Endocrinology
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Endocrinology - Leaderboard
Endocrinology - Details
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| What receptors does DHT bind? | DHT is the most potent androgen, binds delta-4 receptors and get stored by becoming 3a androstendione. |
| What receptors does DHT bind? | DHT is the most potent androgen, binds delta-4 receptors and get stored by becoming 3a androstendione. |
| How is the pathophysiology of Hirsuism? | We have overproduction of testosterone and delta-4- androstendione For testosterone: it can be from ovarian or extra-ovarian origin as the production of 1/3 of testosterone is from ovary and 2/3 is at extraovarian |
| What is Hirsutism? | Excessive hair development in unusual places for females (face and body) It is the most common type of hyperandrogenism for females |
| What is the difference between Hirsutism and Hypertrichosis? | Hypertrichosis is excess hair development in usual places, while Hirsutism is excess in unusual places |
| How does hyperandrogenism cause hair loss on the scalp? | They stimulate sebaceous glands and thus causing hair loss in the scalp |
| What are the signs of virilization that may accompany hyperandrogenism? | Minor signs (acne/ seborrhea- scalp sebaccous accumulation) these signs are not that serious Major signs (clitoris hypertrophy, alopecia (صلع), muscular hypertrophy, mammarian atrophy...) these signs are more serious and may lead to malignancy. |
| What are the main androgens present? | Testosterone and delta-4- androstendione. There is a correlation between their levels and the clinical severity. |
| What are the two types of Hirsutism? | Idiopathic (unknown origin of Hirsutism, hypersensitivity of receptors) Hyperproduction (of androgens and androgen precursors) |
| What are the etiologies for hyperproduction type of Hirsutism? | PCOS (most common type) Enzyme deficiency (Most common is 21-hydroxylase deficiency) Cushing's (syndrome) Tumors (ovarian or adrenal) |
| How is the pathophysiology of Hirsuism? | We have overproduction of testosterone and delta-4- androstendione For testosterone: it can be from ovarian or extra-ovarian origin as the production of 1/3 of testosterone is from ovary and 2/3 is at extraovarian (by bioconversion of delta 4 androstendione in skin, adrenals and lipid...) they diffuse to cells and become DHT by 5a reductase Delta-4- androstendione produced by ovaries and adrenals in equal proportions (50/50) |
| What receptors does DHT bind? | DHT is the most potent androgen, binds delta-4 receptors and get stored by becoming 3a androstendione. |
| What is the pathophysiology for DHEA? | It is mostly of adrenal origin, become delta 4 in skin, may be sulfated in order to have a longer half life. |
| What are the Etiologies for Hirsutism? | Of Adrenal Origin: Congenital adrenal hyperplasia (21 hydroxylase deficiency, 11-hydroxylase deficiency, 3-beta-HSD deficiency) Virilizing tumors (rapid and severe changes) Cushing's (ACTH dependent (either pituitary issue/ ectopic production) and ACTH independent) |
| What is the difference between Cushing's syndrome and disease? | Syndrome= any excess in coritsol Disease= pituitary origin of cortisol excess |
| What is 21-hydroxylase deficiency? | It is an autosomal recessive ch6 short arm disorder It is very polymorphic (could be complete deficiency or incomplete one) if incomplete it may present during puberty not from childhood |
| How is the pathophysiology of 21-hydroxylase deficiency? | Decrease in aldosterone and cortisol production, increase in ACTH, adrenal hyperplasia, and accumulate 17-OH-Progesterone which will eventually give delta 4 androstendione and testosterone This leads to hypotension, hyperkalemia and loss of water (no aldosterone) and hyponatremia. |
| What is the classic form of 21-hydroxylase deficiency? | Complete deficiency, appears at birth, pseudohermaphrodism feminin (looks like a male) loss of 2/3 of salt Rare. |
| What is the non-classic form of 21-hydroxylase deficiency? | It is more common, partial deficiency, appears in peri-puberty, variable from one female to another, mostly can be asymptomatic and only seen with serum testing |
| What are the signs of 21-hydroxylase deficiency? | Android aspect of the body Abnormal Puberty (irregular and late menses) Any Family History |
| How do we get a diagnosis of 21-hydroxylase deficiency primarily? | Dosage of 17-OH-P can be measured in day-3/4 of menses. it can be high (in case of classic type) or moderate (in case of non-classic) We can also perform Synacthene test (ACTH stimulation) to confirm the diagnosis, measure 17-OH-P after 1 hour of administration of ACTH 0.25mg, if higher than 10ng/ml then confirmed. |
| How do we get a diagnosis of 21-hydroxylase deficiency using androgen levels? | We can see an increase in delta 4 by 3 to 4 times of normal values, and of testosterone by 2-3 times and they increase with syncathene test However in partial deficit testosterone appears normal |
| What are the other two congenital adrenal hyperplasia etiologies? | 11-hydroxylase deficiency (rare, presents with HTN and virilization) 3-beta-HSD deficiency |
| What are the virilizing tumors in andrenal glands causing hirsutism? | They are tumors of fasicular or reticular origin of adrenals, tumors have a very rapid and sudden onset of signs, and present with virilizing syndrome (major signs) Aldosterone here is not affected as much as cortisol and androgens |
| What do adrenal tumors cause? | Very brutal hirsutism, with acne, seborrhea, and progressive alopecia Comes with oligo-amenorrhea, virilizing signs (major ones like clitoris hypertrophy, muscular hypertrophy, mammary atrophy |
| What biological changes occur with adrenal tumors? | Increase in DHEA and DHEAS (by 100 times!) Increase in testo and 4-delta (by 2-20 times) |
| What happens if adrenal tumors appear pre puberty? | Rapid bone growth and closing early so they will be taller at first and then block at a low height so they turn out short. Causes primary amenorrhea |
| How is the diagnosis of adrenal tumors? | By imaging (CT scan, they usually appear as huge tumors so easy to dx) Or by catheterization (of both adrenals veins to measure hormone levels and see if there is any variability) |
| Talk about ACTH dependent Cushing's causing hirsutism. | Increase ACTH, increase cortisol and androgens comes with hirsutism, facio-trunck obesity, muscular atrophy (at limbs) Vergetures (skin extended red-puprle) ecchymosis, HTN and osteoporosis and moon face. |
| What are the types of Hirsutism of ovarian origin? | Virilizing tumors of ovaries, Polycystic ovary syndrome (PCOS), Ovarian Hypertrophy syndrome. |
| How are virilizing tumors of ovaries? | They are rare, and have an intense presentation Biologically we have increase in androgens (>2ng/ml testo) with no responsiveness to OCP (oral contraceptives) We can locate them using CT scan, Endovaginal US (Echo), or catheterization of ovarian veins to get testo and delta 4 doses. |
| What are the types of virilizing tumors of ovaries? | Arrhenoblastoma, Gonadoblastoma, Lipidic cell tumors, Luteoma (more for GYN than endocrino dr) |
| What is the polycystic ovary disease? | It presents as anovulation, hirsutism, and multicysts at the ovaries (these are the criteria of dx, if 2 out of 3 are expressed--> PCOS Rotterdam While NIH needs all 3) AKA Stein-Leventhal syndrome presents clinically as disrupted menses (spaniomenorrhea, amenorrhea), acne, hirsutism (not severe), obesity (50% due to insulin resistance), no major virilization, acanthosis nigricans (ببين وسخ الجلد ع الرقبة اسود) |
| How does PCOS present biologically? | Increase in androgens (Testo and delta 4 by 2-3 times normal level) Can be suppressed by OCP (unlike tumors) increase LH but normal FSH due to increase ovarian stroma productions only Has two types I and II, type I is more severe than II |
| What are the tests for PCOS? | GnRH stimulation test (if LH explosive reaction--> PCOS) |
| What is ovarian hypertrophy syndrome? | Very Rare, post menopausal, Hypertrophy of ovarian stroma, presents either like PCOS or as severe as tumors (virilizing pseudotumoral) Treated surgically by GYN, dx by histo study |
| How are the Hirsutism of idiopathic origin? | Most common, when all possibilities are eliminated, present with childhood. Variable severity (could be moderate -->severe) occurs with a family history usually Clinically no vilirlization, no hypercoleserol, normal radio, Biology may be normal and maybe high DHEA Pathophysio: Hypersensitivity of receptors (increase 5a reductase) or/ increase usage by skin |
| What are the Iatrogenic origins of Hirsutism? | Estrogen/Androgen therapies, Danazol (for endometriosis), Adrogens for dermatological disease, Anabolites, Other medications (phenylhydatoine, cyclosporine, diazoxide) |
| How do we get a dx for hirsutism? | Hx (Personal, family, medications...) Physical Exam (Ferriman and Gallway Score (from 0-4 each place, 4-9 --> Hirsutism) Virilizing signs (major and minor)) Test (testosterone (as TeBG) and delta 4/ DHT (not asked for)/ DHEAS (adrenal origin sus)/ LH-FSH ratio (PCOS sus)/ Dynamic Tests (Syncatehene test in case hyperplasia adrenal sus) / Imaging (After hormonal workup to not get haloma)/ Catheterization (if radio not enough) |
| What is amenorrhea? | It is the absence of menses for at least 6 months 2 types, primary (complete absence) and secondary (if it disappears after having at least 1 period per life) |
| How is the physiology of the hypothalamic-hypophyseal axis? | For hypothalamus, there is a pulsatile stable secretion of GnRH every 90 mins throughout the cycle, but difference is in gonadotrophic cells receptors according to the phase we are in (follicular or luteal) and may be influenced by activating factors (VIP and NE) or inhibiting ones (dopa, endorphins, serotonin, GABA) For pituitary LH and FSH prodocution depends on the hormonal phase we are in (Luteal LH, Follicular FSH) There are hormones controlling it (Sexual hormones, monamines, and most importantly Prolactin) |
| How is the physiology at ovaries? | During follicular phase estrogen secretion increases, during luteal both estrogen and progesterone are produced by corpus luteum. There are other steroids (testosterone, delta 4 and 17-OH-P) These control menstruation, uterine mucosa and modulate hypothalamic-hypophyseal axis. |
| What is menstruation? | It depends on sex steroids, estrogen is essential to get progesterone receptors to endometrial wall, when hormones are less this leads to shed of endometrium and thus menstruation Permiability of the lower genital tract is also important during menstruation. |
| What are the means of investigation (gonophoric/ sex exploration) ? | Clinical exam of vagina and cervix Hysterosalpingography/ Hysteroscopy for lesions and malformation exploration (+ synechiae uterus) Oestro-progestative (contraceptive) test: giving estradiol for 21 days and progesterone from day 8 till 21, if we see bleeding withdrawal, then we have a functional endometrium (It is an artificial cycle) |
| What are the means of investigation of ovaries? | US (volume and structure), morning thermal curve (for luteal phase, look for monophasic amenorrhea) Endocrine function test (smears and biopsies estimating estrogen impregnation) Progestative test (duphaston for 10 days then progesterone, if bleeding occurs hen we have normal estrogen else we dont have) Hormonal measurement (not very useful, use only androgens) Karyotype (mainly turner (primary amenorrhea) |
| What are the means of investigating hypothalamic-hypophyseal axis? | PRL and gonadotropin levels (increase of PRL in case of adenoma, if PRL increases endorphins increase and thus GnRH decrease), FSH and LH levels (increase in ovarian pathology) LHRH test (if low LH and FSH, evaluated mobilization of pituitary reserve not very imp) clomiphene citrate test (anti-estrogen for functional pathology trigger a cycle) Anatomic exploration (clinical and bio data) |
| What are the etiologies of primary amenorrhea? | There is with or without normal secondary sexual characteristics, sexual ambiguity and hyperandrogenism |
| What are the origins of secondary amenorrhea? | Utero-vaginal, premature ovarian follicule, hypothalamo-pituitary cause, supra-hypothalamic cause, hyperandrogenism) |
| What are the etiologies of primary amenorrhea with secondary sexual char? | First always rule out pregnancy Then see anatomical malformations (imperforated hymen- pelvic pain, congenital aplasia of vagina- antimullerian duct growth seen by laproscopy/ceoloscopy, Post-TB uterine synechiae seen by hysterography) Then anorexia nervosa (respond to contraceptives) Then simple delay of menarche in case we ruled out all causes |
| What are the signals that we look for in 2ary amenorrhea without secondary sexual characteristics? | Evaluate stature-weight curve, bone age, FSH and LH test, karyotype and finally dysmorphia |
| What are the signs of primary amenorrhea without secondary char that are of gonadal origin? | Gonadal dysgenesis (turner syndrome , could be mosaic) Bone age (normal or slightly delayed) Dysmorphic syndrome with small size. Partial or total estrogen deficiency with elevated gonadotropins Seen with Coelioscopy infantile uterus, fallopian tube underdeveloped, and fibrous stripes at ovaries place (no ovaries) |
| What are the signs of primary amenorrhea without secondary characteristics that are of hypothalamic-hypophysela origin? | LH and FSH low with no response to LHRH dx by hx (growth, headache, anosmia (Kalmann syndrome)) and exam (radio MRI mostly |
| What lesions cause primary amenorrhea without sexual characteristics? | Rarely pituitary adenoma Mostly supra-sellar cause (craniopharyngioma -calcification, diencephalic tumors, and hydrocephalus) Sometimes endocrine abnormalities (pan hypopituitarism with defrientation of hyperprolactinemia, eg: Olfacto-genital kalman syndrome) |
| What is functional amenorrhea in case of primary amenorrhea without secondary char? | Diagnosis of elimination may be pubertal delay or psychogenic cause or malnutrition. |
| What is sexual ambiguity? | Male pseudohermaphrodism (testis but feminin) Usually due to androgen resistance, no sexual pilosity, normal breasts and vulvula , no uterus (AMH) two palpable masses (testicles) Dx: normal testosterone, LH and FSH, but with XY karyotype. could be mosaic/ incomplete form |
| What are utero-vaginal causes of secondary amenorrhea? | Acquired anomaly in genital tract preventing menstruation Characterized by ovulatory type temp curve, normal hormones and spaniomenorrhea with decreased menstrual flow Caused by uterine synechiae (TB, trauma- myomectomy/ seen in hysteroscopy) or stenosis of cervix (cancer, electrocoagualation, curettage) |
| What is premature ovarian insuffeciency? | Clinical signs: hot flashes, estrogen deficiency. Hormonal expression: LH and FSH raised with explosive LHRH, estradiol decreased <30, progestogen test negative Etiologies (induced early menopause (ovariectomy, chemotherapy, radiotherapy) , spontaneous early menopauses (autoimmune ovaritis- may be associated with other auto immune diseases)) |
| What are the spontaneous early menopauses causing premature ovarian insufficiency? | Gonadal dysgenesis (early ovarian failure (<30 yrs , chromosomal abnormalities)) Viral origin (mumps, rubella, coxsackie) Gonadotropin-resistance (primordial follicules blocked at antral stage with normal karyotype) Menopauses of undefined cause |
| What is hypothalamo-pituitary cause of secondary amenorrhea? | Clinical aspect (Isolated amenorrhea or pan pituitary insufficiency) Biology (Low LH and FSH (irresponsive to LHRH), fallen estradiol (- progestogen test), prolactin increase) Look for tumor syndrome using imaging Etiologies (pituitary tumors, craniopharyngiomas, non tumoral origins) |
| What pituitary tumors causing secondary amenorrhea? | Adenomas if <1cm micro if more macro Prolactin adenoma (irresponsive to TRH) GH adenoma (amenorrhea preceeds acromegaly, dx by IGF-1 level, and HGPO dose of GH) Corticotropic adenoma (hypercortisol, dx of free cortisol in urine , midnight cortisol level, and dexamethasone decceleration level) Thyrotropic adenoma (very rare but large) Gonadotropic adenoma (very rare, very high FSH (not frequently LH)) |
| What is craniopharyngioma causing secondary amenorrhea? | Supra-pituitary tumor mostly at rathkes pouch, often cystic with slow evolution. Radio: supra sellar calcification Biology: Gonadal insufficiency with other hypophyseal deficts, hyperprolactinemia |
| What are the non-tumor origins of secondary amenorrhea by hypothalamic axis? | Hemochromatosis, glanuloma (sarcoidosis in pituitary), surgical excision, radiotherapy, empty sella turcica, sheehan syndrome (post-partum necrosis) |
| What are supra-hypothalamic origins of secondary amenorrhea? | Psychogenic, gonadotropic insufficiency due to CNS failure interaction, decrease LHRH frequency due to increase of opiods Healed by psychogenic management. |
| What are the acute complications of DM? | Diabetic Ketoacidosis (DKA) Hyperglycemia Hyperosmolar state (HHS) |
| What is DKA? | Most common cause of hospitalization of young diabetic pt (10-14% of pt) and 30% of them are diagnosed with diabetes post hospitalization for DKA. Mortality 5% It should be directly managed |
| Define DKA? | Acute complication of IDDM (type 1 diabetes) caused by an absolute lack of insulin or lack of its action Characterized by: acidemia, ketonemia, hyperglycemia, hyperosmolarity, osmotic diuresis, dehydration. |
| What are the usual criteria of dx of DKA? | Serum glucose (>250 mg/100ml) bicarbonate (<15meq/l) serum ketones (>5mmol/l) pH <7.3 |
| How is the pathogenesis of DKA? | When Insulin is completely blocked, it will cause glucopenia in cells (lack of glucose) so we have more gluconeogenesis and glycogenolysis causing hyperglycemia, and thus osmotic diuresis. In parallel we have use of other energy source which is lipolysis, which will give free fatty acids that will get oxidized into ketone eventually. |
| What are the precipitating factors of DKA? | Not knowing of the dx of IDDM Non-compliance to treatment Infections Acute medical problems (surgery, CAD...) Emotional stress Drugs (interfering with insulin secretion like steroids, thiazide...) Maybe no apparent factor, it just happens |
| What are the typical history presentations for a DKA patient? | Some with coma, change of treatment, fever, infection, drug intake (steroids), alcohol ingestion |
| What are the symptoms of DKA? | Hyperglycemia (polyuria, polydepsia, dry tongue, weakness, malaise, headache, drowsiness, muscle cramps, weight loss...) Acidosis (abdominal pain, nausea, vomiting, constipation, SoB, deteriorated consciousness. |
| What are the signs of DKA? | Vitals (low bp, rapid weak pulse, high temp if infection, long deep sight with acetone smell breathing (Kussmaul breathing) Dehydration signs (dry tongue) Abdominal tenderness and rigidity Muscle weakness Hemiparesis (inability to move a side of the body) |
| What are the lab findings in DKA? | Very high blood sugar (250-700 mg/100ml) ketone, pH<7.3, low bicarb (increased anion gap) Water and electrolyte deficits (except potassium high since usually its intracellular but to compensate it goes out) Hyperlipoporteinemia, enzyme abnormalities (ALT and AST and amylase), BUN increased by dehydration, CBC (leukocytosis) |
| What is the tx of DKA? | Hydration (for dehydration) Insulin (for other complications) If unconscious put NS or dextrose if sugar low after insulin uptake (if sugar reached <250 mg) 1L for half an hour, then 1L for an hour then 1L for 2 hours |
| How is insulin given in case of DKA? | Simple insulin is given IV (push/drip/pump) Glucose falls differently for each pt, rehydration alone reduces glucose, infection decreases the rate of decrease by 50% 4-6 hours glucose falls to 200-300 mg/dl 8-12 hours correct the acidosis Regimen is 0.2 u/kg IVP, then 0.1 IV every hour till pt is out of acidosis, if pt glucose doesnt decrease by 10% then repeat loading dose of 0.2 Usually when first admitted to hospital we give immediately acting insulin |
| How do we replace deficits due to DKA? | Na (NS), K (it decreases with treatment, replace it orally for 1 week) P (uncertain benefits of replacement, usually for people with anemia/ cardiac issues) Mg (replacement if under <1.2mg/dl) |
| How to treat acidosis using bicarbonate? | Usually with severe acidosis (pH<7), should be given in small amounts, monitor and stop giving bicarb at pH=7.15-7.2 Since rapid alkalinization could cause hypokalemia, paradoxical CNS acidosis, effect on oxygen delivery to tissues (O2 saturation curve goes to the right) |
| What are the general measures taken in case of DKA? | Coma give oxygen if needed (intubation or respirator), bladder catheter if needed and low dose heparin if osmolarity >380mosml (hyperosmolar) |
| What complications could accompany the tx of DKA? | Hypoglycemia, hypokalemia, hypoxia and lactic acidosis, brain edema |
| How does tx of DKA cause hypoglycemia? | With hydration and insulin since glucose fall rapidly (more than ketone) so we stop giving insulin before pt stops being acidotic To prevent it change NS to D/NS IV when sugar falls <250 mg/dl with giving insulin IV |
| How does Tx of DKA cause hypokalemia? | If K is not replaced, we should monitor K every 2 hours. symptoms are muscle weakness, paralytic ileus, cardiac depression, cardiac arrest Flat or inverted T wave and a prominent U wave on the EKG |
| What are the complications of bicarbonate Rx? | Severe hypokalemia, Supressed hyperventilation and CO2 retention and thus CSF acidosis and brain edema, decrease in peripheral oxygenation and thus lactic acidosis |
| How does the Rx of DKA cause brain edema and how to treat it? | Accumulation of glucose in plasma, leads to acidosis in CSF and agressive hydration and rapid correction of acidosis will cause edema in brain. Treated with mannitol, decreased fluid intake and steroids (dexamathasone) |
| How do we prevent DKA? | Education, contacting physicians with symptoms, insulin tx, sugar and ketone level monitoring, Abx if infected, avoid precipitating factors and drugs |
| What is Hyperglycemic Hyperosmolar State (HHS)? | Acute complication of T2DM, characterized by extreme hyperglycemia with dehydration, occurs in elderly Pathogenesis same as DKA but without lipolysis --> no ketosis |
| What causes the absence of ketosis for HHS? | Lower levels of couner regulatory hormones, or lower FFA, or liver is less capable to form ketone, or insulin/glucagon ratio doesn't favor ketoacidosis. |
| What are the PPT factors for HHS? | Elderly (with no adequate water intake), CVA, MI, infection, renal failure, drugs (steroids, mannitol, diuretics...) |
| What is the clinical presentation of HHS? | More insidious than DKA (gradual but harmful), signs and symptoms of dehydration and hyperglycemia, more prominent CNS symptoms than DKA, infection S&S |
| What are the lab findings in case of HHS? | Sugar >600 up to 1000 high serum osmolarity >330 No acidosis or mild metabolic one >7.3 |
| What is the tx for HHS? | Urgently treat since MR=50%, Give IV fluids (10L), give insulin, and electrolytes + Abx if infection. |
| What are the types of chronic complications of DM? | Vascular Complications (microvascular: retinopathy, nephropathy, neuropathy; macrovascular: CAD, CVD, Peripheral artery disease (PAD)) Most common are microvascular Non-vascular Complications |
| What is the inflammatory atherothrombotic syndrome caused by insulin resistance (T2DM)? | Insulin resistance causes HTN and atherosclerosis by factor VII and XII and fibrinogen increase due to hyperinsulinemia thus using cholesterol and increasing it in blood causing atherosclerosis. Hyperglycemia causes foam cell formation and leukocytosis causing atherosclerosis |
| What vascular complications are caused by oxidative stress? | Hyperglycemia causes glucose auto-oxidation and thus oxidative stress, which decreases PGF and TXA causing endothelial dysfunction and thus vascular complications In addition to sorbitol pathways causing decreased antioxidants and thus thrombotic activity increase |
| What are the factors affecting CC of DM? | Duration of DM increases risk of getting the CC Microvascular complications result from chronic hyperglycemia in both DM types. No relation between macrovascular complications and chronic hyperglycemia Genetics, and comorbidities play a role as well |
| How is the prevelance of chronic complications of DM? | They are generally more prominent for pt with T2DM than T1 (US: 1/3 of pt T2DM have them while 1/10 of T1DM accoding to NHANES) |
| Describe the relationship between insulin resistance and diabetes development? | Early diabetes we have increased insulin resistance compensated by insulin level increase. With time beta cells start failing so decrease insulin (IFG and IGT) and get diabetes type 2 level of sugar. Risk of complications start with the diagnosis and increases with the progression of the disease. We should start intervention with the increase in IFG and IGT. |
| What are the possible pathways of developing vascular complications of T2DM? | Sorbitol pathway decreases antioxidants and thus increases free radicals and thrombotic effect. Glucose auto oxidation results in a state of oxidative stress. AGE pathway (CVD, stroke, neuropathy and amputation, nephropathy and retinopathy) |
| What affects the CC of DM? | Risk increases with the duration of DM. Microvascular increases with the duration of DM, macro is less conclusive. Genetics, comorbidities smoking and obesity increase the risk as well |
| What is the DCCT study? | It is a study on T1DM pt clinical trial, showed that good glycemic control reduces the risk for complications and this risk increases with increased HbA1c Randomized intensive and conventional treatment, follow up 6.5 years later and then EDIC 17 years later reduction of MI, stroke or death was seen |
| What is UKPDS study? | 5000 pt T2DM, conventional and intensive group, each 1% reduced HbA1C reduces risk of retinopathy by 35% Post trial after 10 years, |