressive proteinuria and arteriosclerosis ---> hypertension |
| What is meant by Osmotic damage in chronic DM? | Sorbitol accumulation in organs with aldose reductase and decrease or absence sorbitol dehydrogenase |
| What enzyme is deficient or absent in DM which causes Osmotic damage? | Sorbitol dehydrogenase |
| What are the forms in which osmotic damage is manifested in DM patients? | 1. Neuropathy (motor, sensory, and autonomic degeneration) 2. Cataracts |
| How is the sensory loss seen in DM due to osmotic damage described? | Glove and stocking distribution |
| What is the value of HbA1c to diagnose Diabetes mellitus? | Greater or equal to 6.5% |
| What is the primary defect DM 1? | Autoimmune destruction of B-cells |
| What is the cause of autoimmune destruction of B-cells in DM 1? | Due to glutamic acid decarboxylase antibodies |
| Which type of DM ALWAYS requires insulin injections? | Type 1 |
| What is the common age for a patient with DM1? | Less than 30 years old |
| Which DM is associated with obesity? | Type 2 |
| Which DM has a strong genetic association? | Type 2 |
| What are the HLA association for DM type 1? | HLA-DR4 and HLA-DR3 |
| Easy way to relate HLA system and type 1 Diabetes mellitus? | 4 - 3 = 1 |
| Which type of DM has a stronger or more severe glucose intolerance? | Type 1 |
| Which DM is seen commonly developing DKA? | Type 1 |
| What is the histology of Diabetes mellitus type 1? | Islet leukocytic infiltrate |
| What is the primary defect of Diabetes mellitus type 2? | Increase resistance to insulin, progressive pancreatic B-cell failure |
| What is the average age to start develon DM type 2? | Over 40 years old |
| How is the histology of DM type 2 featured? | Islet amyloid polypeptide (IAPP) deposits |
| What is the pathogenesis of DKA? | Excess fat breakdown and increased ketogenesis from elevated free fatty acids, which are then made into ketone bodies |
| Which ketone body is most abundant in DKA? | B-hydroxybutyrate |
| What are the signs and symptoms seen in DKA? | - Delirium/psychosis, - Kussmaul respirations (rapid, deep breathing) -Abdominal pain/N/V -Dehydration |
| What is the characteristic breath odor associated with DKA? | Fruity breath odor |
| Why does DKA has a fruity breath odor | Due to excess exhacked acetone |
| DKA cause what kind of metabolic acidosis? | Anion-gap Metabolic acidosis |
| What are some labs seen with DKA? | -Hyperglycemia, -Acidosis, -Decreased HCO3 - Elevated serum ketone level -Leukocytosis |
| Why is characteristic of the Hyperkalemia exhibited in DKA? | Serum hyperkalemia, but depleted intracellular K+ due to transcellular shift form decreased insulin and acidosis |
| What are the most important compilation of DKA? | 1. Life-threatening mucormycosis 2. Cerebral edema 3. Cardiac arrhythmias, 4. Heart Failure |
| What is the treatment for DKA? | IV fluids, IV insulin, and K+ to replete the intracellular stores; Glucose if necessary to prevent hypoglycemia |
| What is the MC causative organism of Mucormycosis in DKA patients? | Rhizopus infection |
| What is hyperosmolar hyperglycemic state? | State of profound hyperglycemia-induced dehydration and increased serum osmolality |
| What kind of population is at higher risk of developing Hyperosmolar hyperglycemic state? | Elderly type 2 diabetes with limited ability to drink |
| What are the alarming labs seen in Hyperosmolar hyperglycemic state? | Glucose > 600 mg/dL Serum Osmolality >320 mOsm/kg No acidosis (pH >7.35) |
| Why is there no acidosis in Hyperosmolar hyperglycemic state? | Ketone production is inhibited by the presence of insulin |
| Common tumor of alpha pancreatic cells, that over secretes glucagon? | Glucagonoma |
| What are the classic symptoms seen in a patient with a Glucagonoma? | Dermatitis (necrolytic migratory erythema), diabetes (hyperglycemia), DVT, declining weight, depression |
| What is the non-surgical treatment for Glucagonoma? | Octreotide |
| An insulinoma is a tumor from which cells? | Pancreatic B-cells, which oversecrete insulin leading to severe hypoglycemia |
| What is the name of the triad of symptoms often associated with an Insulinoma? | Whipple triad |
| What is the Whipple triad seen with Insulinomas? | 1. Low blood glucose 2. Symptoms of Hypoglycemia (lethargy, syncope, and diplopia) 3. Resolution of symptoms after normalization of glucose levels |
| What kind of syndrome is often associated with an Insulinoma? | MEN 1 |
| Overproduction of Somatostatin causes: | Decrease secretion of secretin, CCK, glucagon, insulin, gastrin, and GIP |
| What are common clinical features of an Somatostatinoma? | Diabetes/glucose intolerance, steatorrhea, gallstones, achlorhydria. |
| Tumor of pancreatic gamma-cells? | Somatostatinoma |
| What is the most common malignancy of the Small intestine? | Carcinoid tumor |
| What is the first organ in which a carcinoid tumor metastasizes? | Liver |
| Carcinoid tumors are derived from which type of cells? | Neuroendocrine cells |
| What is commonly secreted in high amounts in GI carcinoid tumors? | Serotonin (5-HT) |
| What are the common clinical features seen with Carcinoid syndrome? | Recurrent diarrhea, cutaneous flushing, asthmatic wheezing, right-sided valvular heart disease due to lung MAO-A enzymatic breakdown of 5-HT before left heart return |
| What side of the heart is affected more severely in Carcinoid syndrome? | Right side |
| What substance is elevated in urine in Carcinoid syndrome? | 5-hydroxyindoleacetic acid |
| What is the name of the condition due to Niacin deficiency? | Pellagra |
| What markers are associated with Carcinoid syndrome? | Chromogranin A and Synaptophysin |
| What is the most common treatment for Carcinoid syndrome , other than surgery? | Octreotide |
| What syndrome is associated with Gastrin-secreting tumor of Pancreas or duodenum? | Zollinger-Ellison syndrome |
| What is the common gastrin-secreting tumor in ZES? | Gastrinoma |
| ZES hypersecretion of acid causes --> | Recurrent ulcers in duodenum and jejunum |
| What syndrome is most often associated with Zollinger-Ellison syndrome? | MEN 1 |
| How is ZES clinically presented? | Abdominal pain (PUD, distal ulcers), diarrhea (malabsorption) |
| ZES has a _________________ secretin stimulation test. | Positive |
| In a Secretin stimulation test, if gastrin levels remain elevated after administration of secretin, it most likely indicate? | Zollinger-Ellison syndrome |
| What is the inheritance of Multiple Endocrine neoplasias? | Autosomal dominant |
| What are the three neoplasias that compose MEN 1? | Pituitary tumors Pancreatic endocrine tumors Parathyroid adenomas |
| What are the most common substances secreted by Pituitary tumors seen in MEN1? | Prolactin >> GH |
| What are the Pancreatic endocrine tumors seen in MEN 1? | Zollinger-Ellison syndrome, insulinomas, VIPomas, and glucagonomas (rare) |
| What is the associated mutation in MEN 1? | Menin, a tumor suppression, chromosome 11 |
| What thyroid carcinoma is associated with MEN 2A and MEN 2B? | Medullary thyroid carcinoma |
| Parathyroid hyperplasia + Medullary thyroid carcinoma + Pheochromocytoma. Dx? | MEN 2A |
| What does RET code for? | Receptor tyrosine kinase |
| Tumor originated from neural crest cells and secretes catecholamines | Pheochromocytoma |
| What substance is secreted by Medullary thyroid carcinoma? | Calcitonin |
| Which two neoplasias are shared in MEN 2A and MEN 2B? | Medullary thyroid carcinoma and Pheochromocytoma |
| What are the examples of Mucosal neuromas seen in MEN 2B? | Oral/ intestinal ganglioneuromatosis |
| Which MEN is associated with marfanoid habitus? | MEN 2B |
| What are the associated neoplasia of MEN 2B? | Medullary thyroid cancer, Pheochromocytoma, and Mucosal neuromas |
| What are the associated side effects of injectable Insulin preparations? | Hypoglycemia, lipodystrophy, rare hypersensitivity reactions |
| What is the action of insulin in the liver? | Increase glucose stored as glycogen |
| How does insulin work in the muscle? | Increase glycogen and protein synthesis |
| In what organ/tissue does insulin increase the level of glycogen and protein production? | Muscle |
| How is the cell membrane affected by exogenous insulin preparations? | Increase Potassium ion (K+) uptake |
| What are the Rapid acting Insulin preparations? | Lispro, Aspart, Glulisine |
| At what time (hours) is the peak action of Rapid insulin preparations? | 1 hour |
| The maximal effect of an exogenous insulin occurred nearly an hour after administration. Which are some common examples? | Lispro, Aspart, and Glulisine |
| How many hours after administration of Short acting insulin preparations is the maximal effect seen? | 2-3 hours |
| Regular insulin is an: | Short-acting insulin |
| NPH is an: | Intermediate acting insulin |
| NPH will see maximal effect _____ hours after administration. | 4-10 hours |
| What are the two most common Long acting insulin preparations? | Detemir and Glargine |
| Pramlintide is an: | Amylin analog |
| What is the most serious adverse effect of Pramlintide? | Hypoglycemia in the setting of mistimed prandial insulin |
| Drug class of GLP-1 analogs? | Injectables |
| What are examples of GLP-1 analogs? | Exenatide and liraglutide |
| Which kind of diabetes medication increases the glucose-dependent insulin release? | GLP-1 analogs |
| What is the most distinctive adverse effect of GLP-1 analogs? | Pancreatitis |
| What is the preferred type of insulin to be administered in cases of DKA? | Regular insulin |
| What is the most common biguanide? | Metformin |
| What is the mechanism of action of Metformin? | 1. Inhibit hepatic gluconeogenesis and the action of glucagon, by inhibiting mGPD 2. Increase glycolysis 3. Increased peripheral glucose uptake (increase insulin sensitivity) |
| What is the most significant side effect of Metformin? | Lactic acidosis |
| Which kind of patients are often at higher risk of developing lactic acidosis by using metformin? | Renal insufficient |
| What kind of anemia is often an associated adverse effect of metformin toxicity? | Megaloblastic anemia due to Vitamin B12 deficiency |
| Which are the 1st generation Sulfonylureas? | Chlorpropamide and Tolbutamide |
| Which adverse effects are shared by 1st and 2nd Sulfonylureas? | Hypoglycemia (increased risk of renal failure), and weight gain |
| What is an associated side effect of 1st generation Sulfonylureas? | Disulfiram-like effects |
| A patient with diagnosed disulfiram-like effects, is probably taking what kind of diabetic medication? | 1st Generation sulfonylureas |
| Chlorpropamide and Tolbutamide are: | 1st Generation sulfonylureas |
| What are the MC 2nd generation sulfonylureas? | Glimepiride, Glipizide, and Glyburide |
| MOA of Sulfonylureas? | Close K+ channel in pancreatic beta cell membrane --> cell depolarizes --> insulin release via increased Calcium ion influx |
| What is the most significant adverse effect of 2nd generation sulfonylureas? | Hypoglycemia |
| What kind of diabetic oral drug shares mechanism of action with Sulfonylureas? | Meglitinides |
| What is the simple difference in MOA between Sulfonylureas and Meglitinides? | The binding site |
| Nateglinide and Repaglinide are: | Meglitinides |
| What are some DPP-4 Inhibitors? | Linagliptin, Saxagliptin, and Sitagliptin |
| What is the shared suffix for DPP-4 inhibitors? | --gliptin |
| What are the major adverse effects of DPP-4 inhibitors? | Mild urinary or respiratory infections |
| What enzyme deactivated by DPP-4 enzyme inhibition? | GLP-1 |
| What is a secondary MOA of DPP-4 inhibitors? | Increase glucose-dependent insulin release |
| What are the Glitazones/ Thiazolidinediones? | Pioglitazone and Rosiglitazone |
| Suffix of Glitazones/ thiazolidinediones? | --glitazone |
| What does SGLT-2 inhibitors stand for? | Sodium-glucose cotransporter 2 inhibitor |
| What are some examples of SGLT-2 inhibitors? | Canagliflozin, Dapagliflozin, and Empagliflozin |
| What is the mode of action of Glitazones/ thiazolidinediones? | Binds to PPAR-Y nuclear transcription regulator --> Increased insulin sensitivity and levels of adiponectin --> regulation of glucose metabolism and fatty acid storage. |
| What are the side effects seen with Pioglitazone? | Weight gain, edema, HF, increase risk of fractures |
| SGLT2 inhibitors MOA? | Block reabsorption of glucose in PCT |
| SGLT-2 inhibitors adverse effects? | Glucosuria, UTIs, vaginal yeast infections, hyperkalemia, dehydration (orthostatic hypotension), weight loss |
| What kind of electrical imbalance is seen with SGLT-2 inhibitors toxicity? | Hyperkalemia |
| Women with recurrent vaginal infections are probably on which diabetic medication? | SGLT-2 inhibitors |
| What are some common alpha-glucosidase inhibitors? | Acarbose and Miglitol |
| What is the mechanism of action of Acarbose and Miglitol? | Inhibit intestinal brush-border a-glucosidases, which causes delayed carbohydrate hydrolysis and glucose absorption --> decreased postprandial hyperglycemia |
| Which kind of chronic patients are not indicated or suitable candidates to a-glucosidase inhibitors? | Those with impaired kidney function |
| What are the 2 main Thioamides? | Propylthiouracil (PTU) and Methimazole |
| What enzyme is inhibited by PTU? | Thyroid peroxidase |
| What its inhibited by PTU therapy that causes the decrease of TH synthesis? | Thyroid peroxidase inhibition causes the: 1. Inhibition of the oxidation of iodide and the, 2. Inhibition of organification and coupling of iodine |
| In which trimester(s) of pregnancy is Methimazole safe to be used? | Second and Third |
| PTU is used in pregnant women during the _________ trimester. | First |
| Which Thioamide is very teratogenic? | Methimazole |
| What is the associated risk of PTU-therapy in 2nd and 3rd trimesters of gestation? | Hepatotoxicity |
| Which common Hyperthyroidism complication is not treated with Thioamides? | Graves ophthalmopathy |
| What are the most common adverse effects of Thioamides? | Skin rash, agranulocytosis (rare), aplastic anemia, and hepatotoxicity. |
| What is the teratogenic effect caused by Methimazole? | Aplasia cutis |
| What is a non-intended or unhealthy use of Levothyroxine? | Weight loss |
| What are the associated side effects of Levothyroxine? | Tachycardia, heat intolerance, tremors, and arrhythmias |
| What conditions are treated with Levothyroxine? | Hypothyroidism, and Myxedema |
| What are some common ADH antagonists? | Conivaptan and Tolvaptan |
| What are the clinical uses of Conivaptan? | SIADH, block action of ADH at V2-receptor |
| What drug is used to treat Central DI? | Desmopressin |
| Which conditions are treated with Desmopressin? | Central DI, von Willebrand disease, sleep enuresis, hemophilia A. |
| Which congenital syndrome, in women, is treated with Growth hormone? | Turner syndrome |
| How does Oxytocin helps labor induction? | Stimulates uterine contractions |
| What labor complication can be controlled with Oxytocin? | Uterine hemorrhage |
| Octreotide, is used for: | Acromegaly, carcinoid syndrome, gastrinoma, glucagonoma, esophageal varices |
| What is the MOA of Demeclocycline? | ADH antagonist |
| Demeclocycline si a member of which antibiotic family? | Tetracycline |
| What condition is treated with Demeclocycline? | SIADH |
| What are adverse effects associated with Demeclocycline? | Nephrogenic DI, photosensitivity, abnormalities of bone and teeth |
| What is the MOA of Fludrocortisone? | Synthetic analog of aldosterone with little glucocorticoid effects |
| What is the clinical use for Fludrocortisone? | Mineralocorticoid replacement in Primary adrenal insufficiency |
| What are some associated adverse effects seen with Fludrocortisone? | Edema, exacerbation of HF, and hyperpigmentation |
| What is Cinacalcet mode of action? | Sensitizes Ca2+-sensing recepto (CaSR) in parathyroid gland to circulating Ca2+ --> decrease of PTH. |
| What calcium imbalance in seen as adverse effect of Cinacalcet? | Hypocalcemia |
| What are the clinical uses of Cinacalcet? | Secondary hyperparathyroidism in patients with CKD receiving hemodialysis, hypercalcemia in Primary HyperPTH, or in PTH carcinoma. |
| What is Sevelamer? | Nonabsorbable phosphate binder that prevents phosphate absorption from the GI. |
| What is the most common use for Sevelamer? | Hyperphosphatemia in CKD |
| What medication is commonly used to reduce the levels of phosphate in blood in a patient with renal insufficiency? | Sevelamer |
Created by:
rakomi
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