NME Flashcards
Cushing’s Disease
A: Cortisol excess: From steroids, pituitary adenoma (most common), ectopic ACTH secretion (small cell lung cancer), adrenal adenoma/carcoma
S: Central obesity, weight gain, easy bruising, myopathy, thin shiny skin, painful purple striae, oedema, excess hair, deep voice, coarse skin, tiredness, depression, headaches.
D: Dexomethasone suppression test (x2 overnight), inferior petrosal sinus sampling, pituitary MRI.
T: Wean off steroids, tumour removal, bilateral adrenalectomy.
Gallstones
A: Classic 5F’s: Fat, Fair, Fertile, Female of Forty. Also hameolytic disorders, resection of distal bowel for Chron’s.
S: 90% asymptomatic.
May cause: biliary colic, cholecystitis, obstructive jaundice, ascending cholangitis.
D: AXR won’t always show it. Ultrasound, ERCP, MRCP.
T: Doesn’t need treating, but complications do.
Oesophageal cancer
A: Upper 2/3 = squamous cell carcinoma
Lower 1/3 = adenocarcinoma (related to Barrett’s oesophagus)
C: Increased incidence in China and Iran. Achalasia, high nitrosamine diet, alcohol, smoking, ingestion caustic substances (acid/alkali), Plummer-vinson syndrome (web of desquamated tissue from oesophagus causing dysphagia, oesophagitis and iron-deficiency anaemia), Howel-Evans syndrome (dominant genetics condition causing hyperkeratosis of hands and oesophageal cancer).
Local spread may cause recurrent laryngeal nerve palsy, Horner’s syndrome or SVC obstruction.
S: worsening dysphagia, cough, SOB, hematemesis, odynophagia, weight loss (squamous).
D: Oesophago-gastric duodenoscopy (visualisation and biopsy), CT to stage.
T: Curative oesophagectomy + chemo, palliative (chemo, radiotherapy, stent).
P: 5-year survival rate 5%.
Irritable bowel syndrome
A: Common in young females, altered motility and visceral hypersensitivity are implicated in causing symptoms.
S: diarrhea, constipation, abdomen pain, bloating, relieved by defecation, passing mucous, increased flatulence
D: Rule out other causes (e.g coeliac).
Rome 3 criteria: Recent abdominal pain/discomfort at least 3 days per month in the last 3 months and associated with two or more out of Improvement on defecation, onset associated with change in stool frequency, onset associated with change in stool apparence.
T: Low FODMAP diet, antidiarrhoeals (e.g codeine), laxatives. If difficult SSRI’s, hypnotherapy and CBT may be needed.
UTI infection
A: Usually E.coli, enterocci, pseudomonas and candida.
S: Suprapubic tenderness, fever, confusion and sepsis. Cystitis, urinary frequency, hameaturia, odorous and cloudy urine.
D: Dipstick, mid-stream collection for microscopy/culture, consider bladder scan for retention as a cause/consequence.
T: Timethoprim, amoxacillin and nitrofurantoin.
If systemic: Gentamicin, ciprofloxacin or augmentin (co-amoxiclav.
IgA nephropathy (Glomerulonephritis)
A: Most common glomerulonephritis worldwide but the cause is still unknown.
S: High BP and invisible hameaturia (may be visible after airway infection) +/- proteinuria are the commonest findings. Some may develop abdominal pains or Henoch-Schonlein purpura (non blanching rash over legs and buttox)
D: Serum IgA may be elevated, renal biopsy is definitive.
T: ACE inhibitors to control BP, immunosupression if severe.
P: Progressive deterioration in renal function, 1/3 develop failure.
Polycystic kidney disease (dominant)
A: Multiple cysts develop on both kidneys, can lead to progressive CKD. From a mutation in PKD-1 (Chromasone 16) or PKD-2 (Chromasone 4) resulting in reduced amounts of polycystin 1 or 2. May be spontaneous.
S: Ballotable large kidneys, maybe an enlarged cystic liver. Abdominal swelling, satiety, loin pain, recurrent infections, CKD.
D: Renal ultrasound is usually diagnostic, genetic testing is rarely needed.
T: ACE inhibitors, treatment of CKD.
Polycystic kidney disease (recessive)
A: Mutations in PKHD-1
S: Problems develop after birth. Lung failure, HTN, polyurea and thirst. Liver failure can lead to internal bleeding and other symptoms.
D: Renal Ultrasound
T: HTN treatment, dialysis and even a transplant.
Biliary Colic
A: Impaction of gallstone in bladder neck (Hartmann’s pouch) or cystic duct.
S: Right upper quadrant and epigastric pain (colicky), eased by moving, worse at night and after eating fatty foods. Nausea, vomiting.
D: ultrasound.
T: analgesia, nil by mouth, cholecystectomy.
C: Can progress to cholecystitis.
Cholecystitis
A: Impaction of gallstone in bladder neck (Hartmann’s pouch) or cystic duct that causes bile to become infected with gut organisms (E.g Ecoli)
S: Fever, tenderness, rebound, guarding RUQ. Pain worse on moving/breathing, radiating to back and right scapula, anorexia, fever.
Patient catches breath on inspiration when hand placed in RUQ (Murphy’s sign), hyperaesthesia below right scapula (Boa’s sign), fullness in RUQ during early inflammation (Zacahry Cope’s sign).
D: Increased WCC, increased CRP, LFT’s may be elevated. Ultrasound.
T: Conservative, nil by mouth, analgesia, cholecystectomy (within first 72 hours or at 6-8 weeks).
Obstructive Jaundice
A: Gallstone leaves gallbladder and becomes impacted in common bile duct.
S: Dark urine, pale stools, RUQ pain, jaundice, anorexia, nausea, pruritis.
D: Increased ALP, conjugated bilirubin, and amylase (If obstructing pancreatic duct).
Ultasound, MRCP, ERCP.
T: ERCP with stone removal/sphincterectomy/stent. Percutaneous transhepatic cholangiography (tube inserted to drain bowel), cholecystectomy.
C: Ascending cholangitis or acute pancreatitis.
Ascending Cholangitis
A: Gallstone impacted in common bile duct causing infection.
S: Charcot’s triad (jaundice, fever, RUQ pain), Reynold’s Pentad (charcots + hypotension and confusion), Womack’s hexad (Reynold’s + rigors)
D: Increased WCC, CRP, ALP, ALT and bilirubin.
Ultrasound.
T: nil by mouth, analgesia, IV antibiotics, ERCP with stone removal/sphincterotamy/stent, percutaneous transhepatic cholangiography (tube inserted to drain bowel), cholecystectomy.
ANCA-associated glomerulonephritis
A: Other autoimmune conditions cause this vasculitis.
S: HTN, invisible haematuria +/- proteinuria. Rapidly rising creatinine and may have reduced urine output. Pulmonary-renal syndrome with alveolar haemorrhage, haemoptysis, non blanching purpuric rash, mononeuritis, CNS involvement, saddle nose, sinus congestion and epistaxis.
D: immunological testing of blood reveals pANCA or c ANCA posotivity and on ELISA testing MPO or PR3 positivitity is found. Renal biopsy shows crescenteric golmerulonephritis.
T: Plasma-exchange, cyclophosphamide and steroids for initial treatment. Mycophenolate motefil and rituximab in some patients. Steroids and azathioprine for maintenace treatment.
Nephrotic syndrome
A: Membranous nephropathy is the commonest cause in adults. But it can be from focal segmental glomerulosclerosis, renal amyloid, diabetes, and minimal change disease (most common in children).
S: Classic triad of proteinuria, hypoalbuminaemia and oedema, (remember: OAP) also an associated hypercholesterolaemia. Patients may also get pitting oedema, ascites and pleural effusions along with swollen legs, weight gain, lethargy and SOB.
D: Urine dipstick, protein:creatinine ratio, renal biopsy.
T: ACE inhibitors, statins and loop diuretics. Treatment may vary depending on cause (e.g steroids are best in minimal change disease).
Post streptococcal golerulonephritis
A: In children after a streptococcal infection.
S: Gross haematuria, oedema, HTN and fever. Malaise, anorexia, abdomen pain.
D: Serum ASO titre to confirm recent streptococcal infection. Increased urea and creatinine, dipstick (proteinuria and RBC casts), decreased C3 levels in blood.
T: Sodium restriction, diuretics, antihypertensives, penicillin for 10 days. Watch out for encephalopathy.
