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CAS 14 FC Topic 3
| Question | Answer |
|---|---|
| What are the three types of goiters? | Simple, multinodular, and dyshormonogenetic |
| What is a dyshormogenetic goiter? | A genetically-determined thyroid hyperplasia that results from enzyme defects in thyroid hormone synthesis, most commonly thyroid peroxidase. |
| What congenital disorder can a dyshormogenetic goiter cause? | Congenital hypothyroidism (cretinism) |
| How can follicular carcinomas and follicular adenomas be distinguished? | Follicular carcinomas invade through the surrounding capsule while follicular adenomas do not. |
| What is the most common cause of a parathyroid mass? | Solitary adenoma |
| What is the least common cause of a parathyroid mass? | Carcinoma |
| The majority of thyroid adenomas (benign thyroid tumors) are derived from what type of thyroid gland tissue? | Follicular epithelium |
| What physiologic response leads to goiter formation? | An enlarged thyroid gland which has undergone hyperplasia in response to excessive stimulation of TSH receptors |
| A fixed, painless and hard (rock-like) goiter is found in what thyroid disorder? | Riedel thyroiditis |
| Hyperfunctionality of thyroid follicular cells in a patient with a toxic multinodular goiter is the result of what mutation? | TSH receptor |
| What is the effect of a toxic multinodular goiter on T3 and T4 levels? | Release of T3 and T4 is increased, resulting in hyperthyroidism |
| What is a goitrogen? | A substance that interferes with iodine uptake, which suppresses the function of the thyroid gland and results in the enlargement of the thyroid |
| What vegetables are goitrogens? | Broccoli and brussel sprouts |
| Parathyroid hyperplasia is commonly associated with what two MEN syndromes? | MEN 1 and MEN 2A |
| If a patient has a goiter secondary to iodine deficiency, what will their thyroid hormone status be? | Euthyroid |
| What thyroid hormone level is expected in a patient with a multinodular goiter? | Euthyroid |
| What is the etiology of a simple goiter? | The body is unable to produce sufficient thyroid hormone, and the thyroid gland undergoes hyperplasia in response |
| What causes a simple goiter? | Lack of dietary iodine or intrinsic thyroid hormone production defects |
| What endocrine abnormality arises from parathyroid nodules? | Primary hyperparathyroidism |
| In what endocrine disorder do autoantibodies stimulate TSH receptors, resulting in the formation of a diffuse goiter? | Graves disease |
| How are tension headaches different from migraines? | Bilateral headaches that are not disabling |
| Which classes of agents are used as the initial prophylactic pharmacotherapy for migraine headaches? | Beta-blockers (propranolol, timolol, metoprolol), antidepressants (amitriptyline, venlafaxine), antiepileptic agents (topiramate, valproate), and calcium channel blockers (verapamil) |
| Migraines are caused by the abnormal activation of which nerves? | Trigeminal ganglion |
| Which key neuropeptides are involved in migraines? | Calcitonin gene-related peptide, substance P, and neurokinin A |
| Tension headaches are generally associated with what key factors? | Muscular or psychological stressors |
| Which drug is most commonly used as prophylactic therapy for patients that experience frequent/chronic tension headaches? | Amitriptyline |
| What is the first line agent for migraine abortive therapy? | Triptans, such as sumatriptan |
| Monoclonal antibodies with which mechanism of action can be used for migraine headache prophylaxis in individuals with headaches that are refractory to other pharmacotherapies? | Calcitonin gene-related peptide (CGRP) antagonists |
| What lifestyle changes are recommended for patients with frequent migraine headaches? | Sufficient sleep, regular exercise, and dietary modification (avoiding fasting and consumption of migraine triggers) |
| What agent, besides sumatriptan, can be used for migraine abortive therapy? | Ergotamine derivatives such as dihydroergotamine also stimulate serotonin receptors and can be used for migraine abortive therapy. |
| What is the pathology underlying headache secondary to sinusitis? | Edema of the mucosal lining of the paranasal sinuses secondary to inflammation, which leads to obstruction of the sinus opening and accumulation of sinus secretions. |
| What headaches occur ≥ 15 days per month and are caused by the chronic overuse of analgesic medication for >3 months? | Medication overuse headaches |
| What 2 therapies are recommended for the acute treatment of cluster headache attacks? | Triptans or 100% oxygen |
| Headaches due to an intracranial mass can be aggravated by what activities? | Exercise, sexual activity, changing position, and Valsalva maneuvers (expiring forcefully against a closed glottis) such as coughing, sneezing, straining on the toilet) |
| What is the treatment for medication overuse headaches? | Withdrawal of the causative analgesic |
| What headaches are unilateral, brief (15-180 minutes) headaches characterized by periorbital pain as well as ipsilateral autonomic symptoms in the face (e.g., lacrimation, rhinorrhea, sweating, miosis, ptosis)? | Cluster headaches |
| The presence of ipsilateral miosis and ptosis in these patients is referred to as what? | Horner-like syndrome. |
| What time of day are headaches due to intracranial mass most severe? | Morning |
| What is the most common type of recurring headache? | Tension headache |
| What are some common causes of headache that may lead to sinusitis? | Upper respiratory infection and allergies |
| What is the first-line prophylactic agent for individuals with chronic cluster headache? | Verapamil |
| What is the pattern of occurrence in cluster headaches? | Occur repeatedly within a “cluster” period of 3-6 weeks followed by month- or year-long periods without incidences. |
| What symptoms will be found in headache associated with sinusitis? | Purulent nasal discharge, nasal congestion, and facial pain over the sinuses that is worsened by bending down or applying pressure over the affected sinus. |
| What class of drugs is for the acute treatment of tension headaches? | Analgesics such as NSAIDs and acetaminophen |
| What types of headaches are disabling due to excruciating pain? | Migraine headaches and cluster headaches |
| In cases of chronic sinusitis, how does pain and headache differ from that in acute sinusitis? | Mild or absent |
| What is the hallmark presentation of migraine headaches? | Pounding (pulsatile), phonophobia, photophobia; one-day duration; unilateral; nausea or vomiting; disabling due to excruciating pain (ie, so painful that it limits routine activities) |
| What is a migraine aura? | A constellation of neurological symptoms which can affect the auditory, visual or olfactory system. |
| What are some pathological conditions that can cause displacement of the carina from its usual anatomical position? | Metastasis of bronchogenic carcinoma into tracheobronchial lymph nodes, enlargement of the left atrium, and conditions causing tracheal deviation (ex: tension pneumothorax) |
| What is the carina? | The cartilaginous ridge within the trachea that runs anteroposteriorly between the left and right main bronchi. |
| To carry out a tracheostomy, between what cartilage rings should a tube be placed? | Between the second and third tracheal cartilage rings |
| What is the epithelium of the trachea? | Pseudostratified, ciliated columnar |
| What is the purpose of pseudostratified, ciliated columnar epithelium in the airway? | Facilitates the clearance of inhaled debris from the airway. |
| Compression of the trachea may result from what? | Thyroid enlargement (tumor or goiter) or aortic arch aneurysm. In the case of aortic arch aneurysm, the pulse can then be felt through the trachea. |
| What is the trachea composed of? | C-shaped cartilage |
| Smooth muscle cells of the airways extend distally to which portion of the airways? | To the end of the terminal bronchioles. |
| In lymph nodes, what are secondary follicles and when do they form? | In response to antigenic stimulation, secondary follicles form. These contain a pale germinal center (mainly activated, proliferating B cells) and a mantle zone (both antigen-presenting B cells and T helper cells) |
| Describe the cortex of a typical lymph node. | Lymphoid follicles (mostly B-cells within a loose network of antigen-presenting follicular dendritic cells) as well as reticular cells, macrophages, and some scattered CD4 helper T cells. |
| What organs drain to the internal iliac lymph nodes? | Distal rectum to anal canal (above pectinate line), bladder, vagina (middle third), and prostate |
| What two cell types are found in the medullary sinuses of lymph nodes? | Macrophages and reticular cells |
| What areas drain to the axillary lymph nodes? | Deep lymphatics of the arm, the pectoral region (including breast), and the skin above the umbilicus |
| What broad class of events causes lymph node paracortex hyperplasia? | Infections increase the number of circulating lymphocytes and create a large influx of lymphocytes into lymph nodes. |
| Which component of the lymph node medulla is characterized dark masses of lymphoid tissue that contain densely packed lymphocytes and antibody-producing plasma cells? | Medullary cords |
| Which type of lymph node follicles contain dormant B cells? | Primary follicles |
| What areas drain to the superficial inguinal lymph nodes? | Anal canal (below pectinate line), the skin below umbilicus (except popliteal territory), the scrotum, and the vulva |
| What are the 2 major components of the lymph node medulla? | Medullary cords and medullary sinuses |
| What organ(s)/area(s) drain to the para-aortic lymph nodes? | Posterior abdominal wall, kidneys, testes, ovaries, and uterus |
| Interaction between what two cell types are facilitated in lymph nodes? | Lymphocytes and antigen-presenting cells, such as macrophages and dendritic cells, which then activate lymphocytes. |
| How do antibodies produced in lymph nodes exit to the lymphatics? | Via medullary cords, which drain into the medullary sinuses, then into the efferent lymphatics. |
| What organs drain to the inferior mesenteric lymph nodes? | Descending (left) and sigmoid colon |
| The lateral dorsal foot and posterior calf drain to the what lymph nodes? | Popliteal nodes |
| What organs drain to the superior mesenteric lymph nodes? | Distal duodenum, jejunum, ileum, ascending (right) colon, and transverse colon to splenic flexure |
| Which syndrome is marked by a hypoplastic lymph node paracortex? | Thymic aplasia or hypoplasia (for example, DiGeorge syndrome) lowers the amount of circulating lymphocytes. As a result of the lack of lymphocyte influx, the paracortex becomes hypoplastic and smaller than usual. |
| What areas does the thoracic duct drain? | Drains lymph from everything except the right upper quadrant of the body, above the diaphragm. |
| Which organs drain to the celiac lymph nodes? | Stomach, liver, pancreas, spleen, and proximal duodenum |
| Where is the paracortex of a typical lymph node, and what is the predominant cell type? | It is a T-cell rich area that lies between the lymph node cortex and medulla. |
| How do mild decreases in serum magnesium levels affect parathyroid hormone (PTH) secretion? | Stimulate PTH secretion. |
| How do severe decreases in serum magnesium levels affect parathyroid hormone (PTH) secretion? | Inhibit PTH secretion |
| What is the relationship between plasma phosphate concentration and parathyroid hormone? | Plasma phosphate lowers the ionized calcium level, stimulating PTH secretion. |
| The presence of which second messenger in urine reflects parathyroid hormone action at the proximal tubule? | Increased urinary cAMP |
| What effect does parathyroid hormone have on bone? | PTH increases bone resorption of calcium and phosphate. |
| When PTH binds to receptors on osteoblasts, what is secreted in response? | Macrophage colony-stimulating factor (M-CSF) and receptor activator of NF-kB ligand (RANK-L) |
| What occurs when RANK-L binds RANK on osteoclast precursors? | RANK-L binds RANK on osteoclast precursors, promoting their differentiation into mature osteoclasts capable of bone resorption and calcium release. |
| Which eponymous physical exam findings are classically associated with hypocalcemia? | Chvostek sign is facial muscle contraction after tapping the facial nerve pathway. After occlusion of the brachial artery, the Trousseau symptom — carpal spasms — occurs (eg, blood pressure cuff inflated around the triceps) |
| The parathyroid gland contains which two cell types? | Chief cells and oxyphil cells |
| Which of the parathyroid gland cells secretes parathyroid hormone? | Chief cells |
| What is the effect of vitamin D on parathyroid hormone? | Vitamin D reduces PTH secretion by inhibiting PTH transcription. |
| What is responsible for the clinical manifestations of hypoparathyroidism? | The magnitude of hypocalcemia determines the clinical symptoms of hypoparathyroidism, which typically manifest as tetany (decreased serum ionized calcium concentration results in neuromuscular irritability). |
| What is parathyroid hormone-related peptide? | PTHrP behaves like PTH, and is often elevated in cancer (paraneoplastic syndromes). |
| How does parathyroid hormone affect intestinal calcium absorption? | PTH boosts calcium absorption. |
| How does PTH hep absorb calcium in the intestines? | PTH increases 1,25-(OH)2 vitamin D production by stimulating 1-hydroxylase in the kidney. The same goes for vitamin D. |
| What impact does an acute decrease in plasma ionized calcium have on parathyroid hormone (PTH) secretion? | PTH secretion increases when there is an acute decrease in plasma ionized calcium. |
| What are the net effects of parathyroid hormone (PTH) on serum calcium and serum phosphate? | ↑ serum calcium, ↓ serum phosphate, ↑ urine phosphate |
| How does parathyroid hormone affect urinary phosphate excretion? | PTH increases the excretion of phosphate in the proximal renal tubule, decreasing phosphate reabsorption. |
| What is the effect of PTH (parathyroid hormone) on renal calcium reabsorption? | PTH increases renal calcium reabsorption in the distal convoluted tubule. |
| Which class of drug can be used to treat patients with Sjögren's syndrome who have xerophthalmia (dry eye) and xerostomia (dry mouth) that do not respond to more conservative measures (eg, artificial tears or saliva)? | Muscarinic agonists |
| What is the difference between Sicca syndrome and Sjögren's syndrome? | Sicca syndrome is not associated with arthritis. |
| Which autoantibodies are present in the majority (60–80%) of patients with Sjögren's syndrome and are the most specific serologic studies to support the diagnosis? | Anti-Ro/SSA and/or anti-La/SSB autoantibodies |
| What diagnostic test measures the output of the lacrimal gland to determine if enough tears are being produced on a patient with Sjögren's syndrome? | Schirmer's test |
| What is the pathophysiology of Sjögren's syndrome? | Sjögren's syndrome is a lymphocyte-mediated autoimmune destruction of minor salivary and lacrimal glands that may result in fibrosis. |
| What are the major components of the management of patients with Sjögren's syndrome that is characterized by mild xerophthalmia and xerostomia? | Artificial tears and saliva, meticulous oral hygiene, and an annual ophthalmologic and bi-annual dental examinations |
| A pregnant mother with anti-Ro/SSA and/or anti-La/SSB autoantibodies will put the fetus at risk of developing which cardiac pathology? | Congenital heart block |
| Which type of lymphoma is most strongly associated with Sjögren's syndrome? | Marginal zone lymphomas of mucosa-associated lymphoid tissue (ie, MALT lymphomas), which are non-Hodgkin B-cell lymphomas. |
| What is the most common site of these lymphomas in Sjögren's syndrome? | Parotid gland |
| What histologic changes present on a lip biopsy are characteristic of a diagnosis of Sjögren's syndrome? | Loss of lymphoid tissue and evidence of mild salivary gland inflammation (lymphocytic sialadenitis). |
| Which physical exam finding is most commonly associated with parotid gland MALT lymphoma in patients with longstanding Sjögren's syndrome? | Unilateral parotid gland enlargement |
| What is the classic presentation of Sjögren's syndrome? | Keratoconjunctivitis sicca (dry eyes), xerostomia (dry mouth), which can lead to dental caries, and joint pain |
| Sjögren's syndrome most commonly affects individuals of which age and sex? | Middle-aged females (40 to 60 years) |
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jofreayala
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