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SYSTEMIC DISEASES AND GENERAL MEDICINE

SYSTEMIC DISEASES AND GENERAL MEDICINE. Prof. Dr. Sibel ERTAN. Endocrine diseases. Hypothyroidism Hyperthyroidism Hypoparathyroidism Hyperparathyroidism Diabetes mellitus Hypoadrenalism Hyperadrenalism. Hypothyroidism. The neurologic complications of hypothyroidism include: Headache

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SYSTEMIC DISEASES AND GENERAL MEDICINE

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  1. SYSTEMIC DISEASES AND GENERAL MEDICINE Prof. Dr. Sibel ERTAN

  2. Endocrine diseases • Hypothyroidism • Hyperthyroidism • Hypoparathyroidism • Hyperparathyroidism • Diabetes mellitus • Hypoadrenalism • Hyperadrenalism

  3. Hypothyroidism The neurologic complications of hypothyroidism include: • Headache • Disorders of cranial and peripheral nerves • Sensorimotor abnormalities • Changes in cognition and level of consciousness • Cerebellar syndrome

  4. Hypothyroidism Chracteristic findings: • Low circulating T4 and T3, elevated TSH levels • Low radioiodine uptake by the thyroid • Increase of the CSF protein content (values greater than 100 mg/mL are not exceptional) • EEG abnormalities include slowing and generalized decrease in amplitude

  5. Hyperthyroidism The neurologic complications of hyperthyroidism include: • Tremor • Thyrotoxic myopathy (weakness and wasting of the muscles of the pelvic girdle to a lesser extent of the shoulder girdle. DTRes are normal or hyperactive. Fasciculations and myokymia may be noted) Thyrotoxic myopathy needs to be distinguished from myasthenia gravis • Stroke (abnormal cardiovascular and autonomic functions) • Mental disturbances (from mild irritability to psychosis) • Graves ophthalmopathy

  6. Hypoparathyroidism The neurologic complications of hypoparathyroidism include: • Mental deficiency • Tetany (In latent tetany:Chvostek sign, Trousseau sign, Erb sign) • Seizures • Hyper- or hypokinetic movement disorders (intracranial calcifications) • Increased intracranial pressure with papiledema • Hypoparathyroid myopathy

  7. Hyperparathyroidism The neurologic complications of hyperparathyroidism include: • Symmetric proximal limb weakness and muscle wasting • DTRes are normal or hyperactive • Chorea, abnormal movements of the tongue • Mental status changes (memory loss, irritability) • Depression

  8. Diabetes mellitus Primary neurologic complications of DM: • Peripheral neuropathy (mononeuropathies, polyneuropathy, autonomic neuropathy, radiculopathies, entrapment neuropthy) • Hypoglycemic coma • Stroke

  9. Hematologic and related diseases • Polycythemia • Heparin-induced Thrombocytopenia • Leukemia • Antitrombin III deficiency • Protein S deficiency • Protein C deficiency • Factor V Leiden mutation • Hereditary abnormalities of fibrinolysis • Autoantibodies • Hemophilia

  10. Polycythemia • Headache due to increase of the blood viscosity • In 50% to 80% of patients: • dizziness, • tinnitus, • visual disturbances, • cognitive impairment • Predisposes to large and small vessel cerebral infarction and may accelerate atherosclerosis • Thrombocytosis and a platelet disorder that leads to a hemorrhagic diathesis may be seen • Peripheral neuropathy (predominantly sensory axonal, in up to 46%)

  11. Heparin-induced Thrombocytopenia • Immune-mediated disorder • The pathogenic IgG binds a heparin/platelet factor 4 complex platelet activation. • Platelet account by 50% or greater • 50% of patients develop thrombotic complications. • Cerebral infarctions in 3%-4% of patients • Heparin should be stopped, warfarin withheld

  12. Leukemia • Indirectly • Therapy complications (hemorrhage due to thrombocytopenia or infections due to  white blood cell count) • Leukostasis (>150,000/mm3) may occlude cerebral blood vessels) • Directly • In acute myelogenous leukemias CNS involvement is uncommonly the first manifestations • Acute lymphocytic leukemia involves the CNS in 5% to 10% of patients at the time of diagnosis, often without symptoms • Chronic leukemia rarely affects the CNS

  13. Antithrombin III deficiency • Plasma glycoprotein(synthesized by the liver and endothelial cells) • ATIII is required for the anticoagulant action of heparin • Heparin accelerates the inactivation of factor Xa and thrombin • Most common presentation is leg thrombosis and pulmonary embolus • Cerebral venous thrombosis is more common but arterial thrombosis may occur • ATIII deficiency is resistant to anticoagulation with heparin • After a thrombotic event, lifelong warfarin therapy is indicated

  14. Protein S deficiency • Protein S is a vitamin K-dependent plasma protein • PS is synthesized in the liver • PS facilitates the binding of protein C to the platelet membrane (acting as a nonenzymatic cofactor for the anticoagulant activity of activated protein C). • Only 40% of PS is in a free form • The rest is in an inactive form, bound to C4-binding protein. (C4-binding protein levels are elevated during acute inflammation or stress increasing the inactivation of PS) • Up to 20% of patients with stroke have PS deficiency

  15. Protein C deficiency • Protein C is a vitamin K-dependent plasma protein • PC is synthesized in the liver • PC is activated by thrombin-thrombomodulin complex • PS enhances the activity of PC • PC inactivates factors Va and VIIIa • PC deficiency is found in 6% to 8% of patients who have a stroke before age 40

  16. Factor V Leiden mutation • FVL is the most common known genetic risk factor for thrombosis • The incidence of heterozygous FVL is 2% to 8.5%. • A mutation of the FV gene results in factor Va resistance to degradation by activated protein C

  17. Hereditary abnormalities of fibrinolysis • Plasminogen deficiency • Tissue plasminogen activator deficiency • Dysfibrinogenemia • Factor XII deficiency

  18. Autoantibodies • Antiphopholipid antibodies, encompassing Lupus anticoagulant and anticardiolipin antibodies are the most common acquired defects associated with thrombosis • May cause: • Ischemic strokes • Cerebral venous sinus thrombosis • Dementia • Chorea

  19. Paraneoplastic syndromes A praneoplastic syndrome is one that occurs more frequently than expected by chance in association with neoplasm, most often a malignant tumor

  20. Paraneoplastic syndromes • All syndromes are rare • All syndromes together occur in less than 1% of all patients with small cell lung cancer • Conversely, among patients diagnosed with a recognized PNPS 10% to 60% prove to have a tumor • Most PNPSs are autoimmune in origin

  21. Paraneoplastic syndromes Clinical neurologic syndromes • Paraneoplastic cerebellar degeneration • Subacute sebnsory neuropathy/encephalitis • Limbic encephalitis • Brainstem encephalitis • Opsoclonus-myoclonus • Myelitis • Motor neuron diseases • Sensorimotor peripheral Neuropathy • Neuromuscular disorders • Myopathies

  22. Vitamin B12 deficiency • Animal products are the sole dietary sources of cobalamin for humans • Gastric acid is needed for peptic digestion to release the vitamin from proteins • The freed B12 isbound by R proteins and than by gastric intrinsic factor, produced by gastric parietal cells, which is needed for absorption of B12 • Intrinsic factor-cobalamin complex is transported across the teminal ileum and binds to transcobalamin • The complex enters the cells by endocytosis, and the vitamin enters red blood cells in an energy dependent process • Cobalamin is converted to adenosyl or methyl coenzymes, which are necessary for normal neural metabolism • If they are missing, abnormal fatty acids may accumulate in myelin or methylating reactions may be defective

  23. Vitamin B12 deficiency • About 80% of adult-onset pernicious anemia is attributed to lack of gastric intrinsic factor secondary to atrophic gastritis • The disorder is thought to be autoimmune in origin • In the spinal cord white matter is affected more than gray • Symmetric loss of myelin sheaths occurs more often than axonal loss • Changes are most prominent in the posterior and lateral columns • The thoracic cord is affected firstand than the process extends in either direction • Patchy demyelination may be seen in the frontal white matter

  24. Vitamin B12 deficiency • Clinical features: • 40% of all patients with B12deficiency are said to have some neurologic symptoms or signs, and these are often the first or most prominent manifestations of the disease • Most patients are over 60 • Most common symptoms are due to myelopathy or neuropathy • Memory loss, visual loss, orthostatic hypotension, anosmia, impaired taste, sphincter symptoms, and impotance are other symptoms.

  25. Vitamin B12 deficiency • The diagnosis rests on demonstration of blood levels of vitamin B12 less than 200 pg/mL, but low normal values (200-350 pg/mL) may be found in people who respond to therapy • In patients with neurologic signs, only about 20% show severe anemia • Both hematocrit and mean corpuscular volume may be normal • B12 is given intramuscularly in a dosage of 1000 g/day for the first week, followed by weekly injections for the first month, and then monthly injections for life

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