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TIKI TAKA ENDOCRINOLOGY

((HASHIMOTO's THYROIDITIS))
. Anti-TPO Abs (Anti-thyroid peroxidase antibodies).
. 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.
((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.
((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 follicles 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 therapy !!
. 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.
((COMPLICATIONS of UN-TREATED HYPER-THYROID PATIENTS))
-> RAPID BONE LOSS -> due to ++ osteoclastic activity .
-> CARDIAC TACHYARRHYTMIA (AF).
((HYPERTENSION in pts with THYROTOXICOSIS))
. is predominantly SYSTOLIC.
. caused by HYPERDYNAMIC CIRCULATION.

((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))
.1. GLYCOSYLATED HEMOGLOBIN Hb A1C:
. 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
recovery in 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.
((Comparison))***IMP***
. DIABETIC KETOACIDOSIS (DKA) .................... HYPEROSMOLAR HYPERGLYCEMIC
STATE
. Type (1) DM usually.

____________________

. Type (2) DM.

. YOUNGER age.

____________________

. Older.

. LESS confusion.

____________________

. Hyperventilation MORE common _____________

. MORE confusion.
. Less common.

. Abdominal pain MORE common. ___________


. Glucose 250 - 500 mg/dl.
. HCO3 < 18 meq/L.

. LESS common.

___________________

. > 600

____________________

. > 18

. +++++ ANION GAP.

____________________

. POSITIVE serum ketones.

__________________

. Serum osmolality < 320

_________________

. NORMAL.
. NEGATIVE.
. > 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 MICROALBUMIN/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 -> DM 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.
. INSULINOMA:
. BETA CELL TUMOR.
. Normally, blood glucose < 60 mg/dl result in complete suppression of insulin
secretion.
. 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. (<280 mOsm.) & HIGH urine osmolality (>100150mOsm) 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.
SO : CCC (confusion/convulsion/coma) = hypertonic saline
((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:
. Hyponatremia - LOW serum osmolality & inappropriately high urine osmolality.
((P.O.C. ------- # DIABETES INSIPIDUS -------- # PSYCHOGENIC POLYDIPSIA
------ # SIADH))
_____

__________________

-> SERUM osm. --->


(-)

(+)

______________________
(-)

_____

-> URINE osm. --->


(+)

(-)

(-)

((ANDROGEN PRODUCING ADRENAL TUMOR in FEMALES))


. Best indicator is DHEA-S = De-Hydro Epi-Androsterone Sulfate.
(( ++ 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).
((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.
((HYPERCALCEMIA (++Ca) ALGORITHM))
(++Ca)
.|
.Measure PTH level
.|
.|

.|

.(+++)

.(---)

.(PTH dependent)

. (PTH-INdependent)

.|
.Measure urinary Ca
.|
.|

.|
._______________________________________________
.|

.|

.|

.________________
LABs
.|
.|

.+PTHrP

.|

.> 250
.< 100
.HYPERTHYROIDISM

.+1,25(OH)D

.+25(OH)D

.|

.|

.|
.TUMOR

.NORMAL

.Lymphoma-Sarcoid . Vit.D toxicity

.|
.|
.MULTIP MYELOMA
1ry or 3ry
.Familial
.Adrenal tumor
Hyperpara- .Hypercalcemic
.Acromegaly
thyroidism
toxicity

.Hypocalciuria

.Vit.A

.Immobilization
((IMPORTANT CASE SCENARIO))
. Rapid ascend to a height of 10000 feet -> HYPO-calcemia ! HOW ?? (++ Albumin
bound 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.
((ACTH defeciency (2ry adrenal insuffeciency): "-- Glucocorticoids"))
-> Postural hypotension & tachycardia.
-> Fatigue & weight loss.
-> -- libido, hypoglycemia & eosinophilia.
N.B: no hyperkalemia /no salt wasting/-- in skin pigmentation (KAPLAN)
((OSTEOPOROSIS))
. Postmenopausal woman.

. presenting with multiple bony #s.


. NORMAL serum Ca - PO4 & PTH & ALP.

((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.

Condition

Calciu

Phosphat

Alkaline
phosphatas
e

Parathyroi
d hormone

Osteoporosis

unaffected unaffected

normal

unaffected

Osteopetrosis

unaffected unaffected

elevated

unaffected

Comments

decreased
bone mass

thick dense
bones also
known as
marble

Condition

Calciu

Phosphat

Alkaline

Parathyroi

phosphatas

d hormone

Comments

bone

Osteomalacia and ricket


s

Osteitis fibrosa cystica

decreased decreased

elevated

elevated

elevated

elevated

elevated

decreased

soft bones

brown
tumors

abnormal
Paget's disease of bone unaffected unaffected

elevated

unaffected

bone
architectur
e

((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.
((CAUSES of HYPOKALEMIA & --BICARBONATE HCO3 {Metabolic
Alkalosis}&high aldosterone)) -> (Check RENIN):
.. CAUSES of HYPOKALEMIA & ++ ALDOSTERONE & -- RENIN -> PRIMARY HYPERALDOSTERONISM.
.. CAUSES of HYPOKALEMIA & ++ BOTH ALDOSTERONE & RENIN -> (Check URINE
Cl):
(A) WITH ++ URINE CHLORIDE (Check Na):
CHLORIDE:

(B) WITH -- URINE

1- -- Na -----> (Diuretic use).


2- Normal Na -> (Bartter's $).

1- Surreptitious vomiting.
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.
((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 PROTOONCOGENE).

((CONGENITAL ADRENAL HYPERPLASIA (CAH)))


. ++ ACTH.
. -- Aldosterone & cortisol.
. Tx -> Prednisone.
. Types of CAH:
* 21 hydroxylase defeciency - * 11 hydroxylase defeciency defeciency
* ++ Adrenal androgens
androgens
* Hirsutism
hirsutism
* ++ 17 hydroxy-progesterone

* 17 hydroxylase

- * ++ Adrenal androgens

- * -- Adrenal

- * Hirsutism
- * NO

* NO hypertension
HYPERTENSION

- * HYPERTENSION

- * NO
- * NO
-*

((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.
((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).
((NOCTURNAL PENILE TUMESCENCE))
. helps to differentiate psychogenic from organic causes of male erectile
dysfunction.
. +ve in psychogenic causes.
. -ve in organic causes.

Edited by : Dr. ALA HAWA


Written by : Dr. Wael Mohamed

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