What are the normal measurements of JVP
no more than 3cm
what is JVP?
Jugular venous pressure (JVP) provides an indirect measure of central venous pressure. This is possible because the internal jugular vein (IJV) connects to the right atrium without any intervening valves, resulting in a continuous column of blood.
5 causes of raised JVP
- Right sided heart failure (commonly caused by L sided heart failure)
- Pulmonary hypertension
- COPD
- Interstitial lung disease
- Tricuspid regurgitation
- Constrictive pericarditis- chronic pericarditis/ inflammation of pericardium causing scarring, thickening and muscle tightening.
describe kidney filtration in the glomerulus
- Endothelium
- this has relatively large pores (70-100 nanometers in diameter), which solutes, plasma proteins and fluid can pass through, but not blood cells.
• Basement membrane
prevent plasma proteins from being filtered out of the bloodstream.
- Epithelium
- this layer consists of specialized cells called podocytes. These cells are attached to the basement membrane by foot processes (pedicels). They wrap around the capillaries, but leave slits between them, known as filtration slits. A thin diaphragm between the slits acts as a final filtration barrier before the fluid enters the glomerular space
describe kidney filtration in the convoluted tubule
Gs Early proximal convoluted tubule
• Sodium/potassium ATPase, 3 Na+ out, 2K+ in
• Sodium/H+ exchanger, which enables reabsorption of bicarbonate.
• Glucose, amino acids and other substances diffuse out of the epithelial cell down their concentration gradients on passive transporters and are then reabsorbed by the blood capillaries.
• By the time the filtrate has reached the mid part of the proximal tubule, 100% of the filtered glucose and amino acids have been reabsorbed, and large amounts of sodium, bicarbonate, phosphate, lactate, and citrate ions.
Late proximal convoluted tubule
• Chloride/formate anion exchangers driven by the high concentration of chloride in the filtrate. Chloride diffuses out of the cell through channels in the cell wall, and then on into the bloodstream.
• Small solutes e.g. water and sodium chloride are reabsorbed via junctions in the epithelial cells of the tubule wall.
what is reabsorbed in the descending LoH
aquaporins allow water to pass from the filtrate into the interstitial fluid
describe kidney filtration in the thick ascending limb
• Na/K/Cl transporter and Na/K ATPase 1Na+, 2Cl- and 1K+ in to ascending limb from the lumen via three-ion cotransporter, then Na+ out into blood and K+ in to ascending limb via Na/K pump, Cl- and K+ out down electrochemical gradient
impermeable to water
describe kidney filtration in the distal tubule
selectively secretes and absorbs ions to maintain electrolyte balance and pH
describe kidney filtration in the collecting duct
reabsorbs solutes and water from the filtrate
How is GFR calculated
Abbreviated MDRD for eGFR equation: 186 x (Creatinine/88.4)-1.154 x (Age)-0.203 x (0.742 if female) x (1.210 if black)
5 causes of left axis deviation
- Normal variant
- Mechanical shift- ascites, high diaphragm
- Left atrial hypertrophy
- Left bundle branch block
- Wolff-Parkinson-White Syndrome
- COPD
- HyperK
- Right ventricular ectopic rhythms
MICA for calcium carbonate
- MOA: basic inorganic salt that neutralises HCl. Inhibits pepsin by increasing the pH via adsorption. 90% is converted to insoluble calcium salts.
- Indications: heartburn and acid indigestion, nutritional supplement or hypoCa tx, hypophosphataemia
- Contraindications: hypercalcaemia of malignant disease or conditions associated with hypercalciuria
- Adverse effects: constipation, diarrhoea, hypercalcaemia, nausea, hypercalciuria, flatulence, GI discomfort, skin reactions.
- Class of drug: antacid/ calcium
- Metabolism & elimination: not metabolised, excreted in the faeces. Majority is reabsorbed in the ascending limb of the LoH and DCT. Secreted by sweat glands.
MICA for calcium gluconate
- MOA: calcium salt that directly replenishes serum calcium levels.
- Indications: severe acute hypocalcaemia or hypocalcaemic tetany, acute severe hyperK, mild asymptomatic hypocalcaemia
- Contraindications: conditions associated with hypercalcaemia e.g. malignancy, conditions associated with hypercalciuria e.g. malignancy. Cautions: hx of nephrolithiasis, sarcoidosis
- Adverse effects: arrhythmias, circulatory collapse, feeling hot, hyperhidrosis, hypoT, vasodilation, vomiting, GI disorder
- Class of drug: calcium
- Metabolism & elimination: doesn’t need metabolization by the liver. Excretion- 20% renal via urine, 80% faecal.
DRDEACPIMP for chronic kidney disease
• Definition: kidney damage for >3months based on findings of abnormal structure or function or GFR <60ml/min/1.73m2 for >3months with/out evidence of kidney damage.
Risk factors: HT, DM, smoking, obesity, CVD, FHx, hypercholesterolaemia, polycystic kidney disease, long term steroid use and lithium use, age >60, recurrent UTIs, black, Asian and minority ethnic groups are 5 times more likely to develop CKD.
- Ddx: AKI, chronic glomerulonephritis, diabetic nephropathy, multiple myeloma, nephrolithiasis, nephrosclerosis
- Epidemiology: ~3 million people in the UK have CKD, 63000 people are being treated for renal failure, ~1000 children with CKD in the UK, 10% in women, 6% in men.
- Aetiology: two main causes are DM (24%) and HT (11%)
- Clinical features: fatigue, weakness, anorexia, vomiting, metallic taste, pruritus, restless legs, bone pain, impotence, dyspnoea, oedema, pallor, jaundice, brown nails, purpura, pleural effusion.
- Pathophysiology: progressive deterioration of renal function leading to problems with electrolyte and fluid balance and consequent symptoms- anaemia is caused by deficient EPO production.
- Ix: Bloods- normocytic normochromic anaemia, ESR, U&E (high urea and creatinine), glucose, Ca (low), phosphate (raised), PTH (raised), urine MS&C dipstick, 24h urine proteins, renal US, CXR- cardiomegaly, pleural/pericardial effusions or pulm oedema, bone x-rays may show osteodystrophy, renal biopsy considered if cause unclear with normal sized kidneys.
- Mx: refer to nephrologist, treat reversible causes e.g. relieve obstruction, stop nephrotoxic drugs, lifestyle changes- exercise, weight loss, fluid intake, Na restriction, moderate diet, prepare for dialysis/transplantation
- Prognosis: 1 in 50 people will develop kidney failure
MICA for DDAVP (desmopressin)
- MOA: binds to V2 receptors in basolateral membrane of cells of DCT and CD stimulating adenylyl cyclase, leading to an increase in aquaporins. Mimics ADH.
- Indications: many indications including diabetes insipidus tx, primary nocturnal enuresis (inability to control urination), post-op polyuria or polydipsia, renal function testing
- Contraindications: cardiac insufficiency, diuretics, hx of hypoNa, polydipsia in alcohol dependence, psychogenic polydipsia, siADH, von Willebrand’s disease type IIb
- Adverse effects: hyponatraemia, abdo pain, aggression in children, allergic dermatitis, emotional disorder, fluid retention, headache, hyponatraemic seizure, vomiting, increased weight.
- Class of drug: vasopressin and analogues
- Metabolism & elimination: no metabolism by the liver, excreted in the urine
5 diseases that can cause metabolic acidosis
heart failure, drugs, toxins, ketoacidosis due to starvation or alcohol excess, salicylate poisoning, methanol poisoning, renal failure, diarrhoea.
compare and contrast nephrotic syndrome
Nephrotic syndrome is a condition involving the loss of significant volumes of protein via the kidneys (proteinuria) which results in hypoalbuminaemia. The definition of nephrotic syndrome includes both massive proteinuria (≥3.5 g/day) and hypoalbuminaemia (serum albumin ≤30 g/L). e.g. CKD, also have oedema for diagnosis.
Nephritic syndrome is a condition involving haematuria, mild to moderate proteinuria (typically less than 3.5g/L/day), hypertension, oliguria and red cell casts in the urine.
MICA of ramipril
- MOA: inhibits the RAAS system by binding to and inhibiting ACE thereby preventing angiotensin 1 to angiotensin 2 conversion. As these levels fall, there is less activation of angiotensin receptor 1 which mediates vasoconstriction, inflammation, fibrosis and oxidative stress and angiotensin receptor 2 activation which causes vasodilation.
- Indications: hypertension, symptomatic heart failure, prophylaxis post MI, nephropathy
- Contraindications: ACEi plus aliskiren (renin inhibitor) in patients with an eGFR less than 60ml/min/1.732 and in patients with DM.
- Adverse effects: alopecia, angina pectoris, angioedema, arrhythmias, asthenia, chest pain, constipation, dyspnoea, dry mouth, renal impairment, syncope.
MICA of furosemide
- MOA: loop diuretic, promotes diuresis by blocking tubular reabsorption of sodium and chloride in the proximal and distal tubules as well as in the thick ascending LoH. Competitive inhibition of Na/K/Cl cotransporters which prevents Na ion transport from the luminal side into the blood, which increases water excretion.
- Indications: oedema, resistant hypertension
- Contraindications: anuria, comatose and precomatose states associated with liver cirrhosis, renal failure due to nephrotoxic or hepatotoxic drugs, severe hypokalaemia or hyponatraemia.
- Adverse effects: AKI, hepatic disorders, metabolic acidosis, psychiatric disorder, urinary disorders
MICA for warfarin
- MOA: vitamin K antagonist which inhibits vit K production, which plays a role in coagulation. Reduces the synthesis of coag factors.
- Indications: prophylaxis of embolization in rheumatic heart disease and AF, prophylaxis after prosthetic heart valve insertion, prophylaxis and treatment of VTE and pulm embolism, TIA.
- Contraindications: 48h post-partum, haemorrhagic stroke, significant bleeding
- Adverse effects: calciphylaxis, abnormal hepatic function, danger of teratogenicity, haemorrhage, alopecia, nausea, vomiting
MICA for insulin dextrose
- MOA: insulin shifts potassium into cells by stimulating the Na/H antiporter on the cell membrane. This promotes sodium entry into cells, which further leads to activation of the Na/K pump causing an influx of potassium. Dose dependent decline in serum potassium. Dextrose- glucose, exogenous glucose stimulates insulin release from the liver.
- Indications: hyperkalaemia, diluting drugs for IV
- Contraindications: pt at risk of thymine deficiency as it can cause encephalopathy, hyponatraemia, excess use in diabetes.
- Adverse effects: hypoglycaemia, skin reactions, irritation to veins, local pain and thrombosis, has to be given by central line due to irritation.
MICA for iron sucrose
- MOA: dissociates into iron and sucrose, iron is transported as a complex with transferrin to target cells including erythroid precursors. The iron is then incorporated into haemoglobin as the cells mature into RBCs.
- Indications: iron deficiency anaemia
- Contraindications: disturbances in utilisation of iron, iron overload
- Adverse effects: dizziness, flushing, headache, hypertension, hypophosphataemia, hypotension, nausea, skin reactions, altered taste, arrhythmias, arthralgia, bronchospasm.
MICA for EPO
- MOA: binds to its receptor and activates intracellular signal transduction pathways. When it binds to its receptor it induces downstream signalling which activates genes involved in RBC production.
- Indications: anaemia due to CKD, anaemia due to zidovudine in patients with HIV, anaemia due to chemo
- Contraindications: patients unable to receive thromboprophylaxis, pure red cell aplasia following erythropoietin therapy, uncontrolled hypertension.
- Adverse effects: arthralgia, embolism and thrombosis, headache, hypertension, flu like illness, skin reactions, stroke.
MICA for aluminium hydroxide
- MOA: neutralises HCl in gastric secretions, inhibits pepsin by increasing the pH and adsorption. Binds phosphate.
- Indications: heart burn and acid indigestion, hyperphosphataemia.
- Contraindications: known hypersensitive, severe diarrhoea
- Adverse effects: hypomagnesaeia, hypophosphataemia, constipation, anaemia, neurotoxicity- drug related dementia
