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120 Cards in this Set
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SIADH |
1- Characterized by 1- Excess free water retention 2- Euvolemic hyponatremia with continuous urinary NA excretion 3- Urine osmolality > serum osmolality 2- Body respond to water retention by decreasing aldosterone, Increasing AND and BNP — Increase Urinary Na excretion — normalization of extracellular fluid — euvolemic hyponatremia 3- Very low Na can lead to 1- cerebral edema 2- Seizures 4- Correct Na slowly to prevent osmotic demyelination syndrome 5- Cause 1- Ectopic ADH (small cell lung cancer) 2- CNS injury/hard trauma 3- Drugs (SSRI, carbamazepine, cyclophosphamide) 4- Pulmonary disease 6- Treatment 1- Fluid restriction 2- Salt tablet 3- IV hypertonic saline 4- Diuretics 5- Drugs (AHD antagonist Conivapton, talvapton, demeclocycline) |
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Osmotic demyelination syndrome other name |
Central pontine myelinolysis |
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Central Diabetes insipidus |
1- Cause 1- Pituitary tumor 2- Autoimmune 3- Trauma 4- Surgery 5- Ischemic encephalopathy 6- Idiopathic 2- Decrease ADH Urine specific gravity < 1.006 Urine osmolality < 300 Serum osmolality > 290 Hypertonic volume concentration 3- Water deprivation test - Increase urine osmolality by 50% after first ADH analog 4- Treatment 1- Desmpressin 2- Hydration |
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Nephrogenic Diabetes insipidus |
1- Cause 1- Hereditary (mutation of V2 receptor) 2- Hypercalcemia 3- Hypokalemia 4- Lithium 5- ADH analog (demeclocycline) 2- Normal or Increase ADH Urine specific gravity < 1.006 Urine osmolality < 300 Serum osmolality > 290 Hypertonic volume concentration
3- Water deprecation test no change in urine osmolality 4- Treatment 1- HCTZ 2- Indomethacin 3- Amiloride 4- Hydration 5- Dietary salt restriction |
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Diabetes insipidus |
1- Inability to concentrate urine due to lack of ADH or inability to respond to ADH 2- Polyuria and Polydipsia |
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Hypopituitarism |
1- Non secreting pituitary adenoma or craniopharyngioma 2- Sheehan syndrome 3- Empty sella syndrome 4- Pituitary apoplexy 5- Brain injury 6- Radiation |
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Treatment of hypopituitarism |
Hormone replacement |
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Sheehan syndrome |
1- Ischemic infarct of pituitary following postpartum bleeding 2- During pregnancy increase pituitary growth - increase susceptible of hypo-perfusion 3- Presents with 1- Inability to lactate 2- Absent menstruation 3- Cold intolerance |
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Empty sella syndrome |
1- Atrophy or compression of pituitary gland (located in sella turcica) 2- Idiopathic, common in obese women 3- Associated with idiopathic intracranial hypertension |
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Pituitary apoplexy |
1- Sudden hemorrhage of pituitary gland often in the presence of an excising pituitary adenoma 2- Features 1- Sudden onset head 2- Visual disturbance (bitemporal hemianopia, diplopia due to CN 3 palsy) 3- Features of hypopituitarism |
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Acromegaly |
1- Increase GH in adults after due to pituitary adenoma Gigantism in children, HF most common cause of death 2- Features 1- Frontal bossing 2- Course facies with aging 3- Large tongue with deep furrow 4- Deep voices 5- Large hands and feet 6- Diaphoresis 7- Insulin resistant 8- Hypertension 9- Increase risk of colon polyps and colon cancer 3- Diagnosis 1- Increase IGF-1 2- Failure of GH suppression with oral glucose tolerance test 3- Pituitary mass seen on MRI 4- Treatment- 1- Pituitary Adenoma- resection 2- Octreotide (Somatostatin analog) 3- Pegvirimant (GH receptor antagonist) 4- Cabergoline (dopamine agonist) |
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Hypothyroidism features |
1- Neuropsychiatric 1- Hypo-activity 2- Lethargy 3- Fatigue 4- Weakness 5- Depressed mood 6- Decrease reflex 2- Ocular- Periorbital edema 3- Cardiovascular 1- Bradycardia 2- SOB 4- GI 1- Constipation 2- Decrease appetite 5- Reproductive 1- Menorrahgia 2- Decrease libido 3- Infertility 6- MSK 1- Hypothyroid myopathy (proximal weakness increase CK) 2- Carpal tunnel syndrome 3- Myoedema (small lump rising on the surface of a muscle when struck with a hammer) 7- Metabolic 1- Cold intolerance 2- Decrease sweating 3- Weight gain (decrease basal metabolic rate - decrease calorigenesis) 4- Hyponatremia 8- Skin and Hair 1- Dry cool skin 2- Coarse brittle hair 3- Diffuse alopecia 4- Brittle nails 5- Puffy facies and generalized non- pitting edema (myxedema) due to increase GAGs in interstitial spaces — increase osmotic pressure — water retention 9- Labs 1- Increase TSH 2- Decrease free T3/T4 3- Hypercholesteramia (due to decrease LDL receptor expression) |
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Hyperthyroidism features |
1-Neuropsychiatric 1- Hyperactivity 2- Restlessness 3- Anxiety 4- Insomnia 5- Fine tremor (due to increase Beta adrenergic activity 2- Ocular 1- Opthalmopathy in Graves’ disease (Periorbital edema, exopthalmos) 2- Lid lag/retraction (increase sympathetic stimulation of levator palpebra superior tarsal muscle) 3- Cardiovascular 1- Tachycardia 2- Palpitation 3- SOB 4- Arrhythmia (eg atrial fibrillation) 5- Chest pain and systolic HTN due to increase number and sensitivity of Beta- adrenergic receptors, increase expression of cardiac sarcolemmal ATPase and decrease expression of phospholamban 4- GI- 1- Diarrhea 2- Increase appetite 5- Reproductive 1- Amenorrhea 2- Gynecomastia 3- Decrease libido 4- Infertility 6- MSK 1- Thyrotoxic myopathy (proximal muscle weakness, normal CK), osteoporosis/increase fracture rate (T3 directly stimulates bone resorption) 7- Metabolic 1- Heat intolerance 2- Increase sweating 3- Weight loss (increase synthesis of Na/K ATPase- increase nasal metabolic rate- increase calorigensis) 8- Skin and Hair 1- Warm moist skin 2- Fine hair 3- Onycholysis 4- Pretibial myxedema in Graves’ disease 9- Labs 1- decrease TSH 2- Increase free T3/T4 3- Decrease LDL, HDL and total cholesterol
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Cause hypothyroidism |
1- Hashimoto thyroiditis 2- Postpartum thyroiditis 3- Congenital hypothyroidism (cretinism) 4- Subacute granulomatous thyroiditis (de quevain) 5- Riedel thyroiditis 6- Other cause |
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Hashimoto thyroiditis |
1- Most common cause of hypothyroidism in iodine sufficient region 2- Autoimmune disorder with anti thyroid peroxidase (anti microsomal) and anti thyroglobulin antibodies 3- Associated with HL-DR3 and HL-DR5 4- Increase risk of non Hodgkin lymphoma (B cell type) 5- May cause hyperthyroidism in the early course due to thyrotoxicosis during follicular rupture 6- Histology 1- Hurthle cell 2- Lymphoid aggravates with germinal center 7- Finding moderately enlargers painless thyroid |
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Postpartum thyroiditis |
1- Self limited thyroiditis arises with 1 year after delivery 2- Present as transient hyperthyroidism, hypothyroidism or hyperthyroidism followed by hypothyroidism 3- Most women become euthyroid after resolution 4- Histology - lymphoid aggregation with occasional germinal center 5- Findings- normal size painless thyroid |
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Congenital hypothyroidism cretinism |
1- Severe fetal hypothyroidism due to 1- Antibody mediated maternal hypothyroidism 2- Thyroid dysgenesis (agenesis, ectopic, hypoplasia) 3- Iodine deficiency 4- Dyshormonogenic goiter ( due to mutation in thyroid peroxidase) 2- Findings 1- Pot bellies 2- Pale 3- Puffy face 4- Protruding umbilicus 5- Protuberance tongue 6- Poor brain development |
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Subacute granulomatous thyroiditis (de queviran) |
1- Self limiting thyroid following flu like symptoms (viral infection) 2- May cause hyperthyroidism in early course followed by hypothyroidism 3- Histology Granulomatous inflammation 4- Findings Tender thyroid increase ESR |
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Riedel thyroiditis |
1- Thyroid replace with fibrous tissue and inflammatory infiltrate 2- Fibrosis may extend to surrounding structures (trachea, esophagus) 3- 1/3 of patients hypothyroid 4- Considered a manifestation of IgG4 related systemic disease (eg autoimmune pancreatitis, retroperitoneal fibrosis, non infectious aortitis) 5- Finding Fixed hard painless thyroid |
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Other cause of hypothyroidism |
1- Iodine deficiency (with goiter) 2- Goitergens (Amiodarone, lithium) 3- Wolff- Chaishoff effect (thyroid gland downregulate in response to increase iodine) |
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Euthyroid sick syndrome |
Decrease T3/T4 Normal TSH in critical non thyroidal illness |
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Hyperthyroidism causes |
1- Graves’ disease 2- Toxic multi modular goiter 3- Thyroid storm 4- Jod Basedow phenomenon 5- Cause of goiter |
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Graves’ disease |
1- Most common cause of hyperthyroidism 2- Thyroid stimulating immunoglobulin (TSI) (IgG, cause transient neonatal hyperthyroidism, type 2 hypersensitivity) stimulate TSH on 1- thyroid- hyperthyroidism, goiter 2- dermal fibroblast - pretibial myxedema 3- Orbital fibroblast - Exophtalmus 3- Activation of T cells - lymphocytic infiltration of retro orbital space- increase cytokines (TNF- alpha, IFN-y)- increase fibroblast secretion of hydrophilic GAGs- increase osmotic muscle swelling, muscle inflammation and adipose count- exopthalmous 4- Often present during stress eg pregnancy 5- Associated with HLA-DR3, HLA-B8 6- Histology: tall, crowded follicular epithelial cells, scalloped colloid |
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Toxic multi modular goiter |
1- Focal patchy hyperfunctioning follicular cells distended with colloid working independently of TSH 2- Due to mutation of TRH in 60% 3- Increase release of T3 and T4 4- Hot nodules are rarely malignant |
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Thyroid storm |
1- Uncommon but serious complication of hyperthyroidism if treated incompletely/untreated 2- Worst with 1- Acute Stress 2- Infection 3- Trauma 4- Surgery 3- Present with 1- agitation 2- Tachyarrythmia 3- Coma 4- Diarrhea 5- Delirium 6- Fever 4- May cause increase LFT 5- Treat with 1- Beta blocker (propanolol) 2- PTU 3- Corticosteriode (prednisone) 4- Potassium iodine (Lugosi iodine) - decrease T4 synthesis
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Thyroid storm |
1- Uncommon but serious complication of hyperthyroidism if treated incompletely/untreated 2- Worst with 1- Acute Stress 2- Infection 3- Trauma 4- Surgery 3- Present with 1- agitation 2- Tachyarrythmia 3- Coma 4- Diarrhea 5- Delirium 6- Fever 4- May cause increase LFT 5- Treat with 1- Beta blocker (propanolol) 2- PTU 3- Corticosteriode (prednisone) 4- Potassium iodine (Lugosi iodine) - decrease T4 synthesis
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Jod-Basedow phenomenon |
1- Iodine induced hyperthyroidism 2- Occur when a patient with iodine defiency and partially autonomous thyroid tissue is iodine replete 3- Can happen after iodine IV contrast or amiodarone use |
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Thyroid storm |
1- Uncommon but serious complication of hyperthyroidism if treated incompletely/untreated 2- Worst with 1- Acute Stress 2- Infection 3- Trauma 4- Surgery 3- Present with 1- agitation 2- Tachyarrythmia 3- Coma 4- Diarrhea 5- Delirium 6- Fever 4- May cause increase LFT 5- Treat with 1- Beta blocker (propanolol) 2- PTU 3- Corticosteriode (prednisone) 4- Potassium iodine (Lugosi iodine) - decrease T4 synthesis
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Jod-Basedow phenomenon |
1- Iodine induced hyperthyroidism 2- Occur when a patient with iodine defiency and partially autonomous thyroid tissue is iodine replete 3- Can happen after iodine IV contrast or amiodarone use |
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Cause of goiter |
Smooth/diffuse 1- Graves’ disease 2- Hashimoto thyroiditis 3- Iodine deficiency 4- TSH- secreting pituitary adenoma Nodule 1- Toxic multi modular goiter 2- Thyroid adenoma 3- Thyroid cancer 4- Thyroid cyst |
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Most common cause of death in a patient with thyroid storm |
Tachyarrythmia |
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Thyroid adenoma |
1- Benign solitary growth of the thyroid 2- Most are non-functioning (cold) rarely cause I hyperthyroidism via autonomous thyroid hormone production (hot or toxic) 3- Histology - Follicular 2- Absent capsular or vascular invasion |
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Thyroid cancer |
1- Diagnosed with fine needle aspiration 2- Treat with thyroidectomy 3- Complication 1- Hypocalcemia 2- Transection of recurrent laryngeal nerve during ligation of inferior thyroid artery (leads to dysphasia and dysphonia) 3- Injury to external branch of superior laryngeal nerve during ligation of superior thyroid Vasculature (loss of taner in professional singers) |
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Papillary thyroid cancer |
1- Most common 2- Good prognosis 3- Orphan Annie eye nucleus (empty nucleus with central clearing) 4- Psuammoma bodies and nuclear grove 5- Increase risk of RET/PTC rearrangement and BRAF mutation 6- Childhood radiation 7- Lymph node enlargement |
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Papillary thyroid cancer |
1- Most common 2- Good prognosis 3- Orphan Annie eye nucleus (empty nucleus with central clearing) 4- Psuammoma bodies and nuclear grove 5- Increase risk of RET/PTC rearrangement and BRAF mutation 6- Childhood radiation 7- Lymph node enlargement |
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Follicular thyroid cancer |
1- Good prognosis 2- Invade capsule and Vasculature 3- Uniform follicle - hematogenous spread 4- Associated with RAS mutation and PAX8- PPAR-y translocation |
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Papillary thyroid cancer |
1- Most common 2- Good prognosis 3- Orphan Annie eye nucleus (empty nucleus with central clearing) 4- Psuammoma bodies and nuclear grove 5- Increase risk of RET/PTC rearrangement and BRAF mutation 6- Childhood radiation 7- Lymph node enlargement |
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Follicular thyroid cancer |
1- Good prognosis 2- Invade capsule and Vasculature 3- Uniform follicle - hematogenous spread 4- Associated with RAS mutation and PAX8- PPAR-y translocation |
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Medullary carcinoma |
1- Affect parafollicular C cells 2- Increase calcitonin 3- Sheets of polygonal cells in an amyloid stroma 4- Associated with MEN2A and 2B (RET mutation) |
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Undifferentiated/Anaplastic thyroid cancer |
1- Very poor prognosis 2- Older people 3- Rapidly enlarging neck mass with compressive symptoms - dysphagia, Dyspnea, hoarseness 4- Associate with TP53 mutation |
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Hypoparathyroidism |
1- Due to 1- injury to parathyroid gland or their blood supply (especially during surgery) 2- Autoimmune destruction 3- DiGeorge syndrome 2- Finding 1- Tetany 2- Hypocalcemia 3- Hyperphosphatemia 4- Chvostek sign - Tapping of facial nerve, contraction of facial muscle 5- Trousseau sign - Occlusion of brachial artery with BP cuff- carpal spasm |
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Pseudohypoparathyroidism |
1- Autosomal dominant 2- Maternally transmitted mutation (imprinted GNAS gene) 3- GNAS1 inactivating mutation (coupling to PTH receptor) encode for Gs protein alpha subunit - inactivation of adenyle cyclase when PTH bind to its receptor - end organ resistance to PTH (kidney and bone) 4- Findings Albright hereditary osteodystrophy 1- Short 4th and 5th digit 2- Short statue 3- Round face 4- Subcutaneous calcification 5- Developmental delay 5- Labs increase PTH, decrease Ca, increase PO |
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Pseudopseudohypoparathyroidism |
1- Autosomal dominant 2- Paternally transmitted mutation ( imprinted GNAS gene)- without end organ resistance 3- Due to normal maternal alle maintains renal responsiveness to PTH 4- Findings Albright hereditary osteodystrophy 5- Labs normal PTH, Ca and PO |
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Primary hyperparathyroidism |
1- Due to parathyroid adenoma or hyperplasia 2- Hypercalcemia, Hyperurecemia ( renal stones), polyurea (thrones) hypophosphatemia, Increase PTH, increase ALP and increase urinary cAMP 3- Most often asymptomatic 4- Features 1- Abdominal pain/flank pain ( kidney stones, acute pancreatitis) 2- Bone pain 3- Weakness 4- Constipation 5- Neuropsychiatric disturbance |
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Ostitis fibrosa cystica |
1- Cystic bone space filled with fibrosis tissue 2- Brown tumor consist of osteoclast and deposits of hemosiderin from hemorrhage(bone pain) 3- Due to Increase PTH classically associated with primary hyperparathyroidism (can be due to 2 hyperparathyroidism) |
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Secondary hyperparathyroidism |
1- Secondary hyperplasia due to decrease Ca absorption and/or increase phosphate 2- Most due to chronic renal failure with ( hypovitaminosis D and hyperphosphotemia- decrease Ca) 3- Hypocalcemia and hyperphosphatemia in CKD (decrease PO in others) 4- Increase PTH and ALP |
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Tertiary hyperparathyroidism |
1- Refectory (autonomous) hyperparathyroidism resulting from chronic kidney failure 2- Increase PTH and Increase Ca |
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Renal osteodystrophy |
Renal failure — secondary and tertiary hyperparathyroidism- bone lesion |
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Lab value in vitamin D deficiency |
Ca- decrease PO- decrease PTH- increase |
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Lab value in hypopituitarism |
Ca- decrease PO- increase PTH- decrease |
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Lab value in 2 hyperparathyroidism (CKD) |
Ca- decrease PO- increase PTH- increase |
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Lab value in pseudo hyperparathyroidism |
Ca- decrease PO- increase PTH- increase |
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Lab value in hyperphosphatemia |
Ca- decrease PO- increase PTH- Increase |
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Familial hypocalciuric Hypercalcemia |
1- Defective G- couple Ca sensing receptors in multiple tissues (parathyroid and kidney) 2- Higher than normal level of Ca required to suppress PTH 3- Increase Ca reabsorbed by kidney- mild Hypercalcemia and hypocalciuria with normal or increase PTH 4- Autosomal dominant |
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Acute manifestation of DM |
1- Polyuria 2- Polydipsia 3- Polyphagia 4- Weight loss 5- DKA (type 1 DM) 6- HHS (type 2 DM) 7- Rarely due to unopposed GH or epinephrine 8- Seen in glucocorticoids use |
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Chronic manifestation of DM |
Non enzymatic Glycosylation Small vessels 1- Retinopathy 2- Glaucoma 3- Nephropathy 4- Nodular glomerosclerosis - progressive proteinurea (initially microalbinuria) 5- Arteriosclerosis Large vessels 1- CAD 2- MI (most common cause of death) 3- PVD 4- Stroke Osmotic damage 1- Neuropathy 2- Cataract |
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Diagnosis of DM |
1- HBA1c >/= 6.5% 2- Fasting plasma glucose >/= 7 3- 2 hr glucose tolerance test >/= 11.1 |
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Diabetic retinopathy |
NPDR 1- Retina hemorrhage 2- Hard exudate 3- Cotton wool spot 4- Venous needing/AV nipping PDR 1- Neurovascularization 2- Vitreous/Preretinal hemorrhage |
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How long does a patient need to fast before glucose test |
8 hrs |
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Which antihypertensive agents are recommended to prevent proteinuria in diabetic patient |
ACEi ARB |
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Type 1 DM |
1- Autoimmune T cell mediated destruction of Beta cells (eg due to presence of glutamic acid decarboxylase antibodies) 2- Always require insulin 3- <30 years old 4- Not assoc with obesity 5- Weak genetic predisposition 6- Associated with HLA-DR3 and HLA-DR4 7- Glucose intolerance severe 8- Insulin sensitivity High 9- Ketoacidosis 10- Decrease number of beta cells 11- Decrease serum insulin level 12- Classic symptoms 13- Histology islet Leukocytosis infiltrate |
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Type 2 DM |
1- Increase insulin resistance progressive pancreatic beta cell failure 2- Insulin required sometimes 3- > 40 years old 4- Associated with obesity 5- Genetic predisposition relatively strong 90% 6- Not associated with HLA system 7- Glucose intolerance mild to moderate 8- Insulin sensitivity- low 9- Rare ketoacidosis 10- Beta cell number in islet variable (with amyloid deposits) 11- Serum insulin increase initially but decrease in advance disease 12- Classic symptoms 13- Histology islet amylod polypeptide (IAPP) deposits |
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Diabetes ketoacidosis DKA |
1- Insulin absent, Ketone present (excess fat breakdown and ketogenesis from increase free fatty acid - ketone bodies (beta hydroxybutyrate> acetoacetate) 2- Signs and symptoms 1- Delirium/confusion/psychosis 2- Kussmal respiration 3- Abdominal pain/ nausea/vomiting 4- Dehydration 5- Fruity breath (from acetone) 3- Labs 1- Hyperglycemia 2- Increase H 3- Decrease HCO (wide anion gap metabolic acidosis) 4- Increase urinary and serum ketones 5- Leukocytosis 6- Normal/Increase serum K 7- Decrease Intracellular K 4- Complication 1- Life threatening Mucormycoses 2- Cerebral edema 3- Cardiac arrhythmia 4- HF 5- Treatment 1- IV fluids 2- IV insulin 3- K +/- glucose to prevent hypoglycemia |
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Hyperosmolar hyperglycemic state |
1- Insulin present, ketone absent (Profound hyperglycemia- increase osmotic diuresis- Dehydration and increase serum osmolality) 2- Sign/Symptoms 1- Polyuria 2- Polydipsia 3- Fatigue 4- Neurological defects 5- Seizures 3- Labs 1- Hyperglycemia 2- Normal pH 3- No ketones 4- Normal/Increase serum K 5- Decrease Intracellular k 4- Complication 1- Coma and death of left untreated 5- Treatment 1- IV fluid 2- IV insulin 3- K |
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Describe kussmaul respiration |
Deep rapid breathing (hyperventilation) |
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Causes of DKA |
Stressors such as 1- Infection 2- Infarction 3- Insulin omission |
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Why is a hyperosmolar hyperglycemia state more common in elderly with type 2 diabetes |
Less able to sustain oral intake |
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Hypoglycemia in DM |
1- Usually in patients treated with insulin or sulfonalurea in the settings of 1- High dose treatment 2- Inadequate food intake 3- Excess exercise 2- Signs and symptoms Neurogenic 1- Anxiety 2- Hunger 3- Diaphoresis 4- Tachycardia 5- Tremor Neuroglycopenic 1- AMS 2- Seizure 3- Death 3- Treatment 1- Simple carbohydrates (glucose, fruit drink) 2- IM glucagon 3- IV dextrose |
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Cushing syndrome |
1- Increase cortisol due to 1- Exogenous corticosteroids- decrease ACTH- bilateral adrenal atrophy (most common cause) 2- Primary adrenal adenoma, hyperplasia or carcinoma- atrophy of uninvolved adrenal glands 3- ACTH secreting pituitary adenoma (Cushing disease) 4- Paraneoplastic ACTH secretion (small cell lung cancer, bronchial carcinoid) 2- Findings 1- Increase cholesterol 2- Increase urine free cortisol 3- Skin (thinning, purple striae) 4- Hypertension 5- Immunosuppression 6- Neoplasia 7- Growth retardation 8- Sugar (hyperglycemia, insulin resistant) 9- Amenorrhea 10- Moon face 11- Buffalo hump 12- osteopenia 13- Weight gain 14- Hirsutism 3- Diagnosis 1- Increase 24 hr free cortisol urinalysis 2- increase salivation at night 3- No suppression with low dose dexamethasone suppression test |
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Diagnosis of ACTH secreting pituitary adenoma |
MRI |
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Diagnosing e Coptic ACTH secretion |
CT scan |
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What will the adrenal look like in abdominal imaging of a patient with Cushing disease |
Bilateral adrenal hyperplasia |
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Nelson disease |
1- Enlargement of a preexisting pituitary adenoma after bilateral adrenlectomy for refractory Cushing disease 2- Increase ACTH (hyperpigmentation) mass effects (headache, bitemporal hemanopia) 3- Treatment 1- Transphenoidal resection 2- Postoperative pituitary irradiation for residual tumor |
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Adrenal insufficient |
1- Inability of the adrenal glands to generate enough corticosteriod +/- Mineralocorticoid for the bodies need 2- Signs 1- GI disturbance 2- Fatigue 3- Weakness 4- Weight loss 5- Orthostatic hypotension 6- Muscle ache 7- Sugar/Salt craving 3- Treatment 1- Glucocorticoids/Mineralocorticoid replacement |
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Primary adrenal insufficiency |
1- Decrease gland function — decrease cortisol, decrease aldosterone 1- Hypotension 2- Hyperkalemia 3- Metabolic acidosis 4- Skin and mucosa hyperpigmentation 2- Acute 1- Sudden onset (due to massive hemorrhage) 2- May present with shock in acute adrenal crisis 3- Chronic 1- Addison disease 2- Due to adrenal atrophy or distraction from disease (autoimmune or TB most common in developed countries) |
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Waterhouse-Friderichsen syndrome |
1- Acute primary adrenal insufficiency due to adrenal hemorrhage associated with septicemia (from N. Meningitidis), DIC and endotoxic shock |
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Secondary adrenal insufficiency |
1- Decrease ACTH from pituitary gland 2- No skin hyperpigmentation (No ACTH being produce from POMC) 3- No Hyperkalemia (Aldosterone produce from RAAS) |
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Tertiary adrenal insufficiency |
1- In patients with chronic exogenous corticosteroids use precipitated by abrupt withdrawal 2- Aldosterone unaffected |
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Hyperaldosteroism |
1- Increase secretion of aldosterone from adrenal glands 2- Signs 1- Hypertension 2- Decrease or normal K 3- Metabolic alkalosis 3- Hyperaldosteronism does not cause edema due to its aldosterone escape mechanism however certain secondary cause of hyperaldosteronism imp are aldosterone escape mechanism worsening edema |
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Primary hyperaldosteronism |
1- Seen in adrenal adenoma (Conns syndrome) and bilateral adrenal hyperplasia 2- Increase aldosterone decrease renin 3- Leads to treatment resistance hypertension |
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Secondary hyperaldosteronism |
1- Seen in patrons with renovascular hypertension, juxtaglomerular cell tumor ( renin producing) and edema (cirrhosis, heart failure and nephrotic syndrome) |
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Neuroendocrine tumor |
1- Heterogenous group of neoplasm originating from neuroendocrine cells 2- Most common 1- GI (carcinoid, gastrioma) 2- Pancreases (insulinoma, glucogonoma ) 3- Lungs (small cell lung cancer) 4- Thyroid (medullary carcinoma) 5- Adrenal (pheochromocytomtoma) 3- Neuroendocrine cells share common biological function through amine precursor uptake decarboxylase) 4- Treatment 1- Surgical resection 2- Somatostatin analog |
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List at least 4 examples of secretory products of neuroendocrine tumors |
1- Chromogranin A 2- Neuron-specific enolase (NSE) 3- Synaptophysin 4- Serotonin 5- Histamine 6- Calcitonin |
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Neuroblastoma |
1- Most common adrenal medullary tumor in children 2- < 4 years old 3- Originating from neural crest, occurs anywhere along the sympathetic chain 3- Features 1- Abdominal dissension 2- Firm, Irregular mass that extend across midline (vs wilms tumor (smooth and unilateral) 3- Less likely to cause hypertension 4- Opsoclonus-myoclonus syndrome 5- Increase HVM and VMA in urine 6- Homer-Wright rosettes (Neuroblastoma surrender by central lumen characteristic in Neuroblastoma and medullaroblastoma 7- Bombesin and NSE positive 8- Associated with amplification N-myc oncogene |
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Pheochromocytoma |
1- Cause 1- Most common tumor of adrenal medulla in adults 2- Originate from chromoffin cells (arises from neural crest) 3- May be associated with germline mutation 1- NF1 2- VHL 3- RET (MEN 2A and 2B) 2- Features 1- Pressure (hypertension due to increase secretion of epinephrine, norepinephrine and dopamine) 2- Pain (headache) 3- Precipitation 4- Palpitation (tachycardia) 5- Pallor 6- Increase EPO- polycythemia 7- Occurs in spells - relapse and remit 3- Increase catecholamine and metanephrine (HVA, VMA) in plasma and urine 4- Chromogranin, synaptophysin and NSE positive 5- Treatment 1- Alpha antagonist ( phenoxybenzamine) followed by 2- beta blocker prior to tumor removal 3- Alpha blockage before given beta blocker to prevent hypertensive emergency |
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Rule of 10 in pheochromocytoma |
1- 10% malignant 2- 10% bilateral 3- 10% extramedullary (bladder wall, organ of zuckerandl) 4- 10% calcific 5- 10% in kids |
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Multiple endocrine neoplasia pattern of inheritance |
Autosomal dominant |
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MEN 1 |
1- Pituitary adenoma (prolactin or GH 2- Pancreatic endocrine tumor 1- Insulinoma 2- Zollinger Ellison syndrome 3- VIPoma 4- Glucoganoma 3- Parathyroid adenoma 4- Associated with mutation of MEN1 ( menin- tumor suppressor- chromosome 11) angiofibroma, collagenoma and Meningioma |
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MEN2A |
1- Parathyroid hyperplasia 2- Medullary thyroid carcinoma 3- Pheochromcytoma 3- Associate with RET mutation |
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MEN 2B |
1- Medullary thyroid carcinoma 2- Pheochromocytoma 3- Mucosal neuromas (oral/intestinal ganglionoma) 4- Associated with Marfanoid habitus 5- Associated with RET mutation |
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Insulinoma |
1- Tumor of pancreatic beta cells - increase insulin- hypoglycemia 2- Whipple triad 1- Hypoglycemia 2- symptoms of hypoglycemia 3- Resolution of symptoms after normalization of plasma glucose level 3- Symptomatic patients decrease blood glucose and increase C peptide 4- 10% associated with MEN1 5- Treatment 1- Surgical resection 2- Somatostatin analogue (octreotide) |
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Glucagonoma |
1- Tumor of pancreatic alpha cells- overproduction of glucagon 2- Features 1- Dermatitis (necrolytic migratory erythema) 2- Diabetes (hyperglycemia) 3- DVT 4- Decrease Weight 5- Depression 6- Diarrhea 3- Treatment 1- Surgical resection 2- Somatostatin analogue (octreotide) |
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Somatostatinoma |
1- Tumor of pancreatic delta cells - increase Somatostatin- decrease secretion of 1- Secretin 2- Cholecystokinin 3- Insulin 4- Glucagon 5- Gastrin 6- Gastric inhibitory peptide (GIP) 2- Features 1- Diabetes/ glucose intolerance 2- Steatorrhea 3- Gall stones 4- Achlorhydria 3- Treatment 1- Surgical resection 2- Somatostatin analogue (octreotide) |
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Carcinoid tumor |
1- Arises from neuroendocrine cells most common in intestine and lungs 2- Rare and does not occur if it’s limited to the GI tract 3- Prominent rosettes, Chromogranin A and Synaptophysin positive 4- Secrete 5HT- 1- Recurrent diarrhea 2- Wheezing 3- Right sided heart lesion ( Tricuspid regurgitation, pulmonary stenosis) 4- Niacin deficiency (plegra) 4- 5HT undergoes first pass metabolism and enzymatic breakdown by MAO in lungs 5- Treatment 1- surgical resection 2- Somatostatin analogue (octreotide) |
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Rule of 1/3 for carcinoid tumors |
1/3 metastasize 1/3 present with 2nd malignancy 1/3 multiple |
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Zollinger Ellison syndrome (gastrinoma) |
1- Gastrin secreting tumor (gastrinoma) of the pancreas or duodenum 2- Acid hypersectiom leads to recurrent ulcer in the duodenum and jejunum 3- Features 1- Abdominal pain (peptic ulcer) 2- Diarrhea (malabsorption) 4- Positive secretin test - Gastrin levels remain elevated after administering secretin, which normally inhibit Gastrin release 5- May be associated with MEN1 |
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Insulin preparation |
1- 1- Rapid onset (1 hr) 1- Lispro 2- Aspart 3- Glulisin 2- Short actin (2-3 hrs) - regular 3- Intermediate acting (4-10hr) - NPH 4- Long acting 1- Detemir 2- Glargine 2- M.O.A 1- Binds to insulin receptor (tyrosine kinase activity) 2- Liver- increase glucose storage is glycogen 3- Muscle - Increase glycogen, protein synthesis 4- Fat- increase TG storage 5- Cell membrane - increase K uptake 3- A.E 1- Hypoglycemia 2- Lipodystrophy 3- Hypersensitivity reaction 4- Weight gain |
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Drugs that increase insulin sensitivity |
1- Biguanides 1- Metformin 2- Glitazones/Thiozolidinediones 1- Pioglitazone 2- Rosiglitazone |
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Biguanides metformin |
1- M.O.A 1- Inhibit mGPD- inhibition of hepatic gluconeogenesis and the action of glucagon 2- Increase glycolysis and peripheral glucose uptake (increase insulin sensitivity) 2- Adverse effect 1- GI upset (diarrhea) 2- Lactic acidosis (caution in renal insufficiency) 3- Vitamin B12 deficiency 4- Weight loss |
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Glitazones/thiozolidinediones Pioglitazone, rosiglitazone |
1- M.O.A 1- Activates PPAR-y (nuclear receptor)- increase insulin sensitivity and adiponectin 2- Adverse effect 1- Delayed onset of action 2- Edema 3- Weight gain 4- HF 5- Increase risk of fracture 6- Rosiglitazone 1- increase risk of M.I. 2- Increase risk of cardiovascular death
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Drugs that increase insulin secretion |
1- Sulfonylureas (1st gen) 1- Chloroprpamide 2- Tolbutamide 2- Sulfonylureas (2nd gen) 1- Glipizide 2- Glyburide 3- Meglotinides 1- Nateglinide 2- Reaglinide |
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Sulfonylureas and Meglitindes |
1- M.O.A 1- Close K channels- cell depolarization- insulin release via Ca channel open 2- Adverse effect 1- Disulfiram like reaction 2- Hypoglycemia 3- Weight gain |
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Drugs that increase glucose induced insulin secretion |
1- GLP- 1 analogs 1- Exenatide 2- Liraglutide 2- DPP- 4 inhibitor 1- Linagliptin, saxagliptin and sitagliptin |
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GLP-1 analogs |
1- Decrease glucagon release and gastric emptying Increase glucose dependent insulin release 2- Adverse effect 1- Nausea 2- Vomiting 3- Pancrratitis 4- Weight loss 5- Increase satiety |
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DPP 4 inhibitors |
1- Inhibits DPP 4 that inactivated GLP-1 - decrease glucagon release and gastric emptying increase glucose dependent insulin release 2- Adverse effects 1- Respiratory and urinary infections 2- Weight neutral 3- Increase satiety |
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Drugs that decrease glucose absorption |
1- SGLT-1 (sodium glucose co-transporter inhibitor 1- Canagliflozin 2- Dapagliflozin 3- Emapagliflozin 2- Alpha glucosidase inhibitor 1- Acarbose 2- Miitol |
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SGLT 1 inhibitors |
1- Block reabsorption of glucose at proximal convoluted tubule 2- Adverse effect 1- Glucosuria (UTI, vulvovaginal candidiasis) 2- Dehydration 3- Hyperkalemia (not recommended in renal insufficiency) 4- Weight loss |
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Alpha glycoside inhibitor |
1- Inhibit intestinal brush border alpha glucosidase- delay carbohydrate hydrolysis and glucose absorption - decrease post pea dial hyperglycemia 2- Adverse effects 1- GI upset 2- Bloating 3- Not recommend in renal failure |
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Amylin analogs |
1- Decrease glucagon release and gastric emptying 2- Adverse effects 1- Hypoglycemia 2- Nausea 3- Increase satiety |
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Thioamides (PTU and methimazole) |
1- Block thyroid peroxidase- Prevent oxidation and organification of iodine and cooling MIT and DIT- Inhibiting thyroid hormone synthesis PTU- inhibit peripheral conversion of T4-T3 by blocking 5’diodinase 2- Use 1- Hyperthyroidism 2- PTU in first trimester of pregnancy (methimazole is teratogenic) 3- Methimazole in second trimester of pregnancy (PTU hepatoxicity) 3- Adverse effects 1- Agranulocytosis 2- Aplastic anemia 3- Skin rash 4- Hepatotoxicity |
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What is the teratogenic effect of Methamizole |
Aplastic cutis (failure of dermal/epidermal formation, commonly the scalp) |
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What is preferred over thionamides for treatment of graves opthalmopathy |
Corticosteroids |
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Which thionamide associated with ANCA positive vasculitis |
PTU |
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Levothyroxine, liothyronine |
1- Hormone replacement for T4 (levothyroxine) and T3(liothyronine) 2- Use 1- Hypothyroidism 2- Myxedema 3- Weight loss 3- Adverse effects 1- Arrhythmia 2- Tachycardia 3- Tremor 4- Heat intolerance |
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Distinguish exogenous hyperthyroidism from endogenous hyperthyroidism |
1- TSH receptor antibodies 2- Radioactive iodine uptake 3- Measurement of thyroid blood flow on Ultrasound |
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Hypothalamic/pituitary drugs |
1- Canivaptan, tolvaptan - 1- ADH antagonist 2- SIADH (on ADH V2 receptors) 2- Demeclocyline 1- ADH antagonist a tetracycline 2- SIADH 3- Desmopressin 1- Central DI 2- Von willebrand disease 3- Sleep enuresis 4 Hemophilia A 4- GH 1- GH deficiency 2- Turner syndrome 5- Oxytocin 1- Induce labour 2- Control uterine bleeding 6- Somatostatin 1- Acromegaly 2- Pancreatic endocrine cell tumors 3- Carcinoid syndrome 4- Gastrinoma 5- Esophageal varies |
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Fludrocortisone |
1- Synthetic analogue of aldosterone with little glucocorticoids effect 2- Use 1- Mineralocorticoid replacement in primary adrenal insufficiency 3- Adverse effects 1- CUSHINGS |
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Cinacalcet |
1- Sensitize Ca-sensing receptors (CaSR) in parathyroid gland to circulating Ca- Decreasing PTH 2- Use 1- 2’ Hyperparathyroidism in CKD patients on dialysis 2- Hyperalcalcemia in 1’ hyperparathyroidism (if parathyroidectomy fails) 3- Parathyroid carcinoma 3- Adverse effect 1- Hypocalcemia |
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Sevelamer |
1- Non-absorbable phosphate binder that prevents phosphate absorption from the GI tract 2- Use 1- Hyperphosphatemia in CKD 3- Adverse effect 1- Hypophosphatemia 2- GI upset |
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Cation exchange resins |
1- Patiromer, sodium polystyrene sulfonate, zirconium cyclosilide 2- Bine K in the colon in exchange for other cation (Na, Ca)- k is excreted in the feces 3- Use 1- Hyperkalemia 4- Adverse effect 1- Hypokalemia 2- GI upset 3- sodium polystyrene sulfonate Bowel ischemic/necrosis |
