Abdominal pain- kidneys Flashcards
The 5 functions of the kidney
• Excretion of toxins
• Maintenance of fluid homeostasis
• Maintenance of electrolyte homeostasis
• Regulation of acid base balance
• Production of hormones: Vitamin D, erythropoietin and renin
Nephron: Afferent and efferent arteriolr, Glomerular capillaries
• Afferent arteriole: receives blood from the systemic circulation and helps regulate pressure in the glomerulus
• Glomerular capillaries: receives blood from the afferent arteriole. Fluid and electrolytes are forced across the filtration surface into the Bowmans capsule which receives the filtrate
• Efferent arteriole: outflow from the glomerular capillaries, also helps to regulate pressure in the glomerulus
Nephron: Peritubular capillaries, renal tubules, collecting ducts
• Peritubular capillaries- involved in the transfer of substances with the renal tubules (reabsorption and secretion)
• Renal tubules: can be divided into the proximal tubule, Loop of Henle and the distal tubules. Involved in the transfer of substances with the peritubular capillaries (reabsorption and secretion)
• Collecting ducts: involved in the reabsorption of water and the drainage of filtrate away from the nephron
Factors which act upon the glomerulus (1-3)
• Resistance in the afferent arteriole: reduced by factors such as prostaglandins i.e. PGE2 which promote vasodilation
• Pressure in the glomerular capillaries: influenced by resistance in the afferent and efferent arterioles
• Resistance in the efferent arteriole: resistance is increased by factors such as angiotensin II which promote vasoconstriction
Factors which act upon the glomerulus (4-6)
• Pressure in the Bowmans capsule: increased resistance to outflow, for instance due to lower urinary tract obstruction, reduced glomerular filtration
• Permeability of filtration surface: reduced permeability, for instance due to glomerulonephritis will reduce glomerular filtration
• Glomerular filtration is maintained by ensuring resistance in the efferent arteriole is greater than resistance in the afferent arteriole. Glomerular filtration can only occur if there is sufficient (hydrostatic) pressure in the glomerular capillaries
Conditions which reduce the hydrostatic pressure in the glomerulus
Hypotension, renal artery stenosis, ACEi (loss of efferent arteriolar constriction), NSAID’s (loss of afferent arteriole dilation)
Conditions which increase the hydrostatic pressure in the Bowmans capsule
Urinary tract obstruction
Glomerular filtration and AKI
Loss of glomerular filtration is the key symptom in an AK and causes circulation volume overload, hyperkalaemia and acidosis. Causes of reduced glomerular filtration include hypotension, some drugs and urinary tract obstruction
Tubular secretion in the kidneys
Includes potassium, hydrogen ions, buffers, creatinine and some drugs. Tubular secretion plays an important role in potassium and acid base homeostasis and is important in the pharmacology of some drugs.
Potassium in the kidney
• Reabsorption of potassium in the proximal tubule
• Reabsorption of potassium in the ascending loop of Henle, for instance via the sodium potassium chloride co-transporter (target for loop diuretics)
• Secretion of potassium in exchange for sodium in the distal tubule (stimulated by aldosterone)
Potassium in the body
• Whole body potassium does not equate to serum because most bodily potassium is stored within cells
• Serum levels are determined by cellular uptake and release
• Hormones which cause cellular storage: insulin, catecholamine
• What promotes cellular release: acidosis
Acid-base balance in the kidneys
The glomerular filtration of acids from the blood and the tubular reabsorption of bicarbonate and secretion of hydrogen ions
Kidney- drugs
- Nephrotoxic drugs: Gentomycin- due to a variety of mechanisms including tubular epithelial damage
- Which drugs reduce glomerular filtration: ACEi, NSAID’s, antihypertensives and diuretics
- Opiates like morphine and some anticoagulants like low molecular weight heparin rely on the kidneys to be deactivated or excreted
- Nitrofurantoin and diuretics like furosemide rely on glomerular filtration and tubular secretion in order to work.
Function of the kidneys: synthesis of hormones
• Erythropoietin- done in the peritubular capillary cells of the renal cortex, produced in response to hypoxia and stimulates red blood cell production
• 1,25-hydroxyvitamin D3- plays an important role in calcium and phosphate homeostasis. 25-hydroxyvitamin D3 is filtered at the glomerulus and delivered to the tubular epithelium where it undergoes 1 hydroxylation to produce 1,25-hydroxyvitamin D3 which is the active hormone.
• Renin: its released by cells in the juxtaglomerular apparatus in response to hypotension, sympathetic activation and reduced sodium delivery to the macula densa in the distal tubule.
• Loss of endocrine function can contribute to anaemia and renal bone disease, more associated with CKD
Causes of AKI
• Urinary tract obstruction (lower abdominal pain, palpable urinary bladder, renal angle tenderness)
• Sepsis (fever or features of infection and signs of an abnormal host response such as new confusion, increased respiratory rate, tachycardia and hypotension)
Predisposing factors for AKI
• Vasculopathy (absent peripheral pulses, palpable abdominal aortic aneurysm)
• Frailty (walking sticks, cachexia)
• Stigmata of diabetes mellitus (injection or blood glucose test site marks, cataracts, obesity (type 2 diabetes), skin thickening, foot ulcers, special footware and mobility aids, fungal infections)
Complications of an AKI
• Fluid overload (raised JVP, peripheral oedema, bibasal crackles and a third heart sound).
• Acidosis (Kussmaul breathing pattern)
Causes of an AKI
• Pre-renal – Renal hypoperfusion due to relative hypotension (sepsis, dehydration, heart failure) or loss of hydrostatic pressure at the glomerulus (often drug mediated). Sustained renal hypoperfusion will lead to acute tubular necrosis.
• Intrarenal – Glomerular pathology (eg autoimmune disease, drugs, infection, primary glomerulonephritis - uncommon), tubular pathology (eg acute tubular necrosis - for instance due to a prolonged episode of relative hypotension), interstitial disease (drugs, autoimmune disease, infiltration).
• Post renal – Urinary tract obstruction at whatever level; ureteric, bladder outflow, urethra.
Classifications of an AKI- stage 1
Creatinine rise of 26 micromol or more within 48 hours. OR. Creatinine rise of 50-99% from baseline within days. OR. Urine output <0.5mL/kg/h for more than 6 hours
Classifications of AKI: stage 2
100-199% creatinine rise from baseline within 7 days. OR. Urine output <0.5mL/kg/hour for more than 12 hours
Classification of AKI: stage 3
200% or more creatinine rise from baseline within 7 days. OR. Creatinine rise to 3.54 micromol/L or more with an acute rise of 26 micromol/L or more within 48 hours or 50% or more rise within 7 days. OR. Urine output <0.3 mL/kg/hour for 24 hours or anuria for 12 hours
Complications of stage 3 AKI
• Fluid overload – On clinical examination, look for peripheral oedema, bibasal crepitations suggestive of pulmonary oedema, a raised JVP and a third heart sound
• Acidaemia – This can rapidly be excluded with a venous blood gas. A laboratory bicarbonate sample may also be helpful.
• Hyperkalaemia - This can rapidly be excluded with a venous blood gas, and confirmed on a laboratory sample.
Investigations for an AKI
• Bedside: urine dip to assess for albuminuria or haematuria which suggests a glomerular cause. Venous blood gas for estimation of serum potassium and acid base status
• Lab tests: FBC, U&E’s, LFT and bone profile to assess for anaemia, infection, hyperkalaemia, hypocalcaemia and hyperphosphataemia. Check creatinine kinase if history of falls to exclude rhabdomyolysis
• Imaging: USS kidney-ureters-bladders
Second line investigations for an AKI
• Quantification of albumin:creatinine ratio if there is evidence of proteinuria
• Myeloma screen
• Autoantibody profile (ANCA, anti-GBM and anti-dsDNA and complement levels to assess for systemic processes like vasculitis
• Virology screen- rarely AKI is associated with HIV and hepatitis, screen is required if the patient needs dialysis
• Renal biopsy
How best to monitor changes in AKI
In AKI there is a lag between improvement in glomerular filtration and the fall in serum creatinine. Raw trends in serum creatinine and urine output are therefore better indicators of changes in renal function in AKI
Approach to hyperkalaemia
1.Establish if there is myocardial toxicity by looking at his ECG - tented T wave and wide QRS complexes
2. Stabilise the myocardium if necessary with calcium gluconate
3.Reduce serum potassium levels by driving potassium in to cells with salbutamol nebulisers and IV insulin with glucose
4.Promote removal of potassium if feasible and appropriate, for instance by supporting urine output with intravenous fluids, or by seeking help early for consideration of renal replacement therapy if poor urine output. Consider dialysis
5.Correct underlying cause
6. Ensure subsequent follow up and monitoring of potassium
Distinguishing an AKI from a CKD
• An AKI is less than 4 weeks
• A discreet insult suggests AKI, a history of progressive malaise over several months with abnormal kidney function suggests CKD
• Creatinine trends over a number of days- renal function tends to improve in AKI
• Hypocalaemia and Hyperphophataemia imply CKD
• Ultrasound- small kidneys with kidney disruption suggest CKD
Treatment for AKI is generally supportive
Systematic approach to interpreting an abdominal x-ray
• Patient details: name, DOB, hospital number, date and time of radiograph
• Projection: anteroposterior with the patient supine
• Technical adequacy: the entire abdomen should be included, hemidiaphragm down to symphysis pubis and hernia orifices
• Obvious abnormalities i.e. small bowel dilation
• Systematic review (Bowel gas pattern, soft tissue, bones, calcification and other): start from the rectum and go backwards i.e. large bowel, small bowel. Then look at the liver, spleen, kidneys, bladder and psoas edges. Finally look at the bones, and for calcification and foreign bodies
Appearance on x-ray odf bowels
• Large bowel: Presence of haustra (block like appearance usually not across the full bowel), may contain faeces (mottled appearance), <6cm in diameter or <9cm for the caecum
• Small bowel: usually lies centrally, valvulae conniventes (mucosal folds across full width of the bowel), <3cm in diameter
Calcification
• Calcification visible on AXR can include kidney stones and gallstones
• Radio-opaque foreign bodies such as surgical clips or ingested foreign bodies can also be seen
• Other calcifications include phleboliths- venous calcification. These are often seen in the pelvis and are mistaken for kidney stones
• Vascular structures like the aorta can also be calcified
X-ray features of small bowel obstruction
• Dilated loops of small bowel proximal to obstruction
• Often centrally located with dilation >3cm
• Valvulae conniventes are visible
Clinical features of small bowel obstruction
• Abdominal pain
• Abdominal distension
• Vomiting
• Absolute constipation (including flatulence)
• Lack of bowel sounds or tickling bowel sounds
Causes of small bowel obstruction
Adhesions, Hernias, Crohns, Caecal cancer
Large bowel obstruction: abdominal x-ray
• Colonic distension proximal to the obstruction
• Dilation of >6cm for colon, >9cm for caecum
• Haustra for visible
Large abdominal obstruction: Clinical features
• Abdominal pain
• Abdominal distension
• Vomiting
• Absolute constipation (including flatulence)
• Lack of bowel sounds or tinkling bowel sounds
Risk factors and causes of large bowel obstruction
Risk factors: Such as colorectal cancer (weight loss, altered habit), constipation or diverticular disease
Causes: Colorectal cancer, faecal impaction, diverticulitis, volvulus
Sigmoid volvulus and Paralytic ileus
Sigmoid volvulus- due to a twist at the base of the sigmoid mesentery which is in a fixed position in the left iliac fossa. Results in the appearance of a giant ‘coffee bean’
Paralytic ileus: all intestinal loops are generally dilated and there is no clear point of obstruction. Causes include trauma, surgery and infections leading to peritonitis.
Constipation and thumbprinting
Constipation: mottled opacities seen within the bowel loops suggestive of significant faecal loading.
Thumbprinting: shows extensive bowel wall thickening throughout the entire colon. Thickening of the haustral folds results in a ‘thumbprinting’ appearance. This is sometimes seen in acute inflammation caused by inflammatory bowel disease.
Toxic megacolon
Shows significant colon dilation and there are extensive mucosal islands indicating bowel wall inflammation. This is caused by C.difficile colitis, ulcerative colitis or Crohns disease
Chest x-rays for abdominal pain
• Pneumoperitoneum: in cases of suspected bowel perforation, there is pneumoperitoneum (free air under the diaphragm). Can be seen after laparoscopic surgery where the abdomen has been insufflated with carbon dioxide
• Riglers sign: both the inside and outside wall of the of the bowel are visible due to free air in the abdomen.
Chilaiditi’s phenomenon
In patients with a small liver (cirrhosis) or hyperextended lungs (COPD) the upper abdomen can be filled by bowel which can mimic free air in the abdomen
GORD
Where acid from the stomach refluxes through the lower oesophageal sphincter. The oesophagus has squamous epithelial lining meaning its more sensitive to stomach acid, the stomach has columnar epithelial lining so its protected from stomach acid.
Symptoms of GORD
Heartburn, acid regurgitation, retrosternal or epigastric pain, bloating, nocturnal cough, hoarse voice
GORD: Diagnosis- Endoscopy
• can be used to assess for peptic ulcers, oesophageal or gastric malignancy
• Evidence of a GI bleed i.e. melaena or coffee ground vomiting needs admission for urgent endoscopy
Red flags for two week cancer referral: GORD
• Dysphagia (difficulty swallowing) at any age gets a two week wait referral
• Aged over 55 (this is generally the cut off for urgent versus routine referrals)
• Weight loss
• Upper abdominal pain / reflux
• Treatment resistant dyspepsia
• Nausea and vomiting
• Low haemoglobin
• Raised platelet count
GORD- Management: lifestyle advice
• Reduce tea, coffee and alcohol
• Weight loss
• Avoid smoking
• Smaller, lighter meals
• Avoid heavy meals before bed time
• Stay upright after meals rather than lying flat
GORD- Management: Medication and surgery
• Acid neutralising medication when required: Gaviscon, Rennie
• Proton pump inhibitors (reduce acid secretion in the stomach): Omeprazole, Lansoprazole
• Rantidine: alternative to PPI, H2 receptor antagonist (antihistamine), reduces stomach acid
Surgery for reflux is laparoscopic fundoplication. It involves tying the fundus of the stomach around the lower oesophagus to narrow the lower oesophagus sphincter
H.pylori
A gram negative aerobic bacteria which lives in the stomach, causes gastritis, ulcers and increases the risk of stomach cancer. Causes breaks in the mucosa exposing the epithelial cells to acid. Also produces ammonia which directly damages epithelial cells. You need two weeks without using a PPI before testing for H.pylori for an accurate result.
Testing for H.pylori
• Urea breath test- using carbon 13
• Stool antigen test
• Rapid urease test can be performed during endoscopy
Eradication of H.pylori
Triple therapy with a PPI (omeprazole) plus 2 antibiotics (i.e. amoxicillin and clarithromycin) for 7 days
Barretts oesophagus
• Acid reflux causes metaplasia resulting in the change of squamous to columnar epithelium
• Risk factor for adenocarcinoma of the oesophagus, monitored by regular endoscopy
•,Treatment with a PPI (omeprazole)
• Ablation therapy using photodynamic therapy, laser therapy or cryotherapy destroys the epithelium so tis replaced with normal cells
Causes of hypothyroidism
• Hashimoto’s Thyroiditis: an autoimmune inflammation of the thyroid gland, antithyroid peroxidase (anti-TPO) antibodies and antithyroglobulin antibodies. Initially causes a goitre then atrophy of the thyroid gland
• Iodine deficiency- common in the developing world
• Secondary to treatment of Hyperthyroidism: Carbimazole, Propylthiouracil, Radioactive iodine, Thyroid surgery
• Medications: Lithium and Amiodarone
• Central causes (secondary hypothyroidism): where the pituitary gland fails to produce enough TSH. In tumours, infection, vascular i.e. Sheehan syndrome and radiation
Presentation and features of hypothyroidism
Weight gain, fatigue, dry skin, coarse hair and hair loss, fluid retention (oedema, pleural effusion, ascites), heavy or irregular periods, constipation
Management of Hypothyroidism
Replacement of thyroid hormones with oral levothyroxine (synthetic T4) and metabolises to T3 in the body. The dose is titrated till TSH levels are normal. If the TSH level is high, the dose is too low and needs to be increased. If the TSH is low, the dose is too high and needs to be reduced.
Hyperthyroidism
Where there is over production of thyroid hormone by the thyroid gland. Thyrotoxicosis is an abnormal and excessive quantity of thyroid hormone in the body
Types of Hyperthyroidism
• Primary hyperthyroidism: when the thyroid is behaving abnormally and producing excessive thyroid hormone
• Secondary hyperthyroidism: where the thyroid is producing excessive thyroid hormone due to overstimulation by TSH (thyroid stimulating hormone), in the hypothalamus or pituitary
• Graves disease: TSH receptor antibodies mimic TSH and stimulate TSH receptors on the thyroid. Most common cause of hyperthyroidism
• Toxic multinodular goitre: nodules develop on the thyroid gland and produce excessive thyroid hormone
Epohthalmos
Bulging of the eyeball out of the socket sue to graves disease. Due to inflammation, swelling and hypertrophy of the tissue behind the eyeball forcing it forwards
Pretibial myxoedema
Deposits of mucin under the skin on the anterior aspect of the leg (pre-tibial area). Giving a discoloured, waxy oedematous appearance to the skin. Its specific to Graves disease and is a reaction to TSH receptor antibodies.
Causes of Hyperthyroidism
• Grave’s disease
• Toxic multinodular goitre
• Solitary toxic thyroid nodule
• Thyroiditis
Universal features of Hyperthyroidism
Anxiety and irritability, Sweating and heat intolerance, Tachycardia, Weight loss, Fatigue, Frequent loose stools, Sexual dysfunction.
Unique features of graves disease
• Diffuse goitre (without nodules)
• Graves eye disease
• Bilateral exophthalmos
• Pretibial myxoedema
Unique features of toxic multinodular goitre
• Goitre with firm nodules
• Most patients are over 50
• Second most common cause of thyrotoxicosis (after Grave’s)
Solitary toxic thyroid nodule
Where a single abnormal thyroid nodule acts alone to release thyroid hormones, the nodules are usually benign adenomas. Treated with surgical removal of the nodule.
De Quervains thyroiditis
This describes the presentation of a viral infection with fever, neck pain and tenderness, dysphagia and features of hyperthyroidism. There is a hyperthyroid phase followed by a hypothyroid phase as the TSH level falls due to negative feedback. It is a self-limiting condition and supportive treatment with NSAIDs for pain and inflammation and beta-blockers for symptomatic relief of hyperthyroidism is usually all that is necessary.
Thyroid storm
A rare presentation of hyperthyroidism. It is also known as “thyrotoxic crisis”. It is a more severe presentation of hyperthyroidism with pyrexia, tachycardia and delirium. They may need supportive care with fluid resuscitation, anti-arrhythmic medication and beta-blockers.
Hyperthyroidism treatment- Carbimazole and Propylthiouracil
• Carbimazole: the first line anti-thyroid drug, usually successful in causing normal thyroid function in Graves disease after 4-8 weeks. Once the patient has normal thyroid hormone levels they continue on maintenance carbimazole and either the dose it titrated to maintain normal level or the dose is sufficient to block all production and the patient takes levothyroxine (block and replace)
• Propylthiouracil- second line
Hyperthyroidism treatment- radioactive iodine and beta blockers
• Radioactive iodine- the radiation destroys a small proportion of the thyroid cells, remission takes 6 months and patients can be left hypothyroid after wards and require levothyroxine replacement
• Beta-blockers i.e. propranolol: block the adrenaline related symptoms of hyperthyroidism. Control the symptoms but don’t treat the underlying problem, whilst definitive treatment takes time to work. Particularly useful in a thyroid storm
Contradictions of radioactive iodine
• Must not be pregnant and are not allowed to get pregnant within 6 months
• Must avoid close contact with children and pregnant women for 3 weeks (depending on the dose)
• Limit contact with anyone for several days after receiving the dose
Surgery for Hyperthyroidism
Remove the whole thyroid or toxic nodules, stops the productive of thyroid hormones but the patient will be left hypothyroid post thyroidectomy and will require levothyroxine replacement for life.
