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Unit 7 SIGs Cases 1-6
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Identify two male genital abnormalities that commonly occur with cryptorchidism in an infant and explain this association embryologically. (Wild Card WFA 7.3)
Inguinal hernias & hydroceles due to abnorm descent of testicles from abd cavity-> scrotum
Contrast the MOA of octreotide with that of pegvisomant (Wild card WFA 7.1).
O: long-acting somatostatin analog--> decreased secretion of GH; P: GH receptor antagonist; GH analog structurally altered to bind GH receptor w/o activating it
Explain how hypercortisolism led to the development of thin extremities and easy bruising (Wild Card WFA 7.3)
Glucocort-protein metabolism: decr protein synthesis& incr protein breakdown;Chronic + ->lean muscle loss;cortisol inhibits fibroblast prolif & collagen->bruise
Discuss the moa of licorice in its use in hypocortisolism (Wild card WFA 7.3)
Glycyrrhizin= analog endogenous corticoids;binds glucocorticoid & mineralcorticoid R; inhibits 11-beta hydroxysteroid dehydrogenase (cortisol-X->cortisone)
Describe the role of Sertoli cells in providing immune protection to the developing sperm (Wild card WFA 7.3)
Sertoli cells protect germ cells by forming the so-called blood-testis barrier with tight junctions between adjacent Sertoli cells.
Explain how the hormonal contraceptive progestin, alone and in combination with estrogen, prevents conception. (SIGS 7.3a)
Combo: Estrogen: inhibits FSH release ant. pit.; progestin: thickens cervical mucus-> decr. sperm penetration; progestin only: suppress GnRH, LH & FSH
Describe the physiology of achieving and maintaining erection (U7W3 SIGS 7.3b).
parasympathetic-> release acetylcholine-> incr endothelial nitric oxide-> activates guanylate cyclase-> incr cGMP-> decr intracell. free Ca2+-> sm. muscle relax
Describe the clinical features of symptomatic male hypogonadism (U7W3 SIGS7.3b).
decreased libido, fewer spontaneous erections, fatigue, hot flashes, depressed mood, difficulty w/ concentration, decr. muscle mass
Contrast primary and secondary hypogonadism and correlate them to low testosterone. (SIGS 7.3b)
Primary: issue w/ gonads-> decr. testosterone production; Secondary: issue w/ ant. pituitary-> decr. LH & FSH production
Contrast the indications for and efficacy of surgery and pharmacologic androgen inhibitors in the treatment of Cushing syndrome. (SIGS 7.2b)
Surgery always recommended to remove hormone producing tumor to decr excess hormone production; pharm if surgery is contraindicated (ketoconazole; metyrapone)
Rationalize the use of 24-hour urine free cortisol (UFC), late-night salivary cortisol and the low-dose overnight dexamethasone suppression test (DST) in the screening for Cushing syndrome. (SIGs 7.2b)
24 hour: cortisol over time (most accurate); late-night: cortisol usually lowest then; Low dose dexameth.: should suppress cortisol (high= cushing)
Classify the ACTH-dependent and ACTH-independent endogenous causes of Cushing syndrome. (SIGs 7.2b)
Dependent: high ACTH, high cortisol (Cushing Disease)- pituitary adenoma ; Indep: low ACTH, high cortisol (Cushing's syndrome)- adrenal adenoma/corticosteroids)
Explain the pathogenesis of T1DM with emphasis on the genetic and environmental causes. (SIGS 7.2a)
See image: HLA or insulin gene mutations; Environmental triggers: diet, viruses, drugs/toxins, stresses
Rationalize serologic and genetic testing done at the time of new-onset T1DM. (SIGS 7.2a)
Screen for HLA subtypes; Serologic testing for presence of auto-antibody types
Identify the associated clinical features in patients with T1DM and DKA. (SIGS 7.2a)
polyuria, polydipsia, polyphagia, weight loss, DKA (delirium, Kussmaul respirations, abdominal pain/nausea/vomiting, dehydration, fruity breath)
Describe the pathophysiology of type 1 diabetes mellitus (T1DM) and diabetic ketoacidosis (DKA). (SIGS 7.2a)
antibodies to beta-islet cells-> decr. insulin production-> low glucose in cells-> use of glycogen/FA-> ketone bodies->buildup-> acidic->DKA
Review pharmacological agents to manage osteoporosis in patients with hyperparathyroidism and hypoparathyroidism. (SIGS 7.1a)
hyper: bisphosphonate (pyrophosphate analogs that bind to hydroxyapatite binding sites to reduce bone resorption); Hypo: teriparatide- promotes bone growth; PTH
Evaluate lifestyle and integrative approaches to bone health, including vitamins, minerals, specific medicinal foods (fish; soy; tea), weight-bearing exercise, and mind-body techniques.
See image
Characterize the utility of imaging techniques in the evaluation of parathyroid disease (Sigs 7.1a).
US: quick/easy/cheap to check size; Nuclear med: Tc-99m test of choice to characterize hot/cold lesion based on metabolic activity; DEXA: bone density
Relate the physiologic process of bone resorption to the management of osteoporosis with parathyroid hormone analogues (teriparatide). (SIGS 7.1a)
synthetic PTH; regulates calcium metabolism from bone to promote bone growth (other meds promote bone density by prohibiting bone resorption); intermittent use
Contrast alterations in blood and urine levels of calcium, phosphate, vitamin D, and alkaline phosphatase in hyper- and hypoparathyroidism. (SIGS 7.1a)
Hypo: Ca+ low, Vit. D. low, alk phos low, phosphate high, PTH low ;hyper: Ca+ high, Vit D high, alk phos high, phosphate low, PTH high
Describe the actions of PTH in the regulation of calcium by the kidney. (SIGS 7.1a)
Low/intermittent levels: anabolic effects on osteoblasts and osteoclasts (indirect) to build bone; chronically high: catabolic effects;
Describe the endocrine disorders seen in MEN-1, including clinical features and morphologic findings of affected organs (SIGS 7.1b).
3P's: Primary hyperparathyroidism (hypercalcemia, nephrolithiasis), Pituitary adenoma (varies), Pancreatic tumors (gastrinoma is most common; gastric ulcers)
Describe the effect of an anterior pituitary adenoma on regulation of the hypothalamic-pituitary (HP) axis (SIGS 7.1b).
producing tumors = effects of the overproduced hormone, smaller size (i.e. prolactinoma); non-producing tumors = mass effects, larger size


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