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Endocrinology 1.1
UWORLD Endocrine Review
| Question | Answer |
|---|---|
| Which thyroid cancer arises from Parafollicular Calcitonin-secreting cell? | Medullary Thyroid Cancer |
| Sheets of polygonal or spindle-shaped cells with extracellular AMYLOID deposits derived from calcitonin, describes the histology of what malignancy? | Medullary Thyroid Cancer |
| Medullary Thyroid cancer is associated with: | MEN2A and MEN2B |
| Medullary Thyroid cancer develops amyloid deposits, thus, it stains: | Congo Red |
| Development of glandular breast tissue in men is? | Gynecomastia |
| What are the 2 factors involved in the development of Gynecomastia? | 1. Increased Estrogen to Androgen ratio 2. Ductal Epithelial Hyperplasia and stromal fibrosis |
| What are common diseases associated with gynecomastia? | Liver cirrhosis, Obesity, CKD, hypogonadism, 5-a-reductase deficiency. |
| To what drugs is the development of gynecomastia associated? | GnRH agonists, Ketoconazole, Spironolactone, |
| How is the fat around internal organs referred as? | Visceral Obesity |
| Visceral obesity is an indicator of: | Insulin resistance |
| TPO is + for: | Hashimoto's Thyroiditis |
| Which are the two most common INCRETINS? | GLP-1 and GIP |
| Are incretins dependent or independent of serum glucose levels? | Incretins are independent of blood glucose level |
| GI hormone released by gut mucosa after the ingestion of a rich glucose meal that increases insulin release? | Incretins |
| What are the two main causes of Hypothyroidism? | Pituitary and Hypothalamic lesions/disorders |
| What are examples of conditions that may provoke Hypothalamic Hypothyroidism? | Sarcoidosis, Infection and radiation therapy |
| Sheehan Syndrome is a common cause of: | Pituitary Hypothyroidism |
| Mass lesions on the Pituitary are known to cause: | Hypothyroidism and Tunnel Vision |
| Low level of hormones released by the pituitary cause deficiency in: | ACTH, Thyroid hormone, Gonadotropins |
| Deficiency in ACTH is clinically manifested as: | Hypotension, decreased weight, and hypoglycemia |
| Hypothyroid patient presents with: | Fatigue, cold intolerance, slowed deep tendon reflexes |
| Low levels of Gonadotropins lead to ___________________ and ______ in the female, and decreased _________________ and also __________ in the male. | amenorrhea; infertility; libido; infertility |
| In 21-(OH) deficiency, there is a deficient conversion of ______________________ into ____________________, which impairs ___________________ synthesis. | 17-hydroxyprogesterone into 11-deoxycortisol; Cortisol |
| Decreased levels of CORTISOL in 21-(OH) deficiency lead to: | Increased level of ACTH release by the Anterior Pituitary |
| Which specific zona of the adrenal cortex is hypertrophied in 21-(OH) deficiency? | Z. RETICULARIS, which causes increased levels of Androgens |
| Elevated sex hormone + low levels of Cortisol and Aldosterone + Low BP, and increased renin activity. Dx? | 21-(OH) deficiency |
| Which congenital Adrenal enzyme deficiency is presented with skin hyperpigmentation? | All of them due to increased levels of MSH as it is coproduced with ACTH |
| If congenital adrenal deficiency starts with "1" --> | Hypertension |
| If congenital adrenal insufficiency ends with "1" --> | virilization in females |
| DECREASED renin activity is seen in which adrenal deficiency? | 11-B-Hydroxylase |
| In congenital adrenal deficiencies the Blood pressure and the [K+] are ____________________________ proportional. | Inversely |
| Fetal DM leads to INCREASED fetal ____________________, that then presents with _____________________, ____________________ cardiomyopathy, and __________________________ after delivery. | Insulin; macrosomia; Hypertrophic; HYPOGLYCEMIA |
| How is Placental vasculopathy caused by fetal DM, presented most commonly? | Aphasia, growth retardation, and POLYCYTHEMIA. |
| What is the main reason for the severe hypoglycemia seen in babies with diabetic mothers? | The mother created a state of chronic hyperglycemia, which caused the fetus to create an constant hyperinsulinemic environment, which is not compensated at birth. |
| Di George Syndrome: | 1. Failure of 3rd branchial pouch (inferior PTH) to form 2. Failure of 4th branchial pouch (superior PTH) to form |
| Signs seen in Di George Syndrome: | 1. Chovek Sign (twitch of nose and lips) 2. Trousseau sign (carpal spasm) |
| Absent Thymic shadow, low levels of T-cells and cleft lips are key characteristics of: | Di George Syndrome |
| Sulfonylureas MoA? | Increase INSULIN SECRETION by the Pancreatic-B cells, INDEPENDENT of blood glucose levels. |
| Where does the sulfonylurea bind in the Pancreatic B-cell? | ATP-dependent K+ channel |
| The attachment of Sulfonylurea to ATP- dependent K+ channel causes _____ ____________, leading to subsequent exocytosis of ___________. | Calcium influx; Insulin |
| What are common Second Generation Sulfonylureas? | Glyburide, Glipizide and Glimepiride |
| 1st generation Sulfonylureas? | Chlorpropamide and Tolbutamide |
| What is a common side effect of ALL sulfonylureas? | Hypoglycemia and Weight gain |
| What is an important side effect of 1st generation Sulfonylureas? | Disulfiram-like effects |
| 2nd Generation sulfonylureas may cause __________________ as a common side effect. | Hypoglycemia |
| GLP-1 analogues are ___________________. Two very common examples are ____________ and ________________. | Injectables; Exenatide and Liraglutide |
| Linagliptin, saxagliptin and sitagliptin are diabetic control drugs classified as ________________. | DPP-4 inhibitors |
| In DKA the patient has excessive _____________________ breakdown in ___________ tissue due to ____________ deficiency | TRIGLYCERIDE; ADIPOSE; INSULIN |
| What enzyme is responsible for breaking down Triglycerides into Fatty acids? | LIPASE |
| GLYCEROL is broken down in the _______________ by __________ __________, into Glycerol-3-P which then becomes DHAP, which produces _________ via ________________ and __________ via ________. | Liver; GLYCEROL KINASE; Glucose via Gluconeogenesis; ENERGY via GLYCOLYSIS |
| Hyperthyroidism causes the upregulation of ___ -receptors expression, leading to INCREASED ___________________ effect. | B-receptors; CATECHOLAMINE |
| Beta blockers are used in Hyperthyroidism for: | 1. minimize the ADRENERGIC effects 2. inhibit 5'-monoiodide, thus decreasing the conversion of T4 into T3. |
| Beta-blockers in Hyperthyroid patients cause a decrease in T___ production by inhibiting _________________________. | T3; 5'-monoiodide. |
| What is the MC type of Thyroid cancer? | Papillary Thyroid cancer |
| Large cells with nuclei, containing finely dispersed CHROMATIN, giving an empty or "ground-glass" appearance, and intranuclear inclusions, is the histology seen in? | Papillary Thyroid cancer |
| "Orphan-Annie eyes" histological description is seen in what type of thyroid cancer? | Papillary Thyroid cancer |
| Psammoma bodies are seen in what type of Thyroid cancer: | Papillary |
| Laminated Calcium deposits seen in certain malignancies? | Psammoma bodies |
| What are the 2 most common causes of DI? | 1. Inadequate PITUITARY secretion of ADH 2. Kidney disease as it fails to respond to ADH |
| Central DI refers to: | Inadequate pituitary secretion of ADH |
| Nephrogenic DI is due to inability of the collecting duct to respond to _______________. | ADH |
| Administration of analogous ADH produces a positive response in what type of Diabetes Insipidus? | Central DI |
| Post-Pituitary damage produces ___________________ __________ DI. | Transient Central DI |
| Permanent Central DI is caused by: | Hypothalamic nuclei damage. |
| 1. Beta-Oxidation of Fatty Acids 2. TCA cycle 3. Carboxylation of Pyruvate (Gluconeogenesis) | Processes occuring in the MITOCHONDRIA |
| Processes occuring in the CYTOSOL: | 1. Glycolysis 2. Fatty acid synthesis 3. PPP |
| The PPP uses: | Transketolase and Vitamin B1 as cofactor. |
| Where does the 1st step in STEROID synthesis occur? all subsequent steps are done in what organelle? | MITOCHONDRIA. All other steps occur in the SMOOTH ER |
| What is a organelle characteristic of all Steroid producing cells? | Well developed Smooth Endoplasmic reticulum. (SER) |
| Which organs have well-developed SER cells? | Adrenal glands, gonads, adn liver |
| Cells that produce steroids: | Increase also the androgen production which may lead to virilization and male-hair pattern. |
| Cushing Disease main hormone abnormality is: | High levels of ACTH |
| High ACTH levels are commonly due to Cushing's, if the ACTH is suppressed after low dose Dexamethasone test, which are the possible causalities of the elevated ACTH? | 1. Adrenal adenoma 2. Adrenal malignancy 3. Exogenous glucocorticoid intake (MC) (person with chronic inflammatory disease) |
| Suppressed levels of ACTH after High dose Dexamethasone Test, indicative which probable causes? | Pituitary adenoma |
| Failure to suppress level of ACTH with Low and High Dexamethasone tests, most probably indicate? | Ectopic ACTH production (malignant tumor) |
| What is the most common Ectopic ACTH secreting tumor? | Small Cell carcinoma of the Lung |
| Inherited enzyme deficiency causing Lactic Acidosis and neurological disorders? | Pyruvate Dehydrogenase Complex Deficiency |
| In Pyruvate Dehydrogenase complex deficiency, the patient is unable to convert ____________________ into __________________. | PYRUVATE into Acetyl-CoA |
| What is the treatment of PD complex deficiency? | Purely Ketogenic amino acid diet |
| Which are the purely Ketogenic amino acids? | Lysine and Leucine |
| Which are the ACTH-Dependent causes of Cushing Syndrome? | 1. Cushing Disease --> Pituitary ACTH hypersecretion 2. Ectopic ACTH secretion --> secretion of ACTH paraneoplastic |
| What is the ACTH-INDEpendent cause of Cushing Syndrome? | Adrenal adenoma or carcinoma |
| Bilateral adrenal hyperplasia involving the Z. Fasciculata and Z. Reticularis. | ACTH-dependent Cushing Syndrome changes at tissue level |
| At time of GLUCOSE DEPLETION, the body uses which substance to create energy? | KETONE |
| ________________ metabolism occurs in the ________________ in times of prolonged ________________. | Ketone; Liver; Fasting |
| Which cells are not able to use Ketones for energy at all and why? | Red Blood cells because it lacks of Mitochondria |
| Are ketones regularly used as energy source by the brain? | No, the brain cell will only take up ketone for energy in cases in extreme cases. |
| Essential Fructosuria is due to deficiency of ____________________. | FRUCTOKINASE |
| In Essential Fructosuria, the lack of Fructokinase activity, is compensated by increase activity of _____________________, entering then ___________________. | HEXOKINASE; Glycolysis |
| Deficiency of _________________ leads to development of Severe Fructose inherited intolerance. | ALDOLASE B |
| What is the clinical presentation of Fructose Intolerance? | Hypoglycemia and vomit after fructose ingestion , along with Liver and Renal failure. |
| In the synthesis of Insulin, the ___________________________ is translocated into the _________________, by the ______-____________. | PRE-PRO-INSULIN; Rough Endoplasmic Reticulum; N-terminal |
| What is the role of PRP (signal peptide protein)? | cleaves preproinsulin, into PRO-INSULIN enter the Golgi Apparatus. |
| Once Pro-Insulin is cleaved into ___________________ and ____________ in __________________ amounts in the ______________ _______________. | Insulin; C-peptide; Equivalent; secretory granules |
| Defective Lipoprotein Lipase leads to development of? | Familial Chylomicronemia Type 1 |
| What substance is accumulated or elevated in Familial Chylomicronemia? | Chylomicrons |
| What are key features of Type 1 Familial Hyperlipoproteinemia? | 1. ACUTE PANCREATITIS episodes 2. Lipemia retinalis 3. Eruptive Xanthomas |
| Another name for Type 2A Familial Hyperlipoproteinemia? | Familial Hypercholesterolemia |
| What is defective in Type 2A Fam Hypercholesterolemia? | 1. LDL receptor 2. ApoB-100 |
| Type ________ hypercholesterolemia is due to _______ receptor or ___________ deficiency or malfunction. | 2A; LDL receptor; ApoB-100 |
| Elevated LDL is seen in which hyperlipoproteinemia? | Type 2A Familial Hypercholesterolemia |
| Patient with premature atherosclerosis, TENDON XANTHOMAS, and xanthelasmas, suspect of? | Type 2A Familial Hypercholesterolemia |
| Familial Dysbetalipoproteinemia | Type 3 Familial Hyperlipoproteinemia |
| Defective ApoE leads to what cholesterol disorder? | Familial Dysbetalipoproteinemia |
| In Type 3 Familial Hyperlipoproteinemia, what is the substance accumulated, what is the defective enzyme? | Accumulation of: 1. Chylomicrons 2. VLDL remnants Defective ApoE (3 &4) |
| Type 4 Hyperlipoproteinemia is also known as: | Familial Hypertriglyceridemia |
| Accumulation of VLDL only, is seen in Type _______ hyperlipoproteinemia. | 4 |
| Tuberoeruptive and palmar xanthomas are characteristic of? | Familial Dysbetalipoproteinemia |
| What are the xanthomas manifested or characteristic of Type 3 Hyperlipoproteinemia? | Tuberoeruptive and Palmar xanthomas |
| What Familial Hyperlipoproteinemia has LDL and VLDL accumulated? | Type 2B Familial Hypercholesterolemia |
| What are the differences between Type 2A and Type 2B Familial Hypercholesterolemia? | Type 2A is mainly LDL receptor deficient and accumulates LDL, while Type 2B has LDL receptor and ApoB-100 defective and accumulates LDL and VLDL |
| ______________ deficiency, has low CORTISOL and excessive release of _________________. The best treatment is __________________ corticosteroids, in order to suppress ______________ production. | 21-(OH); ACTH; Exogenous; ACTH |
| The excess ACTH seen in 21-(OH) deficiency leads to? | Decreased androgen production, which manifests with a DELAY in SEXUAL development. |
| RET mutation + Increase Calcitonin + Marfanoid Habitus. Dx? | MEN 2B |
| What are the neoplasms associated with MEN2B? | 1. Oral/ Mucosal Neuromas 2. Medullary Thyroid cancer 3. Pheochromocytoma |
| Patient with multiple benign submucosal neoplasm, episodic tachycardia, and serum calcium below normal, and a similar history seen in the father of patient. Dx? | MEN2B |
| Where are the Cortisol receptors located? | Cytoplasm |
| _________________ is different to many of is class of hormones, because it has its receptor in the __________________, and not in the ______________ as normally would be expected. | CORTISOL; Cytoplasm; Nucleus |
| Cortisol is translocated to the ______________ after binding to receptor in the ________________. Once in the _____________, it gets __________________ and enhance hepatic ___________ production. | NUCLEUS; Cytoplasm; Nucleus: transcribed (transcription); glucose |
| High levels of Cortisol = | High levels of Hepatic GLUCOSE synthesis --> Hyperglycemia. |
| Aromatase Inhibitors include: | Anastrozole and Letrozole |
| Enzyme inhibited by Anastrozole? | Aromatase |
| ______________________ is enzyme that carries the conversion of ______________________ into ________________. | Aromatase; Testosterone: Estradiol |
| What type of malignancy is treated with Aromatase Inhibitors? | ER-2 + Breast cancer |
| Cholesterol is converted into Pregnenolone in the ________________, and all subsequent steps in Estrogen synthesis occur in the _____________________________. | Mitochondria; SMOOTH ENDOPLASMIC RETICULUM |
| What is the most important INSULIN stimulator? | Glucose |
| Glucose in Pancreatic B-cell undergoes _____________________ to produce _________, which then binds to the _______________________. | GLYCOLYSIS; ATP: ATP-sensitive K+-channel, allowing for depolarization and subsequent INSULIN release from cell. |
| Anatomically, the ANTERIOR pituitary is just BELOW the __________ ______________, and it drops _____________ than the ____________ pituitary. | Optic Chiasm; Lower; Posterior |
| Exogenous Insulin demonstrates levels of: | Elevated Insulin with DECREASED C-peptide |
| If insulin and C-peptide are both elevated, and there is a Positive drug assay, suspect? | Drug intoxication by person with access to Diabetic drugs (oral hypoglycemics) |
| An Insulinoma: | Produces Elevated Insulin and Elevated C-peptide, with negative drug assay. |
| Injectable Insulin does NOT increase ____________________ | C-peptide |
| Initially, the Increase in Estrogen during pregnancy will lead to a ______________ free ______. | DECREASE; T4 |
| Estrogen's high levels in pregnancy also cause, an increase in _________ and bound ________, but decrease in free ______. The increase _________ _______ promotes the release of new _______ hormone to restore levels of free ______. | TBG: T4: T4; bound-T4; TRH; T4. |
| What enzyme converts Testosterone into DHT> | 5-alpha-reductase |
| What is DHT's role? | Development of External MALE genitalia in the Fetus |
| A male patient with 5-alpha-reductase deficiency will show: | Feminized External Genitalia, until puberty |
| What are 2 conditions highly associated to 5-alpha-reductase deficiency? | 1. HYPOSPADIAS 2. Small phallus |
| What drug inhibits 5a-reductase? | Finasteride |
| By which GLUT is glucose taken into the cell in muscle cells and adipocytes? | GLUT-4 |
| Which GLUT is INSULIN dependent? | GLUT-4 |
| Which GLUT is insulin INDEPENDENT? | GLUT 1, 2, 3, and 5 |
| As the concentration of insulin increases the expression of GLUT-4 ____________________, and the expression of GLUT____________ remains the same. | INCREASES; GLUT 1, 2, 3, 5 |
| What is the MCC of Adrenal Insufficiency? | Hypothalamic-Pituitary-Adrenal suppression by Glucocorticoid therapy. |
| What are some common triggers/situations/events that lead to an adrenal crisis? | Times of high stress, such as surgery and/or illness. |
| What are the labs seen in Adrenal Crisis? | Low Cortisol, Low CTrH, and low ACTH |
| Patient with decreased cortisol, ACTH and CTrH, is about to enter the OR for cholecystectomy. What is a common cause for the patients laboratory results? | Adrenal Crisis |
| Conversion of Oxaloacetate into PEP by using PEP carboxykinase (PEPCK) | First step of GLUCONEOGENESIS |
| What is the cofactor used in the first step of Gluconeogenesis? | GTP is the cofactor used by PEPCK in GLUCONEOGENESIS |
| From which cycle is the GTP used in Gluconeogenesis originated? | From the TCA cycle, as Succinyl-CoA converts into Succinate. |
| What hypothalamic hormone inhibits Prolactin? | Dopamine |
| Dopamine inhibitors may cause: | Hyperprolactinemia |
| What two hypothalamic substances stimulate the release of Prolactin? | TRH and VIP |
| Haloperidol is a ________________ inhibitor that may cause: | Galactorrhea |
| Small Vessel Leukocytoclastic Angiitis is associated with ________, in children 3-11 years old, by deposition of _________ adn _______. | HSP: IgA and C3 |
| Hepatitis C | Associated with Leukocytoclastic Vasculitis |
| What is Leukocytoclastic Vasculitis? | Small Vessel Vasculitis that affects most evidently the skin |
| Skin lesions (multiple red dots) + arthralgias + recent treatment with a Beta-lactam, and the patient got symptoms resolved spontaneously. | Small Vessel Leukocytoclastic Vasculitis |
| Conn's Syndrome: | Primary HyperALDOSTERONISM |
| What is the MCC of Conn's Syndrome? | Bilateral Adrenal Hyperplasia |
| Patient presents with HTN, low serum[K+], pH higher than 7.45, muscle fatigue and paraesthesias, with abdominal CT showing abnormally large adrenal gland. Dx? | Conn's syndrome |
| Elevated plasma Aldosterone and Low plasma RENIN activity. Dx? | Conn's syndrome |
| The muscle weakness and paresthesias seen in Conn's Syndrome, are due to: | Severe hypokalemia |
| Inappropriately high activity of renin-angiotensin-aldosterone system, is the MCC of: | Secondary Hyperaldosteronism |
| Baby presents with Enlarged fontanelle, Protruding tongue, and Umbilical hernia, and mother states is hard to feed. PE shows mild jaundice. Dx? | Congenital Hypothyroidism |
| What are the 3 most used descriptions for Congenital Hypothyroidism? | 1. Enlarged Fontanelle 2. Protruding tongue 3. Association with UMBILICAL hernia |
| The brain, kidneys, intestines, liver and RBCs use what type of GLUT transporters? | Insulin-INDEPENDENT GLUT |
| RBCs and BBB use which GLUT? | GLUT-1 |
| GLUT-2 is used by: | Hepatocytes, B-pancreatic cells, and basolateral layer of renal tubule |
| The ____________ and ________________ transport use GLUT ___ for glucose uptake. | Placenta; Neuronal; 3 |
| GLUT-5 is used by: | Sperm and GI tract |
| An increase in Insulin cause NO upregulation of GLUT expression. | Insulin-INDEPENDENT GLUT |
| Insulin-Dependent GLUT | Increase in INSULIN causes an UPREGULATION of GLUT-4 expression. |
| What is the main role of PTH? | Increase BONE RESORPTION to increase serum Calcium |
| PTH acts INDIRECTLY on_______________________ and DIRECTLY on the ________________________. | Osteoclasts; OSTEOBLASTS |
| Osteoblasts have ____________ receptors | PTH |
| The binding of PTH and osteoblast leads to: | Increased production of RANK-L and M-CSF |
| As ______________ and M-CSF combine, after PTH was bounded PTH-receptor on Osteoblast, it lead to the maturing of ___________________, lead into to an increase bone______________. | RNK-L; Osteoclasts; Resorption |
| RANK-L? | product from PTH and Osteoclast interaction. Associated with elevated levels of PTH and low level of serum Calcium. |
| What are the common Fast-acting Insulins? | Aspart, Lispro, and Glulisine |
| Regular Insulin's effect is completely gone after how many hours approximately? | 7 hours |
| Which effect is longer, NPH or Detemir? | Detemir insulin actions act up to 24 hours, while NPH's act up to 18 hours. |
| Insulin receptor shows: | Tyrosine Kinase activity |
| What are common side effects of Insulin preparations? | 1. Hypoglycemia 2. Lipodystrophy 3. Hypersensitive reactions |
| What happens in the liver as insulin is uptaken? | Increase glucose store as GLYCOGEN |
| Increase in glycogen and protein synthesis, is seen as: | Insulin actions in the MUSCLE |
| How is fat affected upon contact with Insulin release: | Increase Triglyceride storage |
| Regular Insulin is considered __________ acting, while__________ is intermediate acting insulin. | SHORT; NPH |
| What is a desired or advantageous side effect of Metformin: | Loss of weight |
| What are the MoA of Metformin? | 1. Inhibits mGPD, which causes inhibition hepatic gluconeogenesis and the action of glucagon. 2. Increases glycolysis 3. Increases peripheral glucose uptake (increases insulin sensitivity) |
| Biguanide | Metformin |
| Where does the B-oxidation of FA occurs? | Mitochondrial matrix |
| Transported used by Fatty Acids to move across the membrane | Carnitine |
| Main product of the de novo fatty acid synthesis first step? | Malonyl-CoA |
| ______________ inhibits the transport of _______________ by carnite and ______________________. | Malonyl-CoA; Fatty acids; carnitine acyl-transferase |
| Malonyl-CoA: | 1. Major product of the de Novo FA synthesis first step 2. Inhibits carnitine acyltransferase --> no Fatty acid across membrane of the mitochondria. |
| Endometrial tissue outside the uterus. | Endometriosis |
| Chronic endometriosis lead to the formation of ______________ which cause ______ of the ________________ tubes, leading to ___________________. | ADHESIONS; scarring; Fallopian: INFERTILITY |
| What are the 3 main causes of abnormal vaginal bleeding? | Fibroids, Adenomyosis, and Endometrial cancer/hyperplasia. |
| 25 yo female. presents with heavy menses, constipation, frequent urination. She states pelvic pain, and a sensation of "something pulling down" in the pelvic area. PE shows very enlarged uterus. Dx? | Fibroids |
| Fibrinoid key features: | 1. Heavy menses 2. Pelvic pain/heaviness "pull-down" sensation 3. Enlarged uterus |
| Pelvic examination demonstrates a bulky, globular, and tender uterus, and a 7 month Hx of dysmenorrhea. Dx? | Adenomyosis |
| What is a common risk Hx for a patient to develop Endometrial carcinoma> | Hx of Obesity, null parity, or chronic ovulation. |
| 69 yo female complains of vaginal bleeding. Her last menses was over 10 years ago. She has a indicates past gastric bypass surgery 20 years ago, and hysterectomy at age 21. Dx? | Endometrial carcinoma/hyperplasia |
| Most common cause of vaginal bleeding in postmenopausal women? | Endometrial carcinoma/hyperplasia |
| Difference in uterus Physical examination in Fibroids, Adenomyosis, and Endometrial cancer? | Fibroids have enlarged uterus. Adenomyosis have bulky, globular and tender uterus Endometrial cancer have a NON-tender uterus. |
| DKA is a common cause of: | Metabolic acidosis |
| What is adenomyosis? | Condition in which the endometrium (inner lining of uterus) breaks through the Myometrium (muscle wall of uterus), causing vaginal bleeding. |
| DKA produces a ______________ odor in the _______________ and ______________. | Fruity; breath ; urine |
| Sudden onset of polyuria, polydipsia, volume depletion and fruity odor in breath. Dx? | Diabetic Ketoacidosis |
| Compensation of metabolic acidosis is ________________________, which is done by ____________________________. | respiratory alkalosis; HYPERVENTILATION |
| What are common causes of Adrenal insufficiency? | Adrenal hemorrhage or infarct, and acute onset of illness or surgery. |
| What is the treatment for adrenal insufficiency? Common used medication? | The use of glucocorticoids; Dexamethasone |
| Thyrotoxicosis labs show: | 1. Elevated free T4, 2. Suppressed TSH 3. Decreased weight |
| Tremors, suppressed TSH, elevated T4, and loss of weight, describe the clinical profile of which hormonal disorder? | Thyrotoxicosis |
| How is the histology of Exogenous Hyperthyroidism described: | Atrophic thyroid follicles, decrease in colloid, and low/undetectable thyroglobulin. |
| Thyroid tissue biopsy demonstrates LYMPHOCYTIC infiltrate with GERMINAL centers. | Hashimoto's Thyroiditis |
| De ____________ thyroiditis has disruption of follicles and _________ cellular infiltrate with _____________________________ cells. | Mixed; Multinucleated Giant cells |
| What is the histological finding in Grave's disease? | Tall, columnar epithelium with scalloped margins of colloid. |
| What are zinc-motifs? | The most common DNA-binding domain. |
| What is the composition of Zinc-motifs? | chains of amino acids, which mostly include Cysteine and Histidine, around central Zinc atom |
| Which amino acids compose Zinc-motif? | Cysteine and Histidine |
| Transcription factors, steroids, thyroid hormone, adn fat-soluble vitamins, commonly use ____________________ as their DNA-binding domain. | Zinc - motifs |
| Which autoimmune conditions have higher risk of developing in a patient with DM type 1? | Hashimoto's thyroiditis, Grave's disease, and Addison's disease. |
| DM type 1, Hashimoto's, Graves' disease and Addison's disease all are _____________. | HLA-2 |
| What are the electrochemical imbalances of Addison's disease? | 1. HYPOnatremia 2. HyperKalemia and Hyperchloremia 3. Non-anion gap metabolic acidosis |
| Addison's Disease is also classified as: | Chronic Primary Adrenal Insufficiency |
| Addison's Disease has __________________ gland dysfunction, leading to decreased levels of both, ________________ and ____________________. | Adrenal; Cortisol and Aldosterone |
| The hyponatremia seen in Addison's disease accounts for the clinical presentation of _______________________. | Hypotension |
| Patients with Addison's have increased production of ________ as it made with ACTH, and causes ________________________ of the skin. | MSH; HYPERPIGMENTATION |
| What is a common cause of PRIMARY ACUTE adrenal insufficiency? | Waterhouse-Friedshensen Syndrome |
| __________________________ is often caused by __________________ by N. _____________, __________, or _______________________ shock. It causes adrenal gland ________________________. | Waterhouse-Freidshensen Syndrome; Septicemia: N. meningitis; DIC: Endotoxin; hemorrhage. |
| Main differences between PRIMARY and SECONDARY adrenal gland insufficiency? | Secondary adrenal insufficiency is caused by pituitary gland inability to produce ACTH, while Primary is due to Adrenal gland dysfunction. In Secondary Adrenal Insufficiency, there is no Hyperkalemia and no skin pigmentation. |
| Abrupt withdrawal of exogenous steroid use, may produce ____________________ adrenal Insufficiency. | Tertiary |
| The Leydig cell is stimulated by ________, which in turn secretes__________________. | LH: secretes Testosterone |
| By what cell is Testosterone secreted? | Leydig cell in the Testis |
| Testosterone is secreted by Leydig cells in the testes by stimulation of which Pituitary hormone? | LH |
| What substance is secreted by Sertoli cells in the testes with FSH stimulation? | Inhibin B |
| Testosterone INHIBITS both, the ___________________ and _______________ release of GnRH and LH, respectively. | Hypothalamus: Pituitary gland |
| Unlike Testosterone, Inhibin B, only inhibits the release of ______ in the __________________ gland. | FSH; Pituitary gland |
| What is the main function of T-cells and NK cells? | Anti-cancer |
| Which are the two main cancer in which T-cells and NK cells act upon or attack? | Melanoma and Renal Cell carcinoma |
| -- B-cell -- No memory -- Short duration -- NO immunogenicity in infancy | Polysaccharide vaccine |
| Protein-Conjugated vaccine characteristics: | + B/T-cell immunity (Humoral and Cellular) + Memory + Long Duration + Immunogenicity in infancy |
| Passive immunization: | Receiving PREFORMED antibodies -- Rapid onset and short half-lives (3 weeks) |
| Examples of passive immunization | IgA breast milk, maternal IgG crossing the placenta, antitoxin, humanized monoclonal antibody. |
| What is Active Immunity means of acquisition? | Exposure to foreign antigens |
| What type of immunity has a slow onset and creates memory? | Active immunity |
| Natural infections, vaccines, toxoids | Examples of active immunity |
| Preformed antibodies, may be given to a patient that had recent exposure to which toxins or infections? What is the main benefit? | This process is Artificially-acquired Passive Immunity. Done after exposure to Tetanus toxin, Botulinum toxin, HBV, Varicella, Rabies Virus, or diphtheria toxin. Provides a quick or prompt healing. |
| What is the most common treatment for anaphylactic shock? | Epinephrine |
| Symptoms seen in Anaphylactic shock? | Vasodilation, increased vascular permeability, and bronchoconstriction. |
| What is the virulence factor of Strep Pyogenes? | M-protein. |
| Scarlet Fever is caused by what common organism? | Group A strep (S. pyogenes) |
| Pentad of; 1 Fever, 2 pharyngitis, 3 Strawberry-tongue, 4 sand-paper like skin rash, 5 circumoral pallor, describes the clinical manifestation of? | Scarlet Fever |
| Infection of S. pyogenes, with or without development of Scarlet Fever, predisposes a higher risk for development of what 2 other conditions? | 1. Rheumatic Fever 2. Glomerulonephritis |
| Patient with Kawasaki Disease has a higher risk of development of _____________________________. | Coronary Aortic Aneurysm |
| Increased cleavage of C2 and C4, resulting in inappropriate activation of the complement cascade is seen in? | C1 deficiency, which is a common cause of Angioedema |
| The conversion of Kininogen to Bradykinin in C1 deficiency, is done by: | C1INH |
| High levels of ______________________ in Hereditary _______________, are seen due to low levels of __________________________. | Bradykinin; Angioedema; C1 esterase inhibitor |
| What and why, type of medications are highly contraindicated in Hereditary Angioedema patients? | ACE INHIBITORS as these increase Bradykinin levels as a side effect, furthering the angioedema. |
| Multiple Endocrine Neoplasia are all autosomal ______________ disorders. | Dominant |
| What is the most common Pancreatic tumor seen in MEN1? | Gastrinoma |
| Pancreatic tumor, rarely seen in MEN1, characterized by electrolyte abnormalities and watery diarrhea? | VIPoma |
| What type of thyroid cancer is shared by MEN2B and MEN2A? | Medullary |
| Pheochromocytomas are seen in which two MEN syndromes? | MEN2A & MEN2B |
| Pituitary adenoma + PTH neoplasia + Insulinoma | MEN1 |
| Primary PTH hyperplasia + Medullary thyroid cancer + adrenal gland mass + episodic tachycardia | MEN2A |
| MEN 2B | Oral mucosa masses + skin neuromas + episodic and recurrent increased heart rate + thyroid cancer |
| Thin, tall guy, with long arms, but not a swimmer. Complains of episodes of headache and rapid pulses, and several small masses in the inside of the mouth. Recalls mother has similar symptoms. MC Dx? | MEN 2B |
| What enzyme is expressed in granulomatous diseases such as Sarcoidosis, and how is it related to increased levels of serum Ca2+? | Sarcoidosis and other granulomatous diseases activate MACROPHAGES, which then express 1a-HYDROXYLASE, which leads to synthesis of 1,25-(OH)2 Vit D and Hypercalcemia |
| What GI autoimmune disorder is a cause of Secondary Hyperparathyroidism? | Celiac Disease |
| Celiac Disease impairs the absorption of fat-soluble vitamins, such as Vitamin _______, which leads to: ______________ serum __________ and _____________ serum ____________, and __________ serum _______. | Vitamin D; low serum Phosphorus; Increased Serum PTH; Low serum Calcium. |
| Low vitamin D has: | Low urinary phosphorus |
| Why do babies born with non-salt wasting 21-(OH) deficiency are taller? | Increased androgens enhance early linear growth. |
| What's the treatment for 21 - (OH) deficiency? | Low doses of EXOGENOUS corticosteroids to suppress excessive ACTH and reduce stimulation of Adrenal cortex. |
| Females with 21-(OH) deficiency are seen with: | Ambiguous genitalia |
| Increased numbers of catecholamines: | Adrenal MEDULLA hyperplasia |
| Leydig Cell Hyperplasia: | Excessive: Testosterone, Androsterone, and DHEA No increase in 17-(OH) |
| No increase in 17-(OH) with Cortisol dominant symptoms: | Pituitary adenoma |
| Increased FSH, LH. Normal 17-(OH) Excess Cortisol (dominant Cushing Disease symptoms) | Pituitary adenoma |
| What is the key characteristic of MCAD deficiency? | Hypoketotic Hypoglycemia |
| Medium-chain acyl-CoA dehydrogenase deficiency is a disorder of which metabolic process? | Beta-Fatty Acid oxidation in the mitochondria |
| What are the most significant clinical manifestations of MCAD deficiency? | 1. HYPOKETOTIC HYPOGLYCEMIA 2. Seizures and sudden death |
| Fatty acid disorder that presents with Hypoketotic Hypoglycemia, muscle weakness, CARDIOMYOPATHY, and hypertriglyceridemia. | Primary Carnitine deficiency |
| Contrary to MCAD deficiency, which occurs in the _______________, Primary Carnitine deficiency occurs in the ____________________. | Mitochondria; Cytoplasm |
| Patient recently diagnosed with depressive disorder, complains of weakness, very concentrated urine, Dx? | SIADH |
| Most common malignancy associated with development of SIADH? | Small Cell carcinoma of the Lung |
| What is the normal urine osmolarity? | 100 mOsm/Kg |
| 1. Ectopic ADH (small cell lung ca) 2. CNS disorder/Trauma (meningitis, SAH) 3. Pulmonary disease 4. Drugs (cyclophosphamide, SSRIs) | Common causes of SIADH |
| Peripartum hemorrhage causing ischemic necrosis, is known as? | Sheehan Syndrome |
| How is Sheehan Syndrome often presented? | Mother's delay to lactate, due to Prolactin deficiency. |
| Why is the reason for developing Sheehan Syndrome? | During pregnancy there is an increase n estrogen due to enlargement of pituitary gland, but there is NO proportional blood supply to the gland enlargement. |
| Another name for De Quervain's Thyroiditis? | Subacute Granulomatous Thyroiditis |
| De Quervain's is most commonly seen after a _______________. | viral infection |
| Is de Quervain's thyroiditis painful? | Yes, it is painful |
| What are some characteristics of De Quervain's Thyroiditis? | 1. Transient Hyperthyroid symptoms 2. Increased ESR and CRP 3. Decreased in radioiodine uptake. |
| Autoimmune, Painless thyroid enlargement, dominant hypothyroid symptoms, +TPO, and histology shows lymphocytic infiltrate with germinal centers | Hashimoto's Thyroiditis |
| Hurthle cells are seen in histology of _____________________________. | Hashimoto's Thyroiditis |
| How are the eosinophilic epithelial cells seen Hashimoto's thyroiditis called? | Hurthle cells |
| Potassium iodine main action? | Inhibition of radioactive iodine. |
| When is the use of Potassium iodine commonly used? | In nuclear accidents in order to prevent radiation-induced thyroid carcinoma |
| Development of Cushing's that ACTH's and Cortisol production is only suppressed by High-dose Dexamethasone test? | Pituitary adenoma |
| Ectopic ACTH secreting adenoma: | ACTH cannot be suppressed with low or high dexamethasone tests. |
| What is the most common Pituitary adenoma, related to High-Dexamethasone suppression-only ? | Prolactinoma |
| _________________ thyroid caner, is the most common type of thyroid cancer. | Papillary |
| "Orphan Annie eyes" cytoplasm in thyroid cells, indicate | Papillary Thyroid cancer |
| Common risk factor, other than family hx, for Papillary thyroid cancer? | Radiation Exposure |
| RET/PTC rearrangements and BRAF mutations lead to increased risk of developing? | Papillary Thyroid cancer |
| Follicular thyroid carcinoma has a ___________ prognosis. It invades the thyroid ___________________ and vasculatures, and is associated to _______ mutations and _________________ translocations. | GOOD; capsule; RAS; PAX8-PPAR-gamma |
| Parafollicular cells are found in which type of thyroid cancer? | Medullary Thyroid cancer |
| Medullary thyroid cancer cells stain + for ________________________. | Congo red |
| RET mutations: | MEN2A and MEN2B |
| To what autoimmune condition is thyroid lymphoma associated? | Hashimoto's Thyroiditis |
| What are common causes of Secondary Hyperparathyroidism? | Vitamin D deficiency, decrease Ca2+ uptake, and Chronic Renal Failure |
| Hyperplasia, adenoma, and carcinoma of the PTH-gland are? | Causes of Primary Hyperparathyroidism |
| Poor prognosis thyroid malignancy, associated with Pleomorphic cells and biphasic spindle cells? | Anaplastic Thyroid cancer |
| Thyroid malignancy with POLYGONAL or spindle shaped cells and + for calcitonin. | Medullary Thyroid cancer |
| Glucocorticoid therapy a predisposal to ultimately induce a chronic state of ________________________________. | Hyperglycemia |
| Glucocorticoid therapy increases the hepatic synthesis of _____________________ and ___________________ proteins to increase the __________________________ availability. | Glucogenic and glycogenic; Glucose |
| An ________________________ effect is seen in glucocorticoid therapy. | Anti-insulinic |
| What changes occur in adipose tissue in patient with glucocorticoid medications? | Lipolysis and altered fat distribution |
| In glucocorticoid therapy, the side effects cause changes in different tissues, such as, Bone, Immune system, Skeletal muscle, liver, skin? | Bone --> osteoporosis, Immune system --> suppression and T-cell apoptosis, Liver --> increased gluconeogenesis and glycogenesis, Skeletal muscle and Adrenal cortex --> atrophy, and the skin is thinning, striated adn impaired wound healing. |
| What enzyme stimulates GLUCONEOGENESIS by increasing the activity of Pyruvate carboxylase? | Acetyl-CoA. |
| Hyperthyroidism causes an ___________________________, characterized by: _______________________________ and hyperreflexia. | Hyper-adrenergic; Hypertension, palpitations, tachycardia, sweating, heat intolerance, tremor. |
| What antiarrhythmic medication type is used in Hyperthyroidism? SE? | Beta-blockers to minimize adrenergic effects They do not work on exophthalmos |
| What are 2 common medications used to treat Hyperthyroidism? | Methimazole and PTU |
| Agranulocytosis | Side effect of Methimazole and PTU |
| ___________________ is a teratogenic drug during the ________ trimester. | Methimazole; First |
| What is the main side effect of PTU? | Hepatic failure |
| The use of radioiodine ablation in treatment of Hyperthyroidism may worse the _______________________ seen in these patients. | Exophthalmos |
| Surgery of the thyroid gland is a good option for permanent treatment of hyperthyroidism, but, it may also cause _____________ damage, leading to the development of ____________________ of the voice. | Recurrent Laryngeal Nerve; Hoarseness |
| Acetyl-CoA ---------------------------------> Malonyl-CoA, is catalyzed by what enzyme? | Cytosolic Acetyl-CoA carboxylase |
| What is the main action of Malonyl-CoA? | Inhibition of B-oxidation of newly formed fatty acids |
| What enzyme is inhibited by Malonyl-CoA? | mitochondrial carnitine acyltransferase |
| ______________________ is known as a __________________ of the de Novo Fatty acid synthesis and ___________________ of Fatty acids. | Malonyl-CoA: REGULATOR ; Beta-oxidation of FA |
| Events leading to Adrenal Crisis: | 1. Prolonged use of glucocorticoids leads to, 2. Suppression of HPA-axis ---> ---> ADRENAL INSUFFICIENCY, 3. In these patients, increased levels of STRESS lead to, ADRENAL CRISIS. |
| What situations are associated with increased stress leading to adrenal crisis? | A person in route to surgery or diagnosed with a severe disease. |
| A person with known Addison's disease, is about to have knee surgery. The physician should adequately _____________________, in order to prevent Adrenal crisis. | Increase the dosage of glucocorticoids |
| Stimulation of orbital fibroblast by Thyrotropin receptor antibodies and cytokines released by T -cells, leads to development of? | Grave's Ophthalmopathy |
| What is the triad of symptoms seen in Grave's Ophthalmopathy? | Exophthalmos, proptosis, and diplopia |
| ____________________ are most widely used in treatment of _________________ (vision condition) | Glucocorticoids; Grave's Ophthalmopathy |
| Which agents use Protein Kinase A, G-protein adenylate cyclase second messenger? | TSH, glucagon, adn PTH |
| The _____ is the major product of the TH gland. | T4 |
| What is the active form of thyroid hormone? | T3 |
| T3: | active form of TH |
| rT3 is: | inactive form generated by peripheral conversion. |
| G protein-coupled receptors include: | TSH, LH, and FSH. |
| What are 3 major domains of G protein-coupled receptors? | 1. Extracellular N-terminus 2. Transmembrane domain 3. Intracellular C-terminus |
| What type and which amino acids make up the Transmembrane domain G protein-coupled ? | HYDROPHOBIC; Ala, Leu, Phe, Trp, Met, Pro, and Gly |
| Tamoxifen is used in gynecomastia because? | Inhibits the effects of ESTROGEN on breast tissue. |
| Hyperlipidemia associated with eruptive and palmar xanthomas? | Familial Dysbetalipoprotenemia |
| Actions of TPO: | 1. conversion of iodide --> iodine 2. Iodination of thyroglobulin tyrosinase residues and, 3. iodotyrosine coupling reaction that forms T3 and T4. |
| Niacin of MoA: | 1. Decrease hepatic synthesis of triglycerides and VLDL, 2. Reduce clearance HDL |
| hyperlipidemic drug that may cause GOUTY ARTHRITIS? | Niacin |
| Glycogen Storage disease type 2? | Pompe disease |
| Pompe's disease has deficiency of __________________________ | Acid alpha-glucosidase (acid maltase) |
| Patient seen with cardiomegaly, hepatomegaly, generalized hypotonia, and macroglossia. Dx? | Pompe Disease |
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