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General Medicine

General Medicine

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General Medicine

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  1. General Medicine Nutritional & Metabolic Disorders

  2. Revision • water & sodium metabolism • potassium metabolism • calcium metabolism • phosphate metabolism • magnesium metabolism • acid-base metabolism

  3. Understand Nutritional Basics • Macronutrients • Carbohydrates  mono- & polysaccharides • Protein  essential amino acids • Fats  saturated & unsaturated; essential fatty acids • Micronutrients • Vitamins  fat soluble vs water soluble • Minerals • Electrolytes • Nutrient & energy requirements

  4. Vitamins

  5. Any group of substances that are required, in small amounts, for healthy growth & development • Can’t be synthesized by the body, and are therefore essential constituents of the diet • Divided into 2 groups • Water soluble  Vit B complex & Vit C • Fat soluble  Vit A, D, E & K • Lack of sufficient quantities of any specific vitamin results in deficiency disease

  6. Vitamin A (Retinol) Deficiency • 1° deficiency • prolonged dietary deprivation • endemic in areas where rice is staple food (devoid of carotene) • 2° deficiency • Inadequate conversion of carotene to Vit A • Interference with absorption, storage or transport of Vit A • celiac disease; sprue • Cystic fibrosis • Pancreatic disease • Duodenal bypass • Cirrhosis; chronic obstructive liver disease • Mixed common in protein-energy malnutrition • Marasmus • Kwashiorkor

  7. Clinical Features • Severity of the effects inversely related to age • Blindness is the most important consequence: • Impaired dark adaptation and night blindness (rod dysfuntion) • Loss of mucous cells from the cornea dull, hazy appearance (keratinisation)  xerophthalmia • Bitot’s spots  glistening white plaques of desquamated, thickened conjuctival epithelium • Development of keratomalacia  corneal ulceration, scarring & irreversible blindness • Children present with growth retardation • Keratinisation of lung, GI tract & urinary tract epithelia • Increased susceptibility to infections  death • Follicular hyperkeratosis (skin)

  8. Vitamin A (Retinol) Toxicity • Acute toxicity • Usually manifests in children after large doses (>300 000IU) • Irritability, headaches & subsequent peeling of the skin • ICP & vomiting • May lead to death • Recovery spontaneous after discontinuation  no residual damage • Chronic toxicity • Usually in older children & adults • Doses > 100 000IU/day for months • Sparse coarse hair, alopecia of eyebrows, dry rough skin & cracked lips are early signs • Severe headaches & generalised weakness prominent later • Cortical hyperostosis & arthralgia are common • Liver damage, hepatomegally & splenomegally may occur • Hypercarotenosis • Carotene metabolised in liver to form Vit A • Excessive carotene does not cause Vit A toxicity, but carotenemia (>250um/L) • Skin becomes deep yellow (but not the sclera), esp palms & soles • May occour in DM, myxoedema & anorexia nervosa

  9. Vitamin D Disorders • 2 Natural Forms • Ergocalciferol  activaded ergosterol (Vit D2) • Irradiated yeast • Cholecalciferol  activated 7-dehydro-cholesterol (Vit D3) • Human skin on exposure to sunlight (UV)  major source • Fish liver oils & egg yolks • Deficiency • Rickets (children) • Bones don’t harden due to VitD deficiency (not enough Ca2+ salts deposited in bones) • Pronounced in long bones  soft & maleable  bow legs • Osteomalacia • Softening of the bones due to lack of Vit D • Deficiency of Vit D leads to progressive decalcification of bony tissues • Bone pain common • May become irreversible without Vit D treatment

  10. Prohormone (multiple active metabolites that act as hormones)  7-dehydocholesterol  UV light (photochemical reaction)  Vit D3  liver  25(OH)D3 (25-hydroxycholecalciferol) = major circulating form  enterohepatic circulation  Reabsorbed  Undergoes hydrolysation in the Kidneys (under PTH control, or hypophasphataemia)  1,25(OH)2D3 (1,25-dihydroxycholecalciferol; vit D hormone; calcitriol)   calcium absorption from intestines & promote normal bone function & mineralization

  11. Causes of Rickets & Osteomalacia • Vit D deficiency • Low dietary intake • High phosphate intake • Lack of sunlight • Malabsorption syndrome • Defects related to 25(OH)D3 production • Liver disease (advanced parenchymal & cholestatic disease) • Prolonged use of phenobarbitol • Defects related to action of 1,25(OH)2D3 • Defect in hydroxylation enzymes for conversion (Vit-D-dependant rickets type I) • Absent or defective receptors (VitD-dependant rickets type II) • Other • Familial hypophosphataemic rickets (renal tubular defect in PO4- ) • Chronic renal failure (renal osteodystrophy) • Fanconi’s syndrome • Renal tubular acidosis • DM • Hypoparathyroidism

  12. Diagnosis of Rickets & Osteomalacia • Serum level • Healthy individuals • 62-99 mmol/L= 25(OH)D3 • 48-108 mmol/L = 1,25(OH)2D3 • Nutritional causes • 25(OH)D3 levels very low; 1,25(OH)2D3 undetectable • Hypophosphataemia • High serum alkaline phosphatase • Serum calcium low or normal (2° hyperparathyroidism   PTH  compensation) • Low urinary calcium • History of low calcium intake

  13. Vitamin D Toxicity • 1000ug/day produces for 4 months toxicity in infants • 75ug/day can produce toxicity over years • Toxicity occur in adults receiving 2500ug/day over several months • Hypercalcaemia =  serum calcium (>3-4mmol/dL) • toxic symptoms appear • Normal levels = 2.12-2.62mmol/dL • Must be measured weekly/monthly in patients receiving high dose Vit D therapy • Clinical features • Anorexia, N/V • Polyuria & polydipsia • Weakness & nervousness • Pruritis • Impaired renal function  proteinuria, casts & azotaemia • Metastatic calcification • Must differentiate from other hypercalcaemic conditions  history • Vit D toxicity occurs commonly during treatment of hypoparathyrdism

  14. Vitamin E (tocopherol) Deficiency • Vitamin E • Any of a group of 8 chemically related fat soluble compounds • Tocopherols & tocotrienols (α-, β-, γ-, ð-isomers) • α-tocopherol is the only naturally occuring steroisomer & the most potent in biological assays • Serum levels of tocopherol vary with total plasma lipid levels • α-tocopherol = 11.6 – 23.2 umol/L • Functions • Have anti-oxidant properties  prevents oxidation of polyunsaturated fatty acid components • Maintain cell membrane structure • DNA synthesis effects & cell signalling • Anti-inflammatory & immune system functions • Protection against coronary artery disease  anto-oxidant  arthrogenesis • Deficiency • Rare  premature infants & malabsorption syndromes • Myopathies, neuropathies & liver necrosis  CM damage • Mild haemolytic anaemia   erythrocyte haemolysis • Chronic fat malabsorption  ataxia & visual scotomas

  15. Vitamin K Deficiency • Vitamin K • Vitamin K ("Koagulations-Vitamin") denotes a group of lipophilic, hydrophobic vitamins that have coagulation activity • Chemically they are 2-methyl-1,4-naphthoquinone derivatives • Vit K1 (phylloquinone)  found in plants • Vit K2 (menaquinone)  synthesised in the intestines by bacteria • Controls formation of coagulation factors II (prothrombin), VII (proconvertin), IX (christmas factor) & X in the liver • Daily requirement is about 1ug/KG • Deficiency • Haemorrhagic disease of newborns • Uncommon primary deficiency in adults • Vit K antagonists  anticoagulants (e.g. warfarin); megadoses VitA & VitE • Hypothrombinaemia &  Vit K–dependant coagulation factors  defective coagulation & haemorrhage • Biliary obstruction, malabsorption or parenchymal liver disease can cause Vit K deficiency • Easy bruising & mucosal bleeding a sign •  PT & PTT

  16. Vitamin B1 (thiamine) Deficiency • Thiamine (Aneurine) • Active in the form thiamine pyrophosphate (TPP) • Plays an important role in helping the body metabolize carbohydrates and fat to produce energy • Co-enzyme for decarboxylation of pyruvate  acetylcoenzyme A (anaerobic glycolysis) • Co-enzyme for decarboxylation of α-ketoglutamate  succinate (Kreb’s cyc) • It is essential for normal growth and development and helps to maintain proper functioning of the heart and the nervous and digestive systems. • Thiamine is water-soluble and cannot be stored in the body; however, once absorbed, the vitamin is concentrated in muscle tissue. • Deficiency • 1° deficiency  inadequate dietary intake • 2° deficiency •  requirement (e.g. hyperthyroidism; pregnancy; lactation; fever) • Impaired absorption (e.g. prolonged diarrhoea) • Impaired utilization (e.g. severe liver disease)

  17. Beri-Beri(neurological disorder caused by thiamine deficiency) Aetiology • Common in people whose diet consists mainly of polished white rice (very low in thiamine - thiamine-bearing husk has been removed) • chronic alcoholics with an inadequate diet, • If a baby is mainly fed on the milk of a mother who suffers from thiamine deficiency then that child may develop beriberi. Clinical Features • Charactarised by damage to nerves and heart; general symptoms include loss of appetite and feeling of lassitude. • Weight loss, emotional disturbances, impaired sensory perception (Wernicke's encephalopathy), weakness and pain in the limbs, and periods of irregular heart rate. • Oedema is common. • In advanced cases, the disease may cause heart failure and death. • It may also increase the amount of lactic acid and pyruvic acid in the blood.

  18. Types of Beri-Beri • Wet beriberi affects the heart; it is sometimes fatal, as it causes a combination of heart failure and weakening of the capillary walls, which causes the peripheral tissues to become edematous. • Dry beriberi causes wasting and partial paralysis resulting from damaged peripheral nerves. It is also referred to as endemic neuritis. Treatment • Treatment is with thiamine hydrochloride, either in tablet form or injection. • A rapid and dramatic recovery within hours can be made when this is administered to patients with beriberi, and their health can be transformed within an hour of administration of the treatment. • Thiamine occurs naturally in and fresh foods, particularly fresh meat, legumes, green vegetables, fruit, and milk.

  19. Vitamin B2 (riboflavin) Deficiency • Riboflavin • Acts as an essential co-enzyme in many oxidation-reduction reactions (mitochondria) involved with CHO metabolism • It is the central component of the cofactors FAD (flavine adenine dinucleotide) and FMN (flavine mononucleotide), and is therefore required by all flavoproteins • Deficiency • 1° deficiency  inadequate consumption of milk products • 2° deficiency  chronic diarrhoeas; liver disease; chronic alcoholism • Pallor & maceration of mucosa in angles of mouth (angular stomatis) & lip surfaces (cheilosis)

  20. Vitamin B3 (niacin; nicotinic acid) Deficiency • Niacin • Derivitive of pyridine & interchangable with its nicotinamide • Nicotinic acid can be made from tryptophan (EAA) • Derevatives include • Nicotinamide adenine dinucleotide (NAD; coenzyme I) • Nicotinamide adenine dinucleotide phosphate (NADP; CoII) • Among its many functions, niacin derivatives are involved with detoxification of xenochemicals, DNA repair, and the production of steroid hormones in the adrenal gland. • Deficiency • 1° deficiency  areas where maize is the staple diet • 2° deficiency  chronic diarrhoeas; cirrhosis; chronic alcoholism

  21. Pellegra(nutritional disorder caused by nicotinic acid deficiency) Aetiology • Diet poor in nicotinic acid or tryptophan Clinical Features • Charactarised by cutaneous, mucous membrane, CNS & GI symptoms • Symmetric photosensitive rash, scarlet stomatitis, glossitis, diarrhoea & mental abberations • Symptoms may appear alone or in combination • Bilateral cutaneous lesions • Chronic hypertrophy  skin thick, fissured & deeply pigmented • Chronic atrophic lesions  dry, scaly skin • Sunlight causes Casal’s necklace & butterfly lesions on the face

  22. Vitamin B5 (pentothenic acid) Deficiency • Pentothenic acid • Pantothenic acid is used in the synthesis of coenzyme A (CoA). • Coenzyme A may act as an acyl group carrier to form acetyl-CoA and other related compounds; this is a way to transport carbon atoms within the cell. • The transfer of carbon atoms by coenzyme A is important in cellular respiration, as well as the biosynthesis of many important compounds such as fatty acids, cholesterol, and acetylcholine. • Since pantothenic acid participates in a wide array of key biological roles, it is considered essential to all forms of life. • Pantothenic acid is vital for a healthy pregnancy. • Deficiency • Pantothenic acid deficiency is exceptionally rare and has not been thoroughly studied. • In the few cases where deficiency has been seen (victims of starvation and limited volunteer trials), nearly all symptoms can be reversed with the return of pantothenic acid. • Symptoms of deficiency are similar to other vitamin B deficiencies. Most are minor, including fatigue, allergies, nausea, and abdominal pain. • In a few rare circumstances more serious (but reversible) conditions have been seen, such as adrenal insufficiency and hepatic encephalopathy. • Painful burning sensations of the feet were reported in tests conducted on volunteers. • Deficiency of pantothenic acid may explain similar sensations reported in malnourished prisoners of war.

  23. Vitamin B6 (pyridoxine, pyridoxal & pyridoxamine) Deficiency • Vitamin B6 • Pyridoxine assists in the balancing of sodium and potassium as well as promoting red blood cell production. • It is required for the production of the monoamine neurotransmitters serotonin, dopamine, noradrenaline and adrenaline, as it is the precursor to pyridoxal-5- phosphate • Pyridoxal-5-phosphate is the active form in humans  cofactor for the enzyme aromatic amino acid decarboxylase. This enzyme is responsible for converting the precusors 5-hydroxytryptophan (5-HTP) into serotonin and levodopa (L-DOPA) into dopamine, noradrenaline and adrenaline. As such it has been implicated in the treatment of depression and anxiety. • It is linked to cardiovascular health by decreasing the formation of homocysteine. • It has been suggested that Pyridoxine might help children with learning difficulties, and may also prevent dandruff, eczema, and psoriasis • Pyridoxine can help balance hormonal changes in women and aid in immune system.

  24. Vitamin B6 Deficiency • 1° deficiency  rare (most foods contain pyridoxine) • 2° deficiency  malabsorption, alcoholism, OCP, excessive loss & increased metabolism • Seborrheic dermatosis, glossitis, cheilosis, peripheral neuropathy & lymphopenia • Convulsions in infants • Normocytic anaemia is adults

  25. Vitamin B7 (biotin) Deficiency • Biotin • Also known as vitamin H or B7. • Biotin is a cofactor in the metabolism of fatty acids and leucine, and in gluconeogenesis. • Biotin is necessary for cell growth, the production of fatty acids, and the metabolism of fats and amino acids. • It plays a role in the citric acid cycle • Biotin not only assists in various metabolic reactions, but also helps to transfer carbon dioxide. • Biotin is also helpful in maintaining a steady blood sugar level. • Deficiency • Rare • Prolonged consumption of raw egg white (contain avidin  a biotin antagonist) • Scaly dermatitis, alopecia & parasthesia

  26. Vitamin B9 (folate; folic acid) Deficiency • Folic acid • Folate is necessary for the production and maintenance of new cells. This is especially important during periods of rapid cell division and growth such as infancy and pregnancy. • Important in synthesis of nucleic acids  needed to replicate DNA. • The metabolic role of folate is interdependant with Vit B12 (both required by rapidly dividing cells) • Deficiency • Folate deficiency hinders DNA synthesis and cell division, affecting most clinically the bone marrow, a site of rapid cell turnover. • Because RNA and protein synthesis are not hindered by folate deficiency, large red blood cells called megaloblasts are produced, resulting in megaloblastic anemia.. • Both adults and children need folate to make normal red blood cells and prevent anemia

  27. Causes of Folate deficiency • Inadequate diet • Diet lacking fresh, slightly cooked food • Chronic alcoholism • Inadequate absorption • Malabsorption  caeliac; sprue; • Drugs  barbituates; OCP • Congenital folic acid malabsorption • Inadequate utilization • Antagonists; enzyme deficiencies; Vit B12 deficiency; scurvy • Increased requirement • Pregnancy; lactation; infancy; increased haemopoiesis; increased metabolism • Increased excretion • Renal dialysis

  28. Vitamin B12 (cyanocobalamin) Deficiency • Cyanocobalamin • Form of Vit B12 with coenzyme activity is 5-deoxyadenosyl cobalamin  used for synthesis of nucleic acids & maintainence of myelin sheaths • Important for the normal functioning of the brain and nervous system and for the formation of blood. • It is normally involved in the metabolism of every cell of the body, especially affecting the DNA synthesis and regulation but also fatty acid synthesis and energy production. • Maintains proper function of folic acid & other B vitamins • Absorbed only in presence of intrinsic factor, a protein secreted in the stomach • Deficiency • Affects all body tissues, esp those with high cellular turnover • Perinicious anaemia • Degeneration of the nervous system (predominates if folate intake maintains erythropoeisis) • Peripheral neuropathy (d.t. diffuse & uneven demyelination)

  29. Causes of Vit B12 deficiency • Inadequate diet • Veganism (vegan breastfeeding mothers) • Chronic alcoholism • Fad diets • Inadequate absorption • Lack of intrinsic factor  pernicious anaemia  abstruction of gastric mucosa) • Small intestine disorders  celiac; sprue; malabsorption • Inadequate utilization • Antagonists; enzyme deficiencies; Vit B12 deficiency; scurvy • Increased requirement • Pregnancy; lactation; infancy; parasitic infection; Α-thalassemia • Increased excretion • Liver or kidney disease

  30. Vitamin C (ascorbic acid) Deficiency • Ascorbic acid • Most active reducing agent in aqueous phase of living tissues • Essential for collagen formation • Maintains substances of mesenchymal origin (e.g. CT) • Essential in wound healing & facilitates recovery from burns • Strong reducing agent  readily oxidised & reduced in the body (redox system in cells) • Involved in metabolism of phenylalanine & tyrosine • Deficiency • Improper diet  lack of fresh fruits & vegetables • Pregnancy, lactation & thyrotoxicosis increase requirements • Acute & chronic inflammatory disease • Diarrhoea  faecal loss • Achlordynia  malabsorption

  31. Scurvy(disease caused by lack of Vit C) • 3-6 months of VitC < 10mg/day • Defective formation of collagen • impaired wound healing • capillary haemorrhage • subnormal platelet adhesiveness • Clinical Features • Swollen & spongy gums  bleed easily • Perifollicular, petechial or spontaneous bruising • Splinter haemorrhage (nails) • Anaemia • Fresh wounds fail to heal

  32. Minerals

  33. Iron deficiency • Most common nutritional deficiency in the world • Due to insufficient intake (infants, adolescent girls or PG) • Blood loss may produce iron deficiency • Iron deficiency anaemia • microcytic anaemia with anisocytosis & poikilocytosis • smooth tongue & spoon nails • low serum Fe & ferritin • Iron toxicity • Vomiting, diarrhoea & intestinal damage • May accumulate with prolonged, excessive therapy, after repeated transfusions or in chronic alcoholism • Haemochromotosis is a potentially fatal but treatable disease

  34. Iodine deficiency • Iodine intake < 20ug/day • Thyroid gland hypertrophy  concentrates iodide in itself  colloid goitre • Endemic myxoedema (adults) or endemic cretinism (infants) • Major cause of hypothyroidism • Iodine toxicity • Iodine intake 20x greater than RDA (2mg/day) • Some develop goiters • Some develop myxoedema & hyperthyroidism (paradoxical) • Very high doses cause a brassy taste, increased salivation & gastric irritation

  35. Goitre(swelling of neck due to enlargement of the thyroid gland) • Endemic • Gland enlarges  attempt to increase the output of hormone • Dietary lack of iodine  regions where diet lacked iodine • Drugs may decrease hormone production • Neonatal congenital hypothroidism  mental & physical retardism • Euthyroid goitre • An enlargement of the thyroid gland without clinical or laboratory evidence of thyroid dysfunction • More frequent during puberty, pregnancy or menopause • Exophthalmic goitre (Grave’s disease) • Swelling associated with hyperactivity of the gland (hyperthyroidism) • Associated with Grave’s disease & Hashimoto’s disease

  36. Flourine deficiency • Not considered an essential mineral  deficiency state has, reversed by the mineral alone, not been induced • Considered essential for prevention of dental carries and possibly osteoporosis • Flouridation of water that contains less than 1ppm significantly reduces incidence of dental caries • Flourine toxicity (fluorosis) • Excess accumulation of fluorine occurs in teeth & bones in proportion to level & duration fluorine intake • > 10ppm in drinking water • Chalky white, irregularly distributed patches on surface of enamel • Patches become stained yellow-brown, characteristic • Severe flourosis weakens enamel  pitting in surface • Bony changes only seen after prolonged exposure to high flourine (e.g. osteosclerosis; exostoses of the spine; genu valgum)

  37. Zinc deficiency • Anorexia & hypogeusia • Growth retardation • Delayed sexual maturation • Hypogonadism & hypospermia ( plasma testosterone) • Immune disorders (impaired T-lymphocyte function) • Dermatitis • Night blindness • Impaired wound healing ( collagen synthesis  hypofibrinaemia) • Zinc toxicity • Large amounts required (200-800mg/day) • Usually due to consuming acidic food or drink from a calvanised container • Vomiting & diarrhoea • Hypocupraemia  Zn interfers with copper metabolism • Neutropaenia • RBC microcytosis

  38. Chromium deficiency • Very rare • Associated with glucose intolerance & peripheral neuropathy • Chromium toxicity • Trivalent chromium (CrCl3), as found in brewers yeast, may cause skin irritation at high doses

  39. Copper deficiency • Acquired copper deficiency • Environmental or diet abnormalities rarely causes clinically significant copper deficiency • Causes are kwashiokor, persistant infantile diarrhoea (associated with milk), severe malabsorption (e.g. sprue), excess intake of zinc salt • Inherited copper deficiency (Menkes’ syndrome) • Characterised by deficiencies of copper in liver & serum, and deficiencies of essential copper proteins • Causes severe mental retardation • Copper toxicosis • Prolonged contact with copper vessels • Miligrams  nausea, vomiting & diarrhoea • Grams  copper induced haemolytic anaemia & anuria  fatal

  40. Wilson’s Disease(an inherited defect of copper metabolism; inherited copper toxicosis) • Progressive & uniformly fatal disorder of copper metabolism • Liver concentration of copper 20x normal (from birth) • Deficiency of copper plasma protein ceruloplasmin • N.B. these levels are diagnostic, but are present in every infant 2-3months

  41. Fluid & Electrolyte Imbalences

  42. Fluid & Electrolyte Balance • Abnormalities of composition & volumes of bodily fluids are common and clinically important problems. • Understanding and treating these disorders requires knowledge of fluid shifts of EC and IC compartments before and after therapy. • Various factors cause EC & IC volumes to change markedly, e.g: • ingestion of water or dehydration • IV transfusions of various solutions • loss of large amount of fluid from GIT • loss of abnormal fluids through sweating or kidneys • 2 basic principles important for understanding of changes of fluid concentrations: • Water moves rapidly across cell membranes (osmolarities of EC & IC compartments remain almost exactly equal to each other, except for a few minutes after a change in either compartment) • The cell membrane is almost completely impermeable to many solutes (number of osmoles in EC & IC compartments remains relatively constant unless solutes are added to or lost from EC compartment)

  43. H20 Metabolism bodily loss of water ↑ osmolality of ECF (hypertonic blood environment) hypothalamus stimulated (osmoreceptors) sensation of thirst distributed via blood stimulates ADH secretion patient drinks ↑ permeability to H2O restores osmotic consistency epithelial cells of collecting ducts ↓ stimulation of hypothalamus (↓ ADH secretion) ↑ urine volume (↓ H2O reabsorption) ↓ osmolality of ECF

  44. Na+ Metabolism & BP Control juxtaglomerular complex cells of distal tubule monitor minute changes in BP of afferent vessels stimulates enzyme renin release if ↓renal arterial BP detected angiotensin I converted into angiotensin II (angiotensin converting enzyme) renin converts angiotensinogen into angiotensin I stimulates constriction of arterioles & aldosterone secretion (adrenal cortex) aldosterone affects cells in distal convoluted tubule & collecting ducts angiotensin II released into blood increases BP enough to form a –ve feedback loop back to juxtaglomerular complex targets cells to speed up transport of Na+ out of tubule and back into blood H2O follows

  45. Na2+ Control Mechanisms • Glomerular Filtration Rate (GFR) • Renin-Angiotensin-Aldosterone Mechanism • Atrial Natriuretic Peptide • e.g. blood loss/shock  ↓CO  ↓GFR  Na2+/H2O retained ↓ renal arterial pressure ↓[Na2+] distal tubule angiotensinII aldosterone vasoconstiction reabsorption of Na2+ (distal tubules) Renin = Na2+/H2O reabsorbed  ↓urinary output  ↑BP inhibits mechanisms used for Na2+/H2O retention due to atrial dilation