253994296 Tiki Taka Ck Endocrinology

8/20/2019 253994296 Tiki Taka Ck Endocrinology

1/15

ENDOCRINOLOGY TiKi TaKa _________________________ . THYROID DISEASES:

___________________ ___________________ . P.O.C. ___________________ HYPOthyroidism ______________ HYPERthyroidism ---------------- -----------------* Labs ___________________ -- T4 & ++ TSH ______________ ++ T4 & -- TSH* Weight ___________________ Gain ______________ Loss* Intolerance ___________________ Cold ______________ Heat* Hair ___________________ Coarse ______________ Fine* Skin ___________________ Dry ______________ Moist* Mental ___________________ Depressed ______________ Anxious* Heart ___________________ Bradycardia ______________ Tachycardia & Af* Muscles ___________________ Week ______________ Week* Reflexes ___________________ Diminished ______________ Hyperactive* Fatigue ___________________ Yes ______________ Yes

* Menstrual changes ___________________ Yes ______________ Yes. HYPOTHYROIDISM: _________________ * PRIMARY Hypothyroidism * * Secondary Hypothyroidism * * TERTIARY Hypothyroidism * ________________________ _________________________ ___________________

______ . -- T3 & T4. . -- T3 & T4. . -- T3 & T4.. ++ TSH. . -- or normal TSH. . -- or normal TSH. . Ex: Auto-immune Hashimoto's.. HASHIMOTO's THYROIDITIS:

__________________________ . Hypothyroidism symptoms: Slow, tired, fatigued pt with weight gain.

. Anti-TPO Abs (Anti-thyroid peroxidase antibodies). . -- T4 & ++ TSH. . Tx -> T4 or thyroxine replacement. . High risk of developing THYROID LYMPHOMA.. GENERALIZED RESISTANCE to thyroid hormones:

_____________________________________________ . ++ T3 & T4 levels. . ++ or Normal TSH level. . features of HYPO-thyroidism despite having ++ free T3 & T4.. N.B. HYPOTHYROIDISM & MYOPATHY:

_________________________________ . Un-explained ++ ofe serum CPK creatinine kinase. . ANA Anti-nuclear antibodies may be +ve in HASHIMOTO's thyroiditis.

. Serum TSH level is the most sensitive test to diagnose hypothyroidism.. HYPERTHYROIDISM -> "Grave's disease" - "Silent" - "Subacute" - "Pituitary adenoma":

________________________________________________________________________________ __________ . Physical findings: . Eye,skin,nails - Not tender - Tender gland - None.. RAIU scan: . (++) - (--) - (--) - (++).. TTT: . Iodine ablation - None - Aspirin - Surgical removal..1. GRAVE's DISEASE:


2/15

____________________ . Symptoms of thyrotoxicosis (weight loss - insomnia - hperactivity - tachycardia). . Ophthalmopathy (Exophthalmos & proptosis - Abs against the extra-ocular muscles). . Dermopathy (Thickening & redness of the skin just below the knee). . Onycolysis (Separation of the nail from the nailbed). . Peri-orbital lymphocytic infiltration -> Gritty sandy sensation. . Fibroblast proliferation, hyaluronic acid deposition, edema & fibrosis. . Throid stimulating immunoglobulins.. RAIU -> HIGH. . Tx -> Propylthiouracil (PTU) or methimazole. . Use radioactive iodine to ablate the gland (May cause permanent HYPO-thyroidism). . BB (propranolo) to treat sympathetic symptoms, such as tremos & palpitations..2. SILENT Thyroiditis:

_______________________ . Auto-immune process. . Symptoms of thyrotoxicosis (weight loss - insomnia - hperactivity - tachycardia). . NON-tender gland. . No skin, eye or nail diseases. . RAIU -> NORMAL. . Tx -> NONE !

.3. SUB-ACUTE Thyroiditis = De QUERVAIN's THYROIDITIS: ______________________________________________________ . Viral etiology. . ++ ESR > 50 mm/hr. . Thyroid TENDRNESS. . Syms last for < 8 wks due to thyroid depletion. . RAIU -> LOW. . Tx -> ASPIRIN to relieve pain..4. PITUITARY ADENOMA:

______________________ . THE ONLY CAUSE OF HYPERTHYROIDISM WITH ++ T4 & ++ TSH ! . Dx -> Brain MRI. . Tx -> Surgical removal.

.N.B. EXOGENOUS THYROID HORMONE ABUSE: ______________________________________ . ++ T4 & -- TSH. . The galnd will atrophy to the degree of non-palpability on exam.. N.B. THYROID STORM:

_____________________ . Acute, severe life threatening hyperthyroidism. . Tx -> IODINE -> Blocks uptake of iodine into the gland. . Tx -> Propylthiouracil or methimazole -> Blocks the production of thyroxine. . Tx -> Dexamethazone -> Blocks peripheral conversion of T4 to T3. . Tx -> Propranolol -> Blocks target organ effect.# THYROID NODULE APPROACH:

__________________________

A . 1st step -> Cilinical evaluation - TSH level & thyroid ULTRA$OUND. ______________________________________________________________________ B . CANCER risk factors or suspicious U$ findings ?? ____________________________________________________ . YES -> FNAB (Fine Needle Aspiration Biopsy). . NO -> C. (TSH level). C . TSH LEVEL ?? ________________ . Normal or ++ -> FNAB.

. -- Low -------> D. (I 123 scintigraphy).


3/15

D . I - 123 scintigraphy: _________________________ . HYPER-functional (HOT) nodule -> Treat hyperthyroidism. . HYPO-functional (COLD) nodule -> FNAB.. MOST thyroid nodules are BENIGN COLLOID nodules.

__________________________________________________ . SICK EUTHYROID $YNDROME = LOW T3 $YNDROME:

____________________________________________ . Abnormal thyroid function tests with an acute severe illness. . May be due to caloric deprivation. . Fall in total & free T3 levels with NORMAL T4 & TSH.. FACTITIOUS THYROTOXICOSIS:

____________________________ . Due to exogenous thyroid hormone. . H/O of psychiatric illness or attempted weight loss (Herbal remedy!). . Thyrotoxicosis syms (Palpitations - sweating - weight loss - hyperactivity &diarrhea). . Lid lag may be present but NO exophthalmos (Excluding Grave's dis.). . The ingested thyroid hormone disturbs the native thyroid axis ! . RAIU is decreased (-- Radio Active Iodine Uptake). . Dx -> "LOW SERUM THYROGLOBULIN" is the main stay of diagnosis. . Dx -> -- TSH & ++ T3 &/or T4.. TOXIC ADENOMA:

________________

. ++ T4 & -- TSH levels. . Symptoms suggestive of thyrotoxicosis. . Radioactive uptake in the nodule & suppression of uptake ith rest of the thyroid gland. . No infiltrative ophthalmopathy.. THYROID RADIOACTIVE IODINE SCAN:

__________________________________ . HASHIMOTO's THYROIDITIS -> Heterogenous pattern. . GRAVE's DISEASE ---------> Diffusely ++ uptake. . MULTINODULAR GOITER -----> PATCHY. . PAINLESS THYROIDITIS ----> -- markedly reduced uptake.. SIDE EFFECTS OF RADIO-IODINE THERAPY -> HYPO or HYPER thyroidism !!

_____________________________________________________________________

. HYPOTHYROIDISM: _________________ . Destruction of thyroid flollicles by radioactive iodine. . Tx of hypothyroidism is Levo-thyroxine. . Ophthalmopathy may worsen in 10 % of cases. . THYROTOXICOSIS: _________________ . may be a side effect of RADIO-IODINE theray !! . I - 131 is taken up by thyroid follicles & then destroys them by emitting B-rays. . Dying thyroid cells may release excess thyroid hormone into the circulation. . Aggravating the hyperthyroid state.. CONTRA-INDICATIONS to RADIO-ACTIVE IODINE THERAPY:

____________________________________________________ . PREGNANCY. . VERY SEVERE OPHTHALMOPATHY.. SIDE EFFECTS of ANTI-THYROID DRUGS (PROPYLTHIOURACIL):

________________________________________________________ . AGRANULOCYTOSIS (fever & sore throat) -> Stop the drug !. SURGERY SIDE EFFECTS:

_______________________ . Permanent hypothyroidism. . Risk of recurrent laryngeal nerve damage.


4/15

. COMPLICATIONS of UN-TREATED HYPER-THYROID PATIENTS: _____________________________________________________ -> RAPID BONE LOSS -> due to ++ osteoclastic activity . -> CARDIAC TACHYARRHYTMIA (Af).. N.B. HYPERTENSION in pts with THYROTOXICOSIS:

_______________________________________________ . is predominantly SYSTOLIC.. caused by HYPERDYNAMIC CIRCULATION.. N.B. INDICATIONS OF THYROID FUNCTION TESTS:

_____________________________________________ -> HYPERLIPIDEMIA. -> Un-explained hyponatremia. -> Un-exlained ++ CPK.# THYROID MALIGNANCIES:

_______________________ 1 * PAPILLARY CARCINOMA: ________________________ -> MOST COMMON TYPE & BEST PROGNOSIS. -> Slow infiltrative local spread. -> Presence of PSAMMOMA bodies. 2 * MEDULLARY CARCINOMA: ________________________ -> CALCITONIN secretion. 3 * FOLLICULAR CARCINOMA:

_________________________ -> Invasion of the tumor capsule & blood vessels. -> Early metastasis to distant organs.. BIOCHEMISTERY IMPORTANT INFO:

_______________________________ . GLUCONEOGENESIS main substrates:

__________________________________ . Alanine - Lactate - Glycerol 3 phosphate. . PYRUVATE is an INTERMEDIATE of Alaninie.. MULTIPLE ENDOCRINE NEOPLASIA (MEN):

_____________________________________ * MEN TYPE 1:

______________

. Parathyroid adenoma. . Pituitary tumor. . Pancreatic tumor. . {Mutation in the MEN 1 tumor suppressor gene}.* MEN TYPE 2A:

______________ . Medullary thyroid cancer (HARD NODULE - ++ Calcitonin - Malignant cells on FNAB). . Pheochromocytoma. . Parathyroid hyperplasia. . Less aggressive (No associated cancers).* MEN TYPE 2B:

______________

. Medullary thyroid cancer (HARD NODULE - ++ Calcitonin - Malignant cells on FNAB). . Pheochromocytoma (++ urinary metanephrines & nor-epinephrines levels). . Neuromas (mucosal & intestinal). . Marfanoid habitus (-- upper to lower body ratio - hypermobile joints - scoliosis). . {Mutation in the RET proto-oncogene located on chromosome 10}. . DNA testing is used for screening. . More aggressive (Associated cancers).. DM SCREENING TESTS:


5/15

_____________________ .1. GLYCOSYLATED HEMOGLOBIN Hb A 1C:

_____________________________________ . It is used to monitor chronic glycemic control. . It is reflective of the pt's average glucose levels over the past 100-120 days. . Preferred test in non fasting state. . > 6.5 -> DM. . < 5.7 -> Normal. .2. FASTING BLOOD GLUCOSE:

___________________________ . No caloric intake for 8 hours. . > 126 mg/dl -----> DM. . 100 - 125 mg/dl -> Impaired fasting glucose. . 70 - 99 mg/dl ---> NORMAL. .3. RANDOM GLUCOSE LEVEL:

__________________________ . > 200 mg/dl with symptoms of hyperglycemia. .4. ORAL GLUCOSE TOLERANCE TEST:

_________________________________ . MOST SENSITIVE TEST. . 75 g glucose load with glucose testing for 2 hours. . > 200 mg/dl -----> DM.

. 140 - 199 mg/dl -> Impaired glucose tolerance.. DKA DIABETIC KETOACIDOSIS: ____________________________ . Blood glucose level > 250. . pH < 7.3 . Low serum HCO3 < 15-20 . Detection of plasma ketones. . ++ ANION GAP {(Na) - (Cl+HCO3)} ----> AG > 8-12.. H/O of previous stressor e.g. recent GIT infection. . H/O of weight loss, ployurea & polydipsia. . Deep rapid breathing (Kussmaul's respiration). . Osmotic diuresis -- total body K (But : Serum K may be elevated!). . ++ in K level due to EXTRA-CELLULAR SHIFT.

. PARADOXICAL HYPERKALEMIA (The body potassium reserves are actually depleted!) . 1st initial simple step to detect DKA --> FINGER-STICK GLUCOSE ! . DKA MANAGEMENT:

_________________ .1. RAPID INTRAVENOUS NORMAL SALINE (0.9% SALINE). .2. RAPID INTRAVENOUS REGULAR INSULIN. .3. K correction. .4. TTT of infections e.g. Abs.. ARTERIAL pH or ANION GAP is the most reliable indicator of metabolic recoveryin DKA.

________________________________________________________________________________

_______ . HYPER-GLYCEMIC HYPER-OSMOLAR NON-KETOTIC COMA:

________________________________________________ -> Very high glucose levels. -> Very high plasma osmolality. -> NORMAL ANION GAP. -> NEGATIVE SERUM KETONES.. Non ketotic - Hyperglycemic coma management:

______________________________________________ . Fluid replacement with NORMAL SALINE.


6/15

_______________________________ .................... __________________________ ______ . DIABETIC KETOACIDOSIS (DKA) .................... HYPEROSMOLAR HYPERGLYCEMIC STATE

________________________________ .................... __________________________ ______ . Type (1) DM usually. ____________________ . Type (2) DM. . YOUNGER age. ____________________ . Older. . LESS confusion. ____________________ . MORE confusion. . Hyperventillation MORE common ____________________ . Less common. . Abdominal pain MORE common. ____________________ . LESS common. _______________________________________________________________________________

_______ . Glucose 250 - 500 mg/dl. ____________________ . > 600 . HCO3 < 18 meq/L. ____________________ . > 18. +++++ ANION GAP. ____________________ . NORMAL. . POSITIVE serum ketones. ____________________ . NEGATIVE. . Serum osmolality < 320 ____________________ . > 320.. DIABETIC NEPHROPATHY:

_______________________ . Begins with HYPERFILTRATION (++GFR) & MICROALBUMINURIA. . If not ttt well .. Micro becomes Macroalbumiuria > 300 mg/dl. . INTENSIVE BLOOD PRESSURE CONTROL to prevent worsenening of the condition. . Use ACE Is with blood pressure goal 130/80 mmHg.

. Most sensitive screening test is -> RANDOM URINE MICRO-ALBUMIN/CREATININE RATIO.. DIABETIC NEUROPATHY:

______________________ . DISTAL SYMMETRIC SENSORIMOTOR PLOYNEUROPATHY. . STOCKING GLOVE pattern. . It is the most common risk factor of foot ulcerations in diabetics. . Tx -> TCAs (Amitriptyline - Gabapentin).. DIABETIC GASTROPATHY:

_______________________ . Autonomic neuropathy of the GIT. . Symptoms of delayed gastric emptying & gastroparesis. . -- Esophageal dysmotility -> Dysphagia.

. -- Gastric emptying -------> Gastroparesis. . Gastroparesis (Nausea - vomiting - early satiety - postprandial fullness). . -- intestinal function ----> diarrhea - constipation - incontinence. . Tx -> DN control - SMALL FREQUENT MEALS - METOCLOPROMIDE (prokinetic & Antiemitic). . SEs of Metoclopromide -> Extrapyramidal syms -> Tardive dyskinesia (Give Erythromycin).. ERECTILE DYSFUNCTION in D.M.:

_______________________________ . Due to vascular complications & neuropathy. . 1st line of ttt is phosphodiesterase inhibitor (Sildenafil). . Contr'd in pts being ttt with NITRATES. . Sildenafil may predispose to PRIAPISM.

. When combined with an Alpha blocker (Prazosin), it is imp. to give them 4 hrs apart,, . to avoid SEVERE HYPOTENSION.. DIABETIC FOOT management -> DEBRIDEMENT & proper wound care.

______________________________________________________________ . CAUSES OF HYPOGLYCEMIA in NON-DIABETIC pts:

_____________________________________________ 1 - INSULINOMA (BETA cell tumor). 2 - SURREPTITIOUS use of insulin or sulfonylurea.


7/15

. INSULINOMA: _____________ . BETA CELL TUMOR. . Normally, blood glucose < 60 mg/dl result in complete suppression of insulinsecretion. . Hypoglycemia in the presence of inappropriately ++ serum insulin levels = insulinoma. . ++ C-peptide level. . ++ Pro-insulin.. DIABETES INSIPIDUS:

_____________________ . Due to ADH defeciency or resistance. . Urine osmolality is < serum osmolality. . Polyurea & polydipsia. . H/O of tendency to COLD BEVERAGES to QUENCH THIRST. . Exclude psychogenic polydipsia using water deprivation test. . Differentiate bet. central & nephrogenic DI using ARGININE VASOPRESSIN. . Tx -> NORMAL SALINE. . Tx -> CENTRAL -> INTRANASAL SPRAY DDAVP. . Tx -> NEPHROGENIC -> NSAIDs & HCZ.. HOW CAN U DIFFERENTIATE BET. DI & PSYCHOGENIC POLYDIPSIA:

___________________________________________________________ . WATER DEPRIVATION TEST:

__________________________

. Failure to concentrate urine after deprivation -> DI. . Production of concentrated urine ---------------> Psychogenic polydipsia.. HOW CAN U DIFFERENTIATE BET. CENTRAL & NEPHROGENIC DI:

________________________________________________________ . ARGININE VASOPRESSIN (AVP) or DESMOPRESSIN adminstration:

____________________________________________________________ . CENTRAL DI -----> ++ in urine osmolality. . NEPHROGENIC DI -> No significant ++ ! . SYNDROME OF INAPPROPRIATE ADH SECRETION (SIADH):

__________________________________________________ . ++ ADH levels without stimuli of its release. . NORMAL SERUM osmolality -> 275 - 295 mOsm.

. NORMAL URINE osmolality -> 50 - 1400 mOsm. . Dx -> Simultaneous measurment of urine & plasma osmolality. . The normal response to hypotonicity (low plasma osmolality) is , . the production of maximally diluted urine (low urine osmolality -> < 100 mOsm.) . LOW plasma osmolal. (100-150mOsm) is diagnostic.. Tx of SIADH: -> Mild symptoms (forgetfulness & unstable gait) -> Fluid restriction. -> Moderate symptoms (Confusion & lethargy) -> HYPERTONIC SALINE (3%). -> Severe symptoms (seizures & coma) -> Hypertonic saline + Conivaptan. . BOTTOM LINE:

______________ * Diabetes insipidus:

______________________ . Polyurea - polydipsia - excretion of diluted urine with ++ serum osmolality. * 1ry (Psychogenic) polydipsia:

________________________________ . Excessive water drinking -> BOTH plasma & urine are diluted. * SIADH:


8/15

_________ . Hyponatremia - LOW serum osmolality & inappropriately high urine osmolality.. P.O.C.------- # DIABETES INSIPIDUS -------- # PSYCHOGENIC POLYDIPSIA ---------# SIADH _____ __________________ ______________________ _____ -> SERUM osm. ---> (+) (-)

(-)-> URINE osm. ---> (-) (-)

(+). HYPER-VITAMINOSIS "D":

________________________ . H/O of trials of weight loss with vitamin supplementations. . Vit. D ++ Ca absorption -> Hypercalcemia. . Constipation - Abd. pain - Polyurea - Polydipsia.. METABOLIC $YNDROME:

_____________________ 1- ABDOMINAL OBESITY -> Waist circumference (Men > 40 & Women > 35 inches). 2- DIABETIS MELLITIS -> Fasting glucose > 100 - 110 mg/dl. 3- HYPERTENSION ------> Blood pressure > 130/80 mmHg. 4- HYPERLIPIDEMIA ----> Triglycerides > 150 mg/dl & HDL (Men < 40 & Women < 50mg/dl).. The main mechanism of DM development in metabolic $ is INSULIN RESISTANCE.. ACROMEGALY:

_____________ . ++ GROWTH hormone by SOMATOtroph PITUITARY ADENOMA. . GH -> ++ IGF-1. . IGF-1 ++ growth of bones & soft tissues. . Coarse facial features - arthralgia - uncontrolled HTN - skin tags. . Carpal tunnel $. . Dx -> The MOST SENSITIVE TEST is -> IGF-1 level (GH level fluctuations is deceiving). . Suppression of GH by giving glucose excludes acromegaly. . MRI -> Pituitary lesion. . Tx -> Surgical resection with trans-sphenoidal removal. . Tx -> Somatostatin - Cabergoline or bromocriptine.. MOST COMMON CAUSE OF DEATH is CONGESTVE HEART FAILURE.

. Non cardiac causes of death: stroke - cancer colon - renal failure. . ANDROGEN PRODUCING ADRENAL TUMOR in FEMALES:

______________________________________________ . Best indicator is DHEA-S = De-Hydro Epi-Androsterone Sulfate.. PROLACTINOMA:

_______________ . Prolactin secreting micro-adenoma. . Pituitary tumor < 10 mm in diameter is called micro-adenoma. . Amenorrhea & galactorrhea in females. . Hypogonadism in males. . Its small size can't lead to mass effects of ++ ICT. . Tx -> 1st line is medical ttt with Dopamine agonists (CABERGOLINE or BROMOCRI

PTINE). . Cabergoline normalizes the prolactin level & shrinks the tumor's size.# CALCIUM HOMEOSTASIS:

______________________ . 3 forms of calcium (ionized Ca 45% - Albumin bound Ca 40% - Inorganic anionsbound Ca). . Albumin plays an imp. role ! . Pts with hypo-albuminemia can have a low level of total plasma ca, . However ,, They may NOT present with clinical hypocalcemia, . Because their level of ionized calcium (physilologically active form) remain


9/15

ed normal. . So .. it is imp. to calculate the CORRECTED SERUM CALCIUM LEVEL.. CORRECTED SERUM CALCIUM LEVEL = TOTAL Ca + 0.8 (4 - Serum Albumin). . Another rough method,. With every 1 g/dl change in serum albumin level from 4 g/dl, . there is a change in total plasma Ca level by 0.8 mg/dl.# ++ Ca (Hyperclacemia) Approach -> Measure Parathormone (PTH):

_______________________________________________________________ * ++ Ca & ++ PTH -> 1ry hyperparathyroidism (abd. groans - renal stones - bones - moans). ________________ * ++ Ca & -- PTH -> Malignancy - vit. D toxicity - Sarcoidosis. ________________ # -- Ca & ++ PO4 causes -> CRF & Primary hypothyroidism.

________________________________________________________ . CHRONIC RENAL FAILURE:

________________________ . -- Ca & ++ PO4 & ++ PTH.. Exclude CRF by NORMAL renal function tests (urea & creatinine).. PRIMARY HYPO-THYROIDISM:

__________________________ . Causes -> post-surgical- congenital absence - autoimmune. . Post surgical may occur after thyroidectomy & removal of 3.5 out of 4 parathyroids.

. -- Ca -> perioral tingling - numbness - ms cramps - carpopedal spasms - seizures. . EKG -> prolongation of the QT interval.# Causes of ++ Ca & + PTH: 1ry Hyperparathyroidism & familial hypocalciuric hypercalcemia:

________________________________________________________________________________ __________ . Differentiated by 24 hour urinary calcium: ____________________________________________ . Primary Hyper-parathyroidism ---------> > 250 mg. . Familial hypocalciuric hypercalcemia -> < 100 mg.. PRIMARY HYPER-PARA-THYROIDISM:

________________________________

. Causes -> Parathyroid adenoma (90%) - hyperplasia (6%) & carcinoma (2%). . Associated with MEN 1 & 2A. . 80 % of pts are asymptomatic. . Abdominal groans, renal stones, bones #s & psychic moans. . ++ Ca & -- PO4 & ++ or normal PTH. . 24 hours urinary calcium > 250 mg. . Urinary calcium/creatinine > 0.02 (To rule out familial hypo-calciuric hyper-calcemia). . Dx -> 3Ds SESTAMIBI scan + U/$ to locate the hyperactive parathyroid tissue presurgery. . Tx -> Parathyroidectomy for symptomatic pts. . Surgery indications: _____________________

-> Serum Ca level > 1 mg/dl above the upper limit of normal (11mg/dl). -> Young age < 50 ys. -> Bone mineral density < T-2.5 at any stage. -> -- Renal function (GFR < 60ml/min.).. HYPERCALCEMIA of MALIGNANCY:

______________________________ . ++ Ca -> confusion - lethargy - fatigue - anorexia - polyuria & constipation. . Associated with SQUAMOUS cell lung cancer. . CXR finding of lung cancer (lobar mass & perihilar lymphadenopathy). . Malignancy produces PTH related peptide PTHrP -> ++ Ca & -- PO4.


10/15

. HYPERCALCEMIA (++Ca) ALGORITHM: _________________________________ .(++Ca) .| .Measure PTH level __________________ .| .____________________________________________________

.| .| .(+++) .(---) .(PTH dependent) . (PTH-INdependent) ________________ ___________________ .| .| .Measure urinary Ca ._____________________________________________

__.| .| .| .|

.|.________________ .+PTHrP .+1,25(OH)D .+25(OH)D .NORM

AL LABs.| .| .| .| .|

.|.> 250 .< 100 .TUMOR .Lymphoma-Sarcoid .Vit.D toxicity.HYPERTHYROIDISM.| .| .MULTI

P. MYELOMA1ry or 3ry .Familial .Adrenal tumorHyperpara- .Hypercalcemic .Acromegalythyroidism .Hypocalciuria .Vit.A toxicity .Immobilization. IMPORTANT CASE SCENARIO:

__________________________ . Rapid ascent to a height of 10000 feet -> HYPO-calcemia ! HOW ?? (++ Albuminbound Ca).

________________________________________________________________________________ __________ . Respiratory alkalosis = ++ pH level -> ++ the affinity of serum albumin to calcium. . ++ the levels of ALBUMIN-bound Ca -> -- the level of IONIZED Ca (Active form). . -- Ionized Ca (Active form) -> Hypocalcemia manifestations.. PAN-HYPO-PITUITARISM:

_______________________ * Pituitary tumors are the most common cause by exerting pressure on pituitarycells. * ACTH defeciency (2ry adrenal insuffeciency): "-- Glucocorticoids":

____________________________________________________________________ -> Postural hypotension & tachycardia. -> Fatigue & weight loss. -> -- libido, hypoglycemia & eosinophilia. * HYPOTHYROIDISM (Central): ___________________________ -> Fatigue, cold intolerance, -- appetite, constipation & dry skin. -> Bradycardia, delayed relaxation phase of DTRs & anemia.


11/15

* -- GONADOTROPINS: ___________________ -> Women -> Amenorrhea, infertility & hot flashes. -> Men -> -- energy & libido.. OSTEOPOROSIS:

_______________ . Postmenopausal woman. . presenting with multiple bony #s. . NORMAL serum Ca - PO4 & PTH.. OSTEOMALACIA:

_______________ . Vit. D defeciency in ADULTS. . Bony pain & tendrness. . -- serum Ca & PO4. . -- urinary Ca. . ++ ALP & ++ PTH. . -- 25 OH-D. . X-ray -> BILATERAL SYMMETRIC PSEUDO-FRACTURES (LOOSER ZONES).. PAGET's DISEASE:

__________________ . NORMAL serum Ca - PO4 & PTH. . INCREASED ++ ALKALINE PHOSPHATASE. . Tx -> BIPHOSPHONATES -> inhibit OsteoCLASTs asctivity.

. CAUSES of HYPOKALEMIA & --BICARBONATE HCO3 {Metabolic Alkalosis} -> (Check RENIN): ________________________________________________________________________________ ____ .. CAUSES of HYPOKALEMIA & ++ ALDOSTERONE & -- RENIN -> PRIMARY HYPER-ALDOSTERONISM.

_____________________________________________________ .. CAUSES of HYPOKALEMIA & ++ BOTH ALDOSTERONE & RENIN -> (Check Cl):

_____________________________________________________________________ (A) WITH ++ CHLORIDE (Check Na): (B) WITH -- CHLORIDE:

_________________________________ _____________________1- -- Na -----> (Diuretic use). 1- Surreptitious vomiting.2- Normal Na -> (Bartter's $). 2- Factitious diarrhea.

3- ++ Na -----> (Renin secreting tumor).. SURREPTITIOUS VOMITING: _________________________ . Scars & calluses on the dorsum of the hands & dental erosions. . Result from chemical & mechanical injury as the pt uses his hands to induce vomiting. . Dental erosions result due to ++ exposure to gastric acid.. . May lead to hypovolemia & hypochloremia -> Low urine Cl level.. CAUSES OF HYPERTENSION & HYPOKALEMIA:

_______________________________________ . Primary hyperaldosteronism & Reno-vascular hypertension. . Check the PLASMA RENIN ACTIVITY (PRA). . Primary hyperaldosteronism -> LOW PRA.

. Reno-vascular hypertension -> HIGH PRA.# ADRENAL DISORDERS:

____________________ ____________________ .1. CUSHING $YNDROME = HYPER-Corticolism:

_________________________________________ . ++ Cortisol. . Fat redistribution -> Truncal obesity - moon face - buffalo hump - thin arms& legs. . Easy bruising & striae -> Cortisol leads to loss of collagen.


12/15

. Hypertension -> From salt & water retention. . Ms wasting. . Hirsutism -> due to ++ adrenal androgen levels. . Hyperglycemia - Hyperlipidemia - Leukocytosis - Metabolic alkalosis.. Dx -> 1 mg over-night dexamethasone suppression test: _______________________________________________________ . Give dexamethasone at 11 a.m. the night before. . A normal person will will suppress the 8 a.m. level. . A NORMAL 1 mg overnight dexamethasone suppression test EXCLUDES hypercorticolism. . Abnormal test may be false elevated due to stress or alcoholism. . Dx -> 24 hour urine cortisol: _______________________________ . Done to confirm that an overnight dexamethasone suppression test is not falsely ++. _______________________________________________________________________________

_ . Sources of Cushing $ ------> Pituitary tumor - Ectopic - ACTH Adrenal adenoma: _______________________________________________________________________________

_ . ACTH ----------------------> HIGH - HIGH - LOW. . High dose dexamethazone ---> Suppression - No - No. . Specific tests ------------> MRI - CT - CT adrenals.

. Tx ------------------------> Removal - Removal - Removal. . TO DIAGNOSE THE PRESENCE OF CUSHINNG $, Do the following tests:

__________________________________________________________________ 1- 24 hour urine cortisol. 2- 1 mg over night dexamethasone test. . To diagnose the origin of CUSHING $, Check the ACTH level:

_____________________________________________________________ * ACTH -> HIGH -> PITUITARY or ECTOPIC source. * ACTH -> LOW -> ADRENAL source..2. ADRENAL INSUFFECIENCY = ADDISON DISEASE:

____________________________________________

. Fatigue, anorexia, weight loss, weakness & hypotension. . Thin pt with hyperpigmented skin. . Labs -> ++ K, -- Na, -- BP & EOSINOPHILIA. . Dx -> COSYNOTROPIN (Synthetic ACTH) stimulation test: _______________________________________________________ . Measure the level of cortisol bef. & aft. cosynotropin adminstration. . NO RISE IN CORTISOL -> Adrenal insuffeciency. . Dx -> CT adrenals. . Tx -> FLUIDS + Steroid replacement (IV HYDROCORTISONE).. CAUSES:

__________ . 1- Auto-immune adrenalitis -> Responsible of 80% of cases in developed countries.

. 2- Adrenal Tuberculosis -> CT: CALCIFICATION of both glands.. CENTRAL (TERTIARY) ADRENAL INSUFFECIENCY:

___________________________________________ . Due to long term supra-physiologic doses of prednisone. . Suppressing the hypothalamic pituitary adrenal (HPA) axis. . Glucocorticoids suppress Corticotropin Releasing Hormone secretion from hypothalamus,. Also .. Block the action of of CRH on the anterior pituitary to release ACTH. . ACTH acts on adrenal cortex & is responsible for the secretion of cortisol &androgen.


13/15

. ACTH has mild stimulatory effect on Aldosterone secretion,. so .. Aldosterone level is relatively normal in ACTH defeciency in central adrenal def. . NORMALLY, Cortisol suppresses ADH production by the posterior pituitary. . In case of central adrenal def. -> -- cortisol -> ++ ADH secretion. . ++ ADH -> Water retention -> Hyponatremia.. TYPES OF ADRENAL INSUFFECIENCY ALGORITHM:

___________________________________________

.Symptoms & signs of adrenal insuffeciency __________________________________________ .| . 250Mg COSYNOTROPIN stimulation test with CORTISOL & ACTH levels .________________________________________________________________ .|

. Minimal response ._________________ | ._________________________________________________ .| | . Basal cortisol LOW . Basal cortisolLOW

. ACTH HIGH . ACTH LOW

.____________________ .________________ ____ .| .| . PRIMARY AI . SECONDARY or TERTIARY AI.3. PRIMARY HYPER-ALDOSTERONISM:

________________________________ . Hypokalemia + Hypertension + Proximal muscle weakness & numbness. . Hypernatremia + metbaolic alkalosis. . Dx -> Measure (PA:PRA) -> Plasma Aldosterone : Plasma Renin Activity ratio. . Result -> ++ Plasma Aldosterone & -- Plasma Renin Activity i.e. Ratio > 30 ! . (PA:PRA) -> is the most specific test.

. Confirm the diagnosis -> Aldosterone suppression test. . Give oral or IV NaCl then measure 24 hs urinary or plasma aldosterone level. . If Aldosterone level > 14 mg/24 hs despite Na loading -> So Dx is confirmed. . Once u confirm the diagnosis -> Detect the cause, . CT scan of the adrenals -> Adrenal mass -> Adrenal vein sampling.. EVALUATION OF SUSPECTED HYPERALDOSTERONISM:

_____________________________________________

. HYPERTENSION & HYPOKALEMIA _____________________________ | . Measure PLASMA RENIN ACTIVITY (PRA) ______________________________________

.& PLASMA ALDOSTERONE CONCENTRATION (PAC) _________________________________________ | ______________________________________________________ | | | . + PRA & + PAC . - PRA & + PAC . - PRA & - PAC ________________ ________________ ________________ | | | SECONDARY HYPERALDOSTERONISM PRIMARY HYPERALDOSTERONISM Other causes of ++ Aldosterone


14/15

____________________________ __________________________ ____________________ __________ * Diuretic use. * Do a CT ADRENAL to *Congenital adrenal hyperplasia* Liver cirrhosis. * detect the etiology ! * Glucocorticoid resi

stance. * Congestive heart failure. * Exogenous mineralocorticoid. * Reno-vascular hypertension. * Cushing's $yndrome. * Renin secreting tumor.* Malignant hypertension.

* Coarctation of the aorta..4. PHEOCHROMOCYTOMA:

_____________________ . Headache, palpitations, tremors, anxiety & flushing. . Episodic elevations of blood pressue. . Dx -> BEST INITIAL -> ++ catecholamines level in plasma & urine. . Dx -> BEST INITIAL -> ++ metanephrines & VMA levels. . Dx -> MOST ACCURATE -> CT or MRI or MIBG of the adrenal glands. . Tx -> PHENOXYBENZAMINE (Alpha blocker) "FIRST" to control blood pressure. . e'out Alpha blockage, BB may lead to CATASTROPHIC ++ in BP due to unopposed Alpha stim. . Tx -> Propranolol is used "AFTER" an alpha blocker . . Tx -> Surgical resection.

. N.B. It is a part of MEN type 2 A & B (DNA testing is imp. RET PROTO-ONCOGENE)..5. CONGENITAL ADRENAL HYPERPLASIA (CAH):

_________________________________________ . ++ ACTH. . -- Aldosterone & cortisol. . Tx -> Prednisone. . Types of CAH: _______________ ____________________________ ___________________________ ____________________

_________ * 21 hydroxylase defeciency - * 11 hydroxylase defeciency - * 17 hydroxylase defeciency

____________________________ ___________________________ ____________________ _________ * ++ Adrenal androgens - * ++ Adrenal androgens - * -- Adrenal androgens * Hirsutism - * Hirsutism - * NO hirsutism * ++ 17 hydroxy-progesterone- * NO - * NO * NO hypertension - * HYPERTENSION - * HYPERTENSION. LEYDIG CELL TUMORS:

_____________________ . Most common type of testicular sex cord tumors. . ++ ESTROGEN & -- FSH & LH.. ANDROGEN SECRETING NEOPLASM of the OVARY or ADRENAL:

______________________________________________________

. Rapidly developing hyper-androgenism with verilization. . Serum TESTOSTERONE & DHEAS levels are diagnostic. . ++ TESTOSTERONE & NORMAL DHEAS -> OVARIAN source. . NORMAL TESTOSTERONE & ++ DHEAS -> ADRENAL source.. PATHOLOGY of bone diseases:

_____________________________ . OSTEOMALACIA -> -- Mineralization of the bone. . RICKETS ------> -- Mineralization of the bone & CARTILAGE. . PAGET's ------> Disordered remodeling. . OSTEOPOROSIS -> NORMAL mineralization but low bone mass.


15/15

. ERECTILE DYSFUNCTION: _______________________ . Failure to achieve a spontaneous erection. . Causes: . * NEUROGENIC -> injury of the parasympathetic nerve fibers (# pelvis or urethral tear). . * VENOGENIC -> Disruption of tunica albuginea (# penis). . * ENDOCRINOLOGIC -> ++ prolactin & -- Testosterone. . * SITUATIONAL -> Anxiety (Nighttime & morning erctions are preserved). . N.B. NOCTURNAL PENILE TUMESCENCE:

___________________________________ . helps to differentiate psychogenic from organic causes of male erectile dysfunction. . +ve in psychogenic causes. . -ve in organic causes.. PROLACTINOMA = LACTO-TROPH ADENOMA:

_____________________________________ . The MOST COMMON pituitary tumor. . ++ PRL. . Hypogoandism & galactorrhea. Dr. Wael Tawfic Mohamed _________________________

253994296 Tiki Taka Ck Endocrinology

Documents

Transcript of 253994296 Tiki Taka Ck Endocrinology