health facts

Excessive menstrual loss: menorrhagia

2009-05-24T23:37:00.000-07:00

Menorrhagia can be due to uterine or systemic disorders.

Some differential diagnoses and typical outline evidence

Fibroids	Suggested by: (sometimes) urinary frequency, constipation, recurrent abortion, infertility.
	Confirmed by: pelvic examination, ultrasound or CT.
	Management: OHCS pp276â€“7.
Endometrial carcinoma	Suggested by: abnormal uterine bleeding, blood-stained vaginal discharge, postmenopausal bleeding.
	Confirmed by: pelvic ultrasound, tissue sampling of endometrium, hysteroscopy.
	Management: OHCS pp278â€“9.
Pelvic endometriosis	Suggested by: dysmenorrhoea, dyspareunia, infertility, pelvic mass.
	Confirmed by: laparoscopy.
	Management: OHCS p288.
Chronic pelvic inflammatory disease	Suggested by: lower abdominal pain, fever, vaginal discharge, dysuria, â†‘ ESR and â†‘ CRP, leucocytosis.
	Confirmed by: high vaginal swab, pelvic ultrasound, Â± laparoscopy.
	Management: OHCS p286.
Intrauterine contraceptive device	Suggested by: history of its insertion Â± painful periods.
Intrauterine contraceptive device	Confirmed by: symptoms subside after removal of IUCD.
Primary hypothyroidism	Suggested by: cold intolerance, tiredness, constipation, bradycardia.
	Confirmed by: â†‘ TSH, â†“ FT4.
	Management: OHCM p306.
Bleeding diathesis	Suggested by: family history, tendency to bleed, easy bruising.
	Confirmed by: abnormal clotting screen.
	Management: OHCM pp644â€“9.

Sudden diarrhoea, fever and vomiting

2009-05-24T23:36:00.002-07:00

Sudden diarrhoea with fever, Â± malaise, colicky abdominal pain, vomiting.

Some differential diagnoses and typical outline evidence

*Antibiotic induced bacterial opportunist: Clostridium difficile*	Suggested by: diarrhoea with a history of recent antibiotic therapy, â†‘ WBC.
	Confirmed by: Cl. difficile toxin in *stool culture*.
	Management: OHCM pp218, 219.
*Viral gastroenteritis:* Rotavirus	Suggested by: diarrhoea in children <5>
*Viral gastroenteritis:* Rotavirus	Management: OHCM p540.
Norwalk virus	Suggested by: diarrhoea in older children and adults, symptoms resolve in 2 weeks.
*Food poisoning/ toxins Staphylococcus aureus*	Suggested by: eating â€˜doubtfulâ€™ meat, incubation period <6>
	Confirmed by: isolation of Staph. aureus from examination of suspected food.
	Management: OHCM p556.
*Bacillus cereus*	Suggested by: eating â€˜doubtfulâ€™ rice, incubation period <6>
	Confirmed by: *stool microscopy* and culture.
	Management: OHCM pp556, 221.
*Vibrio para haemolyticus*	Suggested by: â€˜doubtfulâ€™ seafood, incubation period 16â€“72 hours.
	Confirmed by: *stool microscopy and culture*.
	Management: OHCM pp596, 621.
*Clostridium perfringens*	Suggested by: eating â€˜doubtfulâ€™ meat, incubation period 8â€“16 hours, abdominal cramps, little vomiting.
*Clostridium perfringens*	Confirmed by: organism *isolation from faeces or suspected food*.
*Botulism*	Suggested by: eating â€˜doubtfulâ€™ canned food, incubation period 18â€“36 hours, but may vary from 4 hours to 8 days, abdominal cramps, dry mouth, diplopia, progressive paralysis.
	Confirmed by: C. botulinum *toxin in serum or faeces;* C. botulinum toxin *isolation from suspected food*.
	Management: OHCM pp591, 830.
*Salmonella typhimurium*	Suggested by: eating â€˜doubtfulâ€™ meat, egg, poultry. Fever (with relative bradycardia), headache, dry cough.
	Confirmed by: *stool microscopy and culture*.
	Management: OHCM p596.

Acute lower central (hypogastric) abdominal pain

2009-05-24T23:36:00.001-07:00

Some differential diagnoses and typical outline evidence

Infective or ulcerative colitis	Suggested by: abdominal pain, diarrhoea with blood and mucus.
	Confirmed by: *stool microscopy and culture, colonoscopy*.
	Management: OHCM pp218â€“19, 244â€“5.
Large bowel obstruction	Suggested by: severe distension, late vomiting, visible peristalsis, resonant percussion, increased bowel sounds. Supine *AXR* showing peripheral abdominal large bowel shadow (with haustra partly crossing the lumen). Fluid levels on erect film.
	Confirmed by: *abdominal ultrasound and laparotomy findings*.
	Management: OHCM p492.
Cystitis	Suggested by: frequency, urgency, dysuria, Â± haematuria.
	Confirmed by: *MSU*for microscopy and culture.
	Management: OHCS p262.
Pelvic inflammatory disease	Suggested by: vaginal discharge, dysuria, dyspareunia, pelvic tenderness on moving cervix, â†‘ ESR and CRP. WBC: leucocytosis.
	Confirmed by: *High vaginal swab, pelvic ultrasound, Â± laparoscopy*.
	Management: OHCS p286.
Pelvic endometriosis	Suggested by: dysmenorrhoea, ovulation pain, dyspareunia, infertility, pelvic mass.
	Confirmed by: *laparoscopy*.
	Management: OHCS p288.
Ectopic pregnancy	Suggested by: constant unilateral pain Â± referred shoulder pain, amenorrhoea, vaginal bleeding (usually less than normal period), faintness with an acute rupture.
	Confirmed by: pregnancy test +ve, bimanual examination reveals slightly enlarged uterus, *pelvic ultrasound* shows empty uterus with thickened decidua.
	Management: OHCS p262â€“3.

Acute lateral abdominal pain

2009-05-24T23:35:00.004-07:00

Some differential diagnoses and typical outline evidence

Pyelonephritis	Suggested by: pain in loin (upper lateral), rigors, fever, vomiting, frequency of micturition, renal angle tenderness
	Confirmed by: *FBC:* leucocytosis. *MSU:* pyuria, urine culture and sensitivities.
	Management: OHCM pp258, 262, 276.
Renal calculus	Suggested by: renal colic mainly in loin (upper lateral), haematuria.
	Confirmed by: *urinalysis, renal ultrasound, IVU, CT/MRI*.
	Management: OHCM p264.
Ureteric calculus	Suggested by: renal colic, moving from loin (upper lateral) down to *RLQ*, haematuria.
	Confirmed by: *urinalysis, renal ultrasound, IVU, CT/MRI*.
	Management: OHCM p264.
Appendicitis	Suggested by: pain initially central, then radiating to right lower quadrant, anorexia, low grade fever, constipation. *RLQ* tenderness and guarding.
	Confirmed by: Inflamed appendix at laparotomy
	Management: OHCM p476.
Salpingitis	Suggested by: fever, nausea, vomiting, muco-purulent cervical discharge, irregular menses. Bilateral lower abdominal tenderness and guarding.
Salpingitis	Confirmed by: *FBC:* leucocytosis. *High vaginal swab, laparoscopy*.

Acute central abdominal pain

2009-05-24T23:35:00.003-07:00

Some differential diagnoses and typical outline evidence

Small bowel obstruction	Suggested by: vomiting, constipation with complete obstruction.
	Confirmed by: *AXR* shows small bowel loops and fluid levels.
	Management: OHCM p492.
Crohn's disease	Suggested by: chronic diarrhoea with abdominal pain, weight loss, palpable RLQ mass or fullness, mouth ulcers.
	Confirmed by: *colonoscopy with biopsy, barium studies* showing â€˜skip lesionsâ€™, string sign in advanced cases.
	Management: OHCM p246.
Mesenteric artery occlusion	Suggested by: vomiting, bowel urgency, melaena, diarrhoea.
	Confirmed by: *mesenteric angiography, exploratory laparotomy*.
	Management: OHCM p488.
Abdominal aortic dissection	Suggested by: tearing pain Â± shock Â± hypotension and peripheral cyanosis.
	Confirmed by: *ultrasound or CT abdomen*.
	Management: OHCM p480.

Acute pain in the upper abdomen

2009-05-24T23:35:00.001-07:00

Trying to localise pain in the upper abdomen to the right, left or middle may be difficult for the patient.

Some differential diagnoses and typical outline evidence

Oesophagitis	Suggested by: retrosternal pain, heartburn.
	Confirmed by: *oesophagogastroscopy*.
	Management: OHCM p216.
Acute coronary syndrome (unstable angina or infarction)	Suggested by: chest tightness or pain on exertion.
	Confirmed by: *exercise ECG* Â± *coronary angiography* if troponin normal, or later if troponin â†‘.
	Management: OHCM pp120â€“4, 782.
Hiatus hernia	Suggested by: heartburn, worsens with stooping or lying, relieved by antacids.
	Confirmed by: *oesophagogastroscopy, barium meal*.
	Management: OHCM p532.
Gastritis	Suggested by: epigastric pain, dull or burning discomfort, nocturnal pain
	Confirmed by: *oesophagogastroscopy, barium meal and pH study*.
	Management: OHCM p214.
Gallstone colic (with no acute inflammation or infection)	Suggested by: jaundice, biliary colic, pain in epigastrium or RUQ radiating to right lower scapula. No fever or â†‘WBC.
	Confirmed by: *ultrasound of gallbladder and biliary ducts*.
	Management: OHCM pp484, 485.
Acute cholecystitis	Suggested by: fever, guarding and positive Murphy's sign (abrupt stopping of inspiration when the palpating hand meets the inflamed gall bladder descending with the liver from behind the sub-costal margin on the right sideâ€”but not on the left side). â†‘WBC.
	Confirmed by: *ultrasound gallbladder and biliary ducts*.
	Management: OHCM p484.
Duodenal ulcer	Suggested by: epigastric pain, dull or burning discomfort, typically relieved by food, nocturnal pain.
	Confirmed by: *oesophagogastroscopy, barium meal and pH study:* (Helicobacter pylori often present in mucosa or serology).
	Management: OHCM p214.
Gastric ulcer	Suggested by: epigastric pain, dull or burning discomfort, typically exacerbated by food, nocturnal pain.
	Confirmed by: *oesophagogastroscopy, barium meal and pH study*.
	Management: OHCM p214.
Gastric carcinoma	Suggested by: marked anorexia, fullness, pain, Troisier's sign (a â€˜Virchow'sâ€™ node i.e. large lymph node in the left supraclavicular fossa).
	Confirmed by: *upper GI endoscopy with biopsy*.
	Management: OHCM p508.
Pancreatitis	Suggested by: pain radiating straight through to the back, better on sitting up or leaning forward.
	Confirmed by: â†‘*serum amylase, CT pancreas*.
	Management: OHCD p478.

Sore throat

2009-05-24T23:34:00.001-07:00

With odynophagiaâ€”painful swallowing.

Some differential diagnoses and typical outline evidence

Viral pharyngitis	Suggested by: sore throat, pain on swallowing, fever, cervical lymphadenopathy and injected fauces. â†‘ lymphocytes, leucocytes normal in WBC.
Viral pharyngitis	Confirmed by: negative *throat swab* for bacterial culture, self-limiting: resolution within days.
Acute follicular tonsillitis (streptococcal)	Suggested by: severe sore throat, pain on swallowing, fever, enlarged tonsils with white patches (like strawberries and cream). Cervical lymphadenopathy especially in angle of jaw. Fever, â†‘ leucocytes in WBC.
	Confirmed by: *throat swab* for culture and sensitivities of organisms.
	Management: OHCS p564.
Infectious mononucleosis (glandular fever) due to Epsteinâ€“Barr virus	Suggested by: very severe throat pain with enlarged tonsils covered with creamy membrane. Petechiae on palate. Profound malaise. Generalised lymphadenopathy, splenomegaly.
	Confirmed by: â†‘ atypical lymphocytes in *WBC. Paulâ€“Bunnel* test positive. *Viral titres*.
	Management: OHCM p570.
Candidiasis of buccal or oesophageal mucosa	Suggested by: painful dysphagia, white plaque, history of immunosuppression/diabetes/recent antibiotics.
	Confirmed by: *oesophagoscopy* showing erythema and plaques, *brush cytology* Â± *biopsy* shows spores and hyphae.
	Management: OHCM p210.
Agranulocytosis	Suggested by: sore throat, background history of taking a drug or contact with noxious substance.
	Confirmed by: low or absent neutrophil count.
	Management: OHCM p662.
Meningococcal meningitits	Suggested by: headache, photophobia, vomiting, sore throat, red fauces without purulent patches, neck stiffness. High blood neutrophil count.
	Confirmed by: lumbar puncture showing pus or neutrophil count and organisms on microscopy or culture.
	Management: OHCM p370.

Obstructive jaundice

2009-05-24T23:33:00.002-07:00

Some differential diagnoses and typical outline evidence

	Suggested by: jaundice with pale stools and dark urine. Bilirubin in urine (i.e. conjugated and thus soluble).
	Confirmed by: â†‘*serum conjugated bilirubin* and thus *urine bilirubin* but no â†‘urobilinogen in urine. Markedly (â†‘â†‘) *alkaline phosphatase*, but less abnormal (â†‘) liver function tests and â†‘â†‘GT.
	Management: OHCM p484.

Some differential diagnoses and typical outline evidence

Common bile duct stones	Suggested by: pain in RUQ Â± Murphy's sign.
	Confirmed by: *ultrasound liver*: dilatation of biliary ducts.
	Management: OHCM pp484, 485.
Cancer of head of pancreas	Suggested by: progressive painless jaundice, palpable gall-bladder (Courvoisier's law), weight loss.
	Confirmed by: *ultrasound liver:* dilatation of biliary ducts. *CT pancreas, ERCP* or *MRCP:* obstruction within head of pancreas.
	Management: OHCM p248.
Sclerosing cholangitis	Suggested by: progressive fatigue, pruritus.
	Confirmed by: â†‘*ALP. Ultrasound liver: no gallstones. ERCP*: (beading of the intra-and extra-hepatic biliary ducts)
	Management: OHCM p238.
Primary biliary cirrhosis	Suggested by: scratch marks, non-tender hepatomegaly, Â± splenomegaly, xanthelasmata and xanthomas, arthralgia.
	Confirmed by: +ve *anti-mitochondrial antibody, â†‘â†‘serum IgM: infiltrate around hepatic bile ducts and cirrhosis on liver biopsy*.
	Management: OHCM p238.
Drug-induced	Suggested by: drug history of oral contraceptive pill, phenothiazines, anabolic steroids, erythromycin, etc.
	Confirmed by: symptoms receding when drug discontinued.
	Management: OHCM p223.
Pregnancy (last trimester)	Suggested by: jaundice during pregnancy.
	Confirmed by: resolution following delivery.
	Management: OHCS p26.
Alcoholic hepatitis or cirrhosis	Suggested by: history of excess alcohol intake, presence of spider naevi and other signs of chronic liver disease.
	Confirmed by: *ultrasound* or *CT liver, liver biopsy*, improvement if abstinence.
	Management: OHCM p254.
Dubinâ€“Johnson syndrome (decreased excretion of conjugated bilirubin, see OHCM p722)	Suggested by: intermittent jaundice, and associated pain in the right hypochondrium. No hepatomegaly.
	Confirmed by: normal *ALP, normal LFT. â†‘urinary bilirubin. Pigment granules on liver biopsy*.

Hepatocellular jaundice (due to hepatitis or very severe liver failure)

2009-05-24T23:33:00.001-07:00

Some differential diagnoses and typical outline evidence

	Suggested by: onset of jaundice over days or weeks, stools and urine pale or dark but dark urine.
	Confirmed by: â†‘serum (conjugated) *bilirubin* and thus â†‘*urine bilirubin. Normal urine urobilinogen. Liver function tests all increasingly abnormal esp. â†‘(ALT*.

Some differential diagnoses and typical outline evidence

Acute (viral) hepatitis A	Suggested by: tender hepatomegaly.
	Confirmed by: presence of *hepatitis A IgM antibody* suggests acute infection.
	Management: OHCM p576.
Acute hepatitis B	Suggested by: history of iv drug user, blood transfusion, needle punctures, tattoos, tender hepatomegaly.
	Confirmed by: presence of *HBsAg in serum*.
	Management: OHCM p576.
Acute hepatitis C	Suggested by: history of iv drug user, blood transfusion, tender hepatomegaly.
	Confirmed by: presence of *anti-HCV antibody, HCV-PCR*.
	Management: OHCM p576.
Alcoholic hepatitis	Suggested by: history of drinking, presence of spider naevi and other signs of chronic liver disease. *AST:ALT* ratio >2.
	Confirmed by: resolution with abstinence.
	Management: OHCM p223.
Drug-induced hepatitis e.g. paracetamol halothane	Suggested by: drug history, recent surgery.
	Confirmed by: drug levels improvement after stopping the offending drug.
	Management: OHCM p223.
Primary hepatoma	Suggested by: weight loss, abdominal pain, RUQ mass.
	Confirmed by: ultrasound/CT liver, liver biopsy, â†‘alpha-fetoprotein.
	Management: OHCM pp242, 243.
Right heart failure	Suggested by: â†‘JVP, hepatomegaly, ankle oedema.
	Confirmed by: *CXR:* large heart. *Echocardiogram:* dilated right ventricle.
	Management: OHCM pp136â€“9.
Glandular fever (infectious mononucleosis)	Suggested by: cervical lymphadenopathy, sharp edge, Â± Splenomegaly, Â± jaundice.
	Confirmed by: *Paul-Bunnell, +ve heterophil antibody* test.
	Management: OHCM p570.

Hepatic jaundice due to congenital enzyme defect

2009-05-24T23:32:00.002-07:00

Some differential diagnoses and typical outline evidence

	Suggested by: jaundice. Normal looking stools and normal looking urine.
	Confirmed by: â†‘*serum bilirubin* (unconjugated), but no (conjugated) bilirubin in urine. No *urobilinogen in urine* and *normal haptoglobin. Normal liver function tests*.

Some differential diagnoses and typical outline evidence

Gilbert's syndrome (Normal lifespan)	Suggested by: above evidence of impaired conjugation, asymptomatic.
	Confirmed by: demonstration of unconjugated hyperbilirubinaemia with normal LFT, no haemolysis. Rise in *bilirubin when fasting and after nicotinic acid*.
	Management: OHCM p724.
Criglerâ€“Najjar syndrome (Type I: Severe, neonatal and often fatal Type II: Normal lifespan)	Suggested by: above evidence of impaired conjugation.
	Confirmed by: unconjugated hyperbilirubinaemia with otherwise normal LFT, no haemolysis. No rise in *bilirubin when fasting or after nicotinic acid*.
	Management: OHCM pp222, 720.

Pre-hepatic jaundice due to haemolysis

2009-05-24T23:32:00.001-07:00

Suggested by: jaundice and anaemia (the combination often seen as â€˜lemonâ€™ or pale yellow). Normal dark stools and normal looking urine.
	Confirmed by: â†‘(unconjugated and thus insoluble) *serum bilirubin* but normal (conjugated and thus soluble) bilirubin and in turn no bilirubin in urine. Evidence of haemolysis as: â†‘*urinary urobilinogen* and â†“*serum haptoglobin. â†‘Reticulocyte count. Normal liver function tests, Hb*â†“.

Some differential diagnoses and typical outline evidence

Hereditary haemolytic anaemia	Suggested by: family history, anaemia, splenomegaly, leg ulcers.
	Confirmed by: above evidence of haemolysis, â†‘*osmotic fragility; enzyme deficiency e.g. G6PD, pyruvate kinase*.
	Management: OHCM pp624, 636, 638.
Acquired haemolytic anaemia	Suggested by: sudden onset, in later life, and on medication.
	Confirmed by: above evidence of haemolysis, *blood film, +ve Coombsâ€™ test* in autoimmune type.
	Management: OHCM pp624, 636, 638.
Septicaemic haemolysis due to pneumonia, UTI, etc	Suggested by: fever, Â± shock symptoms and signs of infection.
	Confirmed by: evidence of haemolysis, *blood culture* positive.
	Management: OHCM pp624, 636, 638.
Malaria	Suggested by: recent travel to malaria zone, periodic paroxysms of rigors, fever, sweating, nausea.
	Confirmed by: Plasmodium in *blood smear*.
	Management: OHCM pp549, 560â€“3

Jaundice

2009-05-24T23:28:00.001-07:00

This can be a symptom reported by the patient or a physical sign. It is confirmed by â†‘bilirubin in the plasma. Yellow sclerae and skin usually becomes visible when serum bilirubin level is >35Âµmol/L, so urine tests may provide the first clue. First subdivide into the 5 leads below. Remember that haemolysis causes â†‘urinary urobilinogen and â†“serum haptoglobin. Hepatic failure causes â†‘serum unconjugated bilirubin but intrahepatic or extra hepatic biliary obstruction results in â†‘serum conjugated bilirubin.

Some differential diagnoses and typical outline evidence

Carotinaemia	Suggested by: onset over months. Skin yellow with white sclerae, normal stools and normal urine. Diet rich in yellow vegetables/fruits).
Carotinaemia	Confirmed by: no bilirubin, no *urobilinogen* in the urine and normal *serum bilirubin. Normal liver function tests*. Response to diet change.
â€˜Pre-hepaticâ€™ jaundice due to haemolysis	Suggested by: jaundice and anaemia (the combination seen as â€˜lemonâ€™ or pale yellow). Normal dark stools and normal looking urine.
	Confirmed by: â†‘ (unconjugated and thus insoluble) *serum bilirubin* but normal (conjugated and soluble) bilirubin and thus no â†‘bilirubin in urine. â†‘*urobilinogen in urine* and â†“*serum haptoglobin. Normal liver function tests. â†‘Reticulocyte count, Hb*â†“.
	Management: OHCM pp222â€“3.
â€˜Hepaticâ€™ jaundice due to congenital enzyme defect	Suggested by: Normal looking stools and normal looking urine.
	Confirmed by: â†‘*serum bilirubin* (unconjugated), but no (conjugated) bilirubin in urine. No *urobilinogen in urine* and *normal haptoglobin. Normal liver function tests*.
	Management: OHCM pp222â€“3.
â€˜Hepatocellularâ€™ jaundice (â€˜hepaticâ€™ with element of â€˜obstructiveâ€™ jaundice)	Suggested by: onset of jaundice over days or weeks, stools pale or normal but dark urine.
	Confirmed by: â†‘serum (conjugated) *bilirubin* and thus â†‘*urine bilirubin. Normal urine urobilinogen. Liver function tests all abnormal esp. â†‘(ALT*.
	Management: OHCM pp222â€“3.
â€˜Obstructiveâ€™ jaundice	Suggested by: onset of jaundice over days or weeks with pale stools and dark urine. Bilirubin â†‘ (i.e. conjugated and thus soluble) in urine.
	Confirmed by: â†‘*serum conjugated bilirubin* and thus â†‘ *urine bilirubin* but no â†‘urobilinogen in urine. Markedly (â†‘â†‘) *alkaline phosphatase*, but less abnormal liver function tests and â†‘â†‘GT.
	Management: OHCM p484.

Vomiting alone (unrelated to food and without abdominal pain or headaches)

2009-05-24T23:27:00.003-07:00

Some differential diagnoses and typical outline evidence

Gastroenteritis	Suggested by: diarrhoea, decreased bowel sounds.
	Confirmed by: *stools for WBC and culture*.
	Management: OHCM p556.
Sliding hiatus hernia	Suggested by: occasional chest pain precipitated by heavy meals, lying flat.
	Confirmed by: *barium meal* showing reflux.
	Management: OHCM p216.
Acute viral labyrinthitis	Suggested by: vertigo, nystagmus.
	Confirmed by: being self-limiting over days.
	Management: OHCM p346â€“7.
MÃ©niÃ¨re's disease	Suggested by: vertigo, tinnitus, deafness.
	Confirmed by: *audiometry:* sensory hearing loss.
	Management: OHCM p346, OHCS p554.
Pregnancy	Suggested by: being worse soon after waking, amenorrhoea.
Pregnancy	Confirmed by: pregnancy test +ve.
Anaphylaxis	Suggested by: bronchospasm, laryngeal oedema, flushing, urticaria, angioedema.
	Confirmed by: relief with antihistamines or steroids.
	Management: OHCM p780, OHCS p237.
Renal failure (CRF)	Suggested by: fatigue, pruritus, anorexia, nausea, â€˜lemon-tingeâ€™ skin.
	Confirmed by: â†‘*serum creatinine, â†“creatinine clearance. If chronic CRF: Hb low, and small kidneys on renal ultrasound*.
	Management: OHCM pp272â€“4.
Addison's disease	Suggested by: lethargy, weakness, dizziness, pigmentation (buccal, scar), hypotension.
	Confirmed by: 9 a.m. plasma cortisol low â†“ and impaired response to short ACTH stimulation test (*short Synacthen test*).
	Management: OHCM p312.
Drugs e.g. antibiotics, cytotoxics, any overdose, excessive alcohol ingestion etc.	Suggested by: history of drug ingestion.
	Confirmed by: response of symptoms to avoidance of drug.
Functional	Suggested by: vomiting during or soon after a meal Â± other psychological disturbance and no symptoms and physical signs of organic disease.
Functional	Confirmed by: response to psychotherapy.

Vomiting with headache alone (unrelated to food and no abdominal pain)

2009-05-24T23:27:00.001-07:00

Some differential diagnoses and typical outline evidence

Migraine	Suggested by: throbbing headache with preceding visual auras or other transient sensory symptoms and â€˜triggerâ€™ factors e.g. pre-menstrual, stress, particular foods.
	Confirmed by: history, but if in doubt *MRI scan* to exclude anatomical abnormalities.
	Management: OHCM p342.
Raised intracranial pressure	Suggested by: being worse in morning, on coughing and leaning forward, papilloedema.
	Confirmed by: *CT scan head* showing flattening of sulci and darkening of brain tissue.
	Management: OHCM p816.
Meningitis *(viral or bacterial)*	Suggested by: photophobia, fever, neck stiffness.
	Confirmed by: *CT scan:* no signs of â†‘intracranial. pressure and *LP:* â†‘lymphocytes in viral, â†‘neutrophils in bacterial with organisms on staining and culture.
	Management: OHCM pp370â€“1.
Haemorrhagic stroke	Suggested by: sudden onset of headache, hemiparesis, sparing of upper face, dysarthia Â± dysphasia, extensor plantar response.
	Confirmed by: *CT brain scan:* high attenuation area representing haemorrhage.
	Management: OHCM pp354â€“8.
Severe hypertension	Suggested by: continuous throbbing headache (non-severe hypertension is usually asymptomatic) but headache Â± visual disturbance in malignant hypertension.
	Confirmed by: *serial BP measurement:* usually >140mmHg diastolic and/or >240mmHg systolic.
	Management: OHCM pp140â€“2.
Epilepsy	Suggested by: aura, altered consciousness, abnormal movements.
	Confirmed by: *EEG* result: spikes and waves over focus.
	Management: OHCM p380.
Acute glaucoma	Suggested by: blurred vision, painful red eye, coloured haloes.
	Confirmed by: â†‘*intraocular pressure* on measurement.
	Management: OHCM p430.
Addison's disease	Suggested by: lethargy, weakness, dizziness, pigmentation (buccal, scar), hypotension.
	Confirmed by: 9 a.m. plasma cortisol â†“ and impaired response to short ACTH stimulation test (*short Synacthen test*).
	Management: OHCM p312.

Vomiting with abdominal pain alone (unrelated to food and no fever)â€”metabolic causes

2009-05-24T23:26:00.002-07:00

This is associated with a wide variety of GI and systemic disorders. It is non-specific.

Some differential diagnoses and typical outline evidence

Drugs overdose e.g. digoxin	Suggested by: drug history.
	Confirmed by: *serum drug levels*.
	Management: OHCM p830.
Diabetic ketoacidosis	Suggested by: polyuria, dehydration, Â±Kussmaul respiration.
	Confirmed by: â†‘*blood glucose, â†“pH,ketonuria* or *plasma bicarbonate* <15mmol/l.
	Management: OHCM p818.
Hypercalcaemia	Suggested by: lethargy, confusion, constipation, muscle weakness, polydipsia and polyuria.
	Confirmed by: â†‘*serum Ca*²⁺.
	Management: OHCM p696.
Acute intermittentporphyria	Suggested by: family history, constipation, peripheral neuropathy, hypertension, psychoses, urine darkens on standing.
	Confirmed by: Elevated *urinary-aminolevulinic acid and porphobilinogen, plasma porphyrins*.
	Management: OHCM p708.
Lead poisoning	Suggested by: anorexia, personality changes, headaches, metallic taste.
	Confirmed by: elevated whole *blood lead concentration* >2.4Âµmol/L.
	Management: OHCM pp210, 628.
Vitamin A intoxication	Suggested by: â†‘intracranial pressure, headache, irritability.
Vitamin A intoxication	Confirmed by: symptoms and signs disappearing within 1â€“4 weeks after stopping vitamin A ingestion.
Phaeochromocytoma	Suggested by: headache, sweating, palpitations, pallor, nausea, hypertension (intermittent or persistent), tachycardia.
	Confirmed by: *24 hour urinary metanephrines* â†‘, *serum catecholamines* â†‘â†‘**(adrenaline, noradrenaline), CT abdomen, MRI scan**.
	Management: OHCM pp314, 822.

Vomiting with abdominal pain alone (unrelated to food and no fever)â€”non-metabolic causes

2009-05-24T23:26:00.001-07:00

This is associated with a wide variety of GI and systemic disorders it is non-specific.

Some differential diagnoses and typical outline evidence

Large bowel obstruction e.g. malignancy, strangulated hernia	Suggested by: faecal vomiting, abdominal distension.
	Confirmed by: *AXR showing bowel dilation, barium enema, colonoscopy*.
	Management: OHCM p492.
Hepatic carcinoma, primary or secondary	Suggested by: RUQ pain and mass, jaundice.
	Confirmed by: *weight loss over weeks to months, ultrasound/CT of liver* showing hepatic mass.
	Management: OHCM pp242â€“3.
Mesenteric artery occlusion	Suggested by: periumbilical pain, diarrhoea, melaena.
	Confirmed by: *mesenteric angiography* showing filling defect.
	Management: OHCM p488.
Intussusception	Suggested by: child, usually between 6â€“18 months of life, acute onset of colicky intermittent abdominal pain, red currant â€˜jellyâ€™ PR bleed, Â± a sausage shape mass in upper abdomen.
	Confirmed by: *barium enema*, may reduce with appropriate hydrostatic pressure.
	Management: OHCM p494.
Ectopic pregnancy, miscarriage	Suggested by: cramping pain, spotting, PV bleeding.
	Confirmed by: positive pregnancy test, *USS of pelvis*.
	Management: OHCS p262â€“3.
Renal calculi	Suggested by: colicky loin pain, haematuria.
	Confirmed by: *plain abd X-ray, ultrasound, IVU*.
	Management: OHCM p264.
Acute inferior myocardial infarction	Suggested by: retrosternal chest pain, sweating, nausea.
	Confirmed by: â†‘ST on *ECG, â†‘cardiac enzymes* e.g. *CK-MB or troponin*.
	Management: OHCM pp120â€“4.
Congestive cardiac failure (and liver congestion)	Suggested by: dyspnoea, orthopnoea, PND, liver enlargement and tenderness, leg oedema.
	Confirmed by: *CXR and echocardiogram*.
	Management: OHCM pp136â€“9

Vomiting with abdominal pain and fever

2009-05-24T23:25:00.004-07:00

The vomiting is usually unrelated to eating.

Some differential diagnoses and typical outline evidence

Gastroenteritis	Suggested by: diarrhoea, â†‘bowel sounds.
	Confirmed by: *stools for WBC and culture*.
	Management: OHCM p556.
Food poisoning	Suggested by: associated with diarrhoea, eating companions affected.
	Confirmed by: *stools for WBC and culture, cultures of vomitus, food and blood*.
	Management: OHCM p556.
Urinary tract infection	Suggested by: dysuria, frequency, abnormal dipstix.
	Confirmed by: *MSU microscopy and culture*. (US scan for possible anatomical abnormality.)
	Management: OHCM p262.
Acute appendicitis, mesenteric adenitis	Suggested by: RLQ pain anorexia, low grade fever.
	Confirmed by: RLQ guarding or right sided rectal tenderness.
	Management: OHCM p476.
Hepatitis A or B	Suggested by: *RUQ* pain, jaundice.
	Confirmed by: ALT â†‘â†‘ and bilirubin â†‘, *hepatitis serology*.
	Management: OHCM p576.
Toxic shock syndrome	Suggested by: use of tampons, high fever, vomiting and profuse watery diarrhoea, confusion, skin rash, hypotension, myalgia.
	Confirmed by: *cultures of blood, stool, vaginal swab* for Staphylococcus and toxin. Thrombocytopenia on *FBC. â†‘CPK*.
	Management: OHCM p590.
Pneumonia (lower lobe)	Suggested by: cough, dyspnoea, fever.
	Confirmed by: *CXR* shows consolidation. *Sputum and blood cultures. Serology* if atypical.
	Management: OHCM p172.
Pelvic inflammatory disease	Suggested by: lower abdominal pain, fever, vaginal discharge.
	Confirmed by: high vaginal swab, elevated *ESR* and *CRP. FBC:* leucocytosis, *pelvic ultrasound, Â±laparoscopy*.
	Management: OHCS p286.
Haemolytic uraemic syndrome	Suggested by: haematuria, fever, confusion.
	Confirmed by: *FBC:* thrombocytopaenia, fragmented RBCs on *blood film, renal failure on U&E*.
	Management: OHCM p282.
Malaria	Suggested by: recent travel to malaria zone, periodic paroxysms of rigors, fever, sweating, nausea.
	Confirmed by: Plasmodium in *blood smear*.
	Management: OHCM pp560â€“2.

Vomiting shortly after food

2009-05-24T23:25:00.003-07:00

Some differential diagnoses and typical outline evidence

Gastritis/peptic ulcer disease	Suggested by: epigastric pain, dull or burning discomfort, (gastric ulcer pain typically exacerbated by food and duodenal ulcer pain relieved by it), â€˜waterbrashâ€™.
	Confirmed by: *oesophagogastroscopy, barium meal and pH study*.
Gastroparesis due to diabetes mellitus	Suggested by: intermittent vomiting, abdominal fullness or bloating, distended upper abdomen, succussion splash, history of diabetes.
	Confirmed by: *oesophagogastroscopy, double contrast barium meal* showing normal mucosa but dilatation.
Gastric outlet obstruction e.g. carcinoma, lymphoma, chronic scarring, congenital pyloric stenosis in newborn	Suggested by: intermittent vomiting, abdominal fullness or bloating, distended upper abdomen, succussion splash.
	Confirmed by: *oesophagogastroscopy, double contrast barium meal* shows structural abnormality.
Small intestinal tumour e.g. lymphoma	Suggested by: abdominal pain, anorexia, weight loss.
	Confirmed by: *small bowel barium meal and follow-through* showing filling defect, *CT abdomen* showing abnormal tumour in wall, *flexible enteroscopy* with biopsy showing abnormal histology.
Acute cholecystitis due to cholelithiasis	Suggested by: symptoms after fatty food with colicky abdominal pain.
	Confirmed by: â†‘*serum amylase, ultrasound scan* of biliary tree/gallbladder.
	Management: OHCM pp484â€“5.
Acute pancreatitis	Suggested by: severe epigastric/central abdominal pain, jaundice, tachycardia, Cullen's sign (periumbilical discolouration) or Grey Turner's sign (discolouration at the flank).
	Confirmed by: â†‘â†‘*serum amylase, â†“Ca²⁺*.
	Management: OHCM p478.

Vomiting without weight loss

2009-05-24T23:25:00.001-07:00

Some differential diagnoses and typical outline evidence

Pharyngeal pouch	Suggested by: no pain, regurgitation of undigested food.
	Confirmed by: *barium swallow* showing saccular opacification outside pharynx.
	Management: OHCS p572.
Achalasia	Suggested by: vomiting after large meals, undigested solid food and fluid, dysphagia to fluid, nocturnal regurgitation.
	Confirmed by: *barium swallow* demonstrating the absence of peristaltic contractions, *oesophagogastroscopy* showing dilatation.
	Management: OHCM p212, OHCS p572.
Oesophagitisand ulceration	Suggested by: retrosternal pain, heartburn, dyspepsia, â€˜waterbrashâ€™.
	Confirmed by: *oesophagogastroscopy* showing inflammation and/or ulceration.
	Management: OHCM p216.

Vomiting with weight loss

2009-05-24T23:24:00.000-07:00

Some differential diagnoses and typical outline evidence

Oesophageal carcinoma	Suggested by: dysphagia to solid food first, then semisolid and finally fluid.
	Confirmed by: *barium swallow* showing filling defect, *fibreoptic gastroscopy* with mucosal biopsy of visible tumour.
	Management: OHCM pp508, 718.
Gastric carcinoma	Suggested by: satiety after small meal.
	Confirmed by: *oesophagogastroscopy* showing and allowing biopsy of visible tumour, *barium meal* showing filling defect.
	Management: OHCM p508.
Achalasia	Suggested by: vomiting after large meals, undigested solid food and fluid, dysphagia to fluid, nocturnal regurgitation.
	Confirmed by: *barium swallow* demonstrating the absence of peristaltic contractions, oesophagogastroscopy showing dilatation.
	Management: OHCM p212.
Oesophageal stricture	Suggested by: undigested solid food and fluid in vomitus.
	Confirmed by: *barium swallow, oesophagogastroscopy* showing food residue and fixed narrowing.
	Management: OHCM p212.
Small intestinal tumour e.g. lymphoma	Suggested by: abdominal pain, anorexia.
Small intestinal tumour e.g. lymphoma	Confirmed by: *small bowel follow-through, CT abdomen, flexible enteroscopy with biopsy*.

Vomiting

2009-05-24T23:23:00.000-07:00

Vomiting is not only a feature of GI disorders, but is also associated with a wide variety of local and systemic disorders. Therefore, more leads are needed. Ask about the amount, frequency and nature of vomitusâ€”red blood, â€˜coffee-groundâ€™, timing of vomit i.e. in relation to meals, AND ask about weight loss, fever, headache and abdominal pain.

Try subdividing into

Vomiting with weight loss
Vomiting without weight loss
Vomiting (within hours) of food
Vomiting unrelated to food but with abdominal pain AND fever
Vomiting unrelated to food, with abdominal pain but NO fever (non-metabolic)
Vomiting unrelated to food, with abdominal pain but NO fever (metabolic)
Vomiting unrelated to food without abdominal pain but with headaches
Vomiting unrelated to food and without abdominal pain or headaches

Severe weight loss over weeks or months

2009-05-24T23:22:00.000-07:00

The degree and speed of weight loss is relevant; the more severe, the more likely is it to be due to a demonstrable cause.

Some differential diagnoses and typical outline evidence

Any advancedmalignancy	Suggested by: progressive onset over weeks or months of specific symptoms e.g. neurological deficit, haemoptysis, rectal bleeding, change of bowel habit, etc.
Any advancedmalignancy	Confirmed by: metastases on *CXR, metastases on ultrasound scan of liver* or leukaemic changes on *FBC* or tumour on *bronchoscopy, or GI endoscopy*, etc.
Depression	Suggested by: sleep disorders, poor concentration, social withdrawal, lack of interest in usual activities etc.
	Confirmed by: response to antidepressants. Psychotherapy.
	Management: OHCS pp336â€“41.
Thyrotoxicosis	Suggested by: heat intolerance, tremor, nervousness, palpitation, frequency of bowel movements, goitre, fine tremor, warm and moist palm.
	Confirmed by: *TSHâ†“, â†‘FT4, â†‘FT3*.
	Management: OHCM p304.
Uncontrolled diabetes mellitus	Suggested by: thirst, polydipsia, polyuria.
	Confirmed by: *Fasting blood glucose* â‰¥7.0 mmol/L (on two occasions) OR fasting, random or *GTT* glucose â‰¥ 11.1mmol/L once only in the presence of symptoms.
	Management: OHCM pp292â€“6.
Infection e.g. tuberculosis	Suggested by: night sweats, fever, malaise, cough.
	Confirmed by: *CXR* showing opacification of pneumonia and presence of *AFB in sputum* on microscopy and culture.
	Management: OHCM pp564â€“6.
Addison's disease	Suggested by: lethargy, weakness, dizziness, pigmentation (buccal, scar), hypotension.
	Confirmed by: 9 a.m. plasma cortisol â†“ and impaired response to short ACTH stimulation test (*short Synacthen test*).
	Management: OHCM p312.

Bilateral ankle swelling

2009-05-24T23:20:00.000-07:00

Think of â†‘ pressure within the veins or lymphatic vessels or low albumin in the vascular space, bilateral damage to veins, lymphatics or capillaries due to local inflammation.

Some differential diagnoses and typical outline evidence

Right ventricular failure due to pulmonary hypertension or congestive cardiac failure	Suggested by: â†‘JVP, liver enlargement and pulsation, RV heave. Onset over months usually.
	Confirmed by: dilated RV on *echocardiogram*.
	Management: OHCM pp136â€“9.
Poor venous return due to abdominal or pelvic masses, post-phlebitic or thrombotic venous damage	Suggested by: onset over months. Worse on prolonged standing or sitting, varicosities, venous eczema, pigmentation or ulceration. Non-pitting oedema if chronic.
	Confirmed by: clinically with Trendelenberg test showing filling along extent of communicating valve leaks or on venous *Doppler ultrasound*.
Low albumin states caused by liver failure, nephrotic syndrome, malnutrition, etc.	Suggested by: generalised oedema often including face after lying down. Onset usually over months.
	Confirmed by: low *serum albumin*.
	OHCD p694.
Bilateral cellulitis often associated with diabetes mellitus	Suggested by: warm, red and tender legs, thrombophlebitis and tracking, ulcers etc. Onset over days.
	Confirmed by: positive blood cultures (usually streptococcal or staphylococcal). (*Blood sugar* â†‘ in diabetes.)
	Management: OHCM pp298, 456, 486, 548.
Inferior vena cava obstruction due to prolonged immobility, carcinoma, and oral combined contraceptive use)	Suggested by: bilateral leg swelling onset over hours, assoc. risk factors (obesity, smoker, FH). Symptoms of PE.
	Confirmed by: *CT abdomen, low flow on Doppler ultrasound scan* or filling defect on *venogram*.
	Management: OHCM p194.
Bilateral thromboses	Suggested by: onset over hours, risk factor of obesity, history of immobility, carcinoma, contraceptive. Assoc. PE. Leg(s) firm, warm, tender.
	Confirmed by: no flow on *Doppler ultrasound scan* or filling defect on *venogram*.
	Management: OHCM pp446, 456, 457.
Impaired lymphatic drainage	Suggested by: firm non-tender, non-pitting oedema of gradual onset over months to years.
Impaired lymphatic drainage	Confirmed by: obstruction to flow *lymphangiogram*.

mesothelioma

2008-12-10T05:36:00.000-08:00

a tumour of the pleura, peritoneum, or pericardium.
Symptoms of mesothelioma may not appear until 20 to 50 years after exposure to asbestos. Shortness of breath, cough, and pain in the chest due to an accumulation of fluid in the pleural space are often symptoms of pleural mesothelioma.

symptom:
chest wall pain
pleural effusion, or fluid surrounding the lung
shortness of breath
fatigue or anemia
wheezing, hoarseness, or cough

Acephalus

2008-10-05T18:03:00.001-07:00

Acephalus is a condition in which a fetus without a head

Muscle stiffness or pain

2008-09-21T19:11:00.000-07:00

Usually worse in the early morning often with pain and stiffness

Some differential diagnoses and typical outline evidence

Normal response to strenuous exercise	Suggested by: fit healthy, unaccustomed exercise 1â€“2 days before.
Normal response to strenuous exercise	Confirmed by: spontaneous resolution.
Polymyalgia rheumatica	Suggested by: onset over weeks or months, stiff, painful, and tender proximal muscles. Fatigue, fever in elderly person.
	Confirmed by: â†‘â†‘*ESR. Rheumatoid factor* -ve, prompt response to prednisolone, no other cause (e.g. infection on follow-up).
	Management: OHCM p424.
Rheumatoid arthritis	Suggested by: early morning stiffness. Fingers showing â€˜swan neckâ€™ or â€˜boutonniÃ¨reâ€™ deformities. Thumbs show Z-deformities. MCP joints and wristsâ€”sublux giving ulnar deviation. Kneesâ€”valgus or varus deformity and popliteal â€˜Baker'sâ€™ cysts. Feetâ€”subluxation of meta-tarsal heads with hallux valgus, clawed toes.
	Confirmed by: *rheumatoid factor* +ve, â†‘*anti-IgG autoantibody. FBC:* Normochromic anaemia, â†‘*ESR* when active.
	Management: OHCM p414.
Ankylosing spondylitis	Suggested by: onset over months or years. Stiffness and progressive loss of spinal movement. Kyphosis and spinal extension.
	Confirmed by: â€˜bambooâ€™ spine on *back X-ray* and loss of sacroileal joint space. *Rheumatoid factor* -ve, *HLA-B₂₇* +ve.
	Management: OHCM pp410, 418.
Primary muscle disease	Suggested by: onset over weeks to years. Predominant weakness.
	Confirmed by: *CPK* â†‘, electromyography and muscle biopsy.
	Management: OHCM p420.
Primary hypothyroidism	Suggested by: onset over weeks to months. Predominant fatigue. Also cold intolerance, depression.
	Confirmed by: â†‘*TSH, â†“FT4*.
	Management: OHCM p306.
Early manifestation of occult malignancy	Suggested by: onset over weeks or months. Weight loss, anorexia.
Early manifestation of occult malignancy	Confirmed by: subsequent appearance of malignancy, especially spinal secondary deposits.
â€˜Fibromyalgiaâ€™	Suggested by: variable onsetâ€”weeks to years. Diffuse pain and stiffness but no features of specific diagnosis.
â€˜Fibromyalgiaâ€™	Confirmed by: no â€˜subsequentâ€™ development of features of a specific diagnosis, normal ESR, Rheumatoid factor -ve, CPK normal, TSH & FT4 normal.

Enter the Twilight Zone: The Hypnagogic State

2008-09-14T23:19:00.000-07:00

Hypnagogia, or the hypnagogic state, is a brief period of altered consciousness that occurs between wakefulness and sleep, typically as people "doze off" on their way to normal sleep. During this period, thoughts can become loosely associated, whimsical, and even bizarre. Hallucinations are very common and may take the form of flashes of lights or colors, sounds, voices (hearing your own name being called is quite common), faces, or fully formed pictures. Mental imagery may become particularly vivid and fantastical, and some people may experience synaesthesia, in which experiences in one sense are experienced in anothersounds, for example, may be experienced as visual phenomena.

It is a normal stage of sleep and most people experience it to some degree, although it may go unnoticed or be very brief or quite subdued in some people. It is possible, however, to be more aware of the hypnagogic state as it occurs and to experience the effects of the brain's transition into sleep more fully.

HOW

Although there is no guaranteed technique to extend or intensify the hypnagogic state, sometimes it can be enough to simply make a conscious effort to be aware of any changes in consciousness as you relax and drop off, if practiced regularly. Trying to visualize or imagine moving objects and scenes, or passively noting any visual phenomena during this period might allow you to notice any changes that take place. Extended periods of light sleep seem more likely to produce noticeable hypnagogia, so being very tired may mean you enter deep sleep too quickly. For this reason, afternoon dozing works well for some.

Some experimenters have tried to extend or induce hypnagogia by using light arousal techniques to prevent a quick transition into deep sleep. A microphone and speaker were used in one study to feed the sound of breathing back to the sleeper. Another method is the use of "repeat alarm clocks" (like the snooze function on many modern alarm clocks)on entering sleep, subjects are required to try and maintain enough awareness to press a key every 5 minutes; otherwise, a soft alarm sounds and rouses them.

Try this yourself on public transport. Because of the low background noise and occasional external prompting, if you manage to fall asleep, dozing on buses and trains can often lead to striking hypnagogic states. In spite of this, this is not always the most practical technique, as you can sometimes end up having to explore more than your own consciousness if you miss your stop.

WHY

Very little research has been done on brain function during the hypnagogic state, partly because conducting psychology experiments with semiconscious people is difficult at the best of times and partly because many of the neuroimaging technologies are not very soporific. fMRI scanning tends to be noisy and PET scanning often involves having a drip inserted into a vein to inject radioactive tracer into the bloodstreamhardly the most relaxing of experiences. As a result, most of the research has been done with EEG (electroencephalogram) readings that involve using small scalp electrodes to read electrical activity from the brain.

Hideki Tanaka and colleagues¹ used EEG during sleep onset and discovered that the brain does not decrease its activity evenly across all areas when entering sleep. A form of alpha wave activity (electrical signals in the frequency range of 8-12 Hz that are linked to relaxed states) spreads from the front of the brain to the other areas before fading away. The frontal cortex is associated with attention (among other things), and it may be that the hypnagogic state results from the progressive defocusing of attention. This could cause a reduction in normal perception filtering, resulting in loosely connected thoughts and unusual experiences.

Electroencephalography (EEG) measures electrical activity from the brain, through small electrodes attached to the skull. The electrical signals are generated by neurons and the amount of synchronous neural activity results in characteristic EEG waveforms. Beta activity (above 14 Hz) is usually linked to high levels of mental effort and cortical activation, characteristic of the waking EEG. As mental activation decreases and sleepiness appears, both alpha (8-13 Hz) and theta (4-7 Hz) activity become more prominent. Delta activity (activity below 4 Hz) is associated with deep, "slow-wave" sleep.

Some scientists have argued that the hypnagogic state is not necessarily sleep-related and may be the result of a reduction in meaningful perceptual information, perhaps leading to defocused attention or other similar effects. A study published in 20022 aimed to test this by comparing hypnagogic states with a condition in which awake participants were fed unstructured sensory information in the form of white noise and diffuse white light. The researchers used EEG recordings and found that, although participants in both conditions reported unusual visual experiences, the pattern of brain activation were quite different, suggesting that hypnagogia is more than just the result of relaxation and lack of structured sensory input.

One problem with recording electrical activity from the scalp is that activity from structures that lie deep in the brain may not be detected. This means we could be missing important information when it comes to understanding what happens as we slip from consciousness into sleep, and even back again into wakefulness (known as the hypnopompic state)particularly as deep structures (such as the brain stem, pons, thalamus, and hypothalamus) are known to be crucial in initiating and regulating sleep.

An ingenious study published in Science did manage to investigate the role of some of the deeper brain structures in hypnagogia,³ specifically the medial temporal lobes, which are particularly linked to memory function. The researchers asked five patients who had suffered medial temporal lobe damage to play several hours of Tetris. Damage to this area of the brain often causes amnesia, and the patients in this study had little conscious memory for more than a few minutes at a time. On one evening, some hours after their last game, the players were woken up just as they started to doze and were asked for their experiences. Although they had no conscious memory of playing the game, all of the patients mentioned images of falling, rotating Tetris blocks. This has given us some strong evidence that the hypnagogic state may be due (at least in part) to unconscious memories appearing as unusual hypnagogic experiences.

You Are What You Think

2008-09-14T23:14:00.000-07:00

The concept of priming runs all the way through explanations of how perception influences behavior. Subliminal perception of photographs can prime you to prefer those photos in the future , and simply spending time with someone who is, say, rubbing his face can infect you with his mannerism . It's not necessary to consciously perceive the photographs or the gestures for them to automatically alter our behavior.

Nowhere is this truer than in exemplar activation: being exposed to ideas of stereotypes of people (the exemplars), not even the people themselves, will prime the characteristic traits of those people, and you'll begin to act in that way. It's very odd, and very cool.

HOW

Here's what John Bargh, Mark Chen, and Lara Burrows did¹: they gave 30 psychology undergraduates word puzzles to do (undergraduates are the raw material for most psychology studies). In half of the experiments, the puzzles included words associated with the elderly, like "careful," "wise," "ancient," and "retired." In the other half, all the puzzle words were neutral and not deliberately associated with any single concept. Immediately after individual students had completed the puzzle, they were free to go.

Bargh and team timed, using a hidden stopwatch, how long it took each undergraduate to walk down the corridor to the elevator. Students who had been given the puzzle featuring elderly related words took, on average, a whole second longer to make the walkan increase from 7.3 to 8.3 seconds. They had picked up one of the perceived traits of the elderly: slower walking speed.

WHY

The specifics of how exemplar activation works is still an open question, but the basic mechanism is the same as how we pick up mannerisms . It's a feature of the brain that perceiving something requires activating some kind of physical representation of the thing being perceived: simply making that representation primes that behavior, making us more likely to do what we see. Exemplar activation takes this a little further than we're used to, because it's the reading of wordsin an apparently unrelated task to walking along the corridorthat primes the concept of "the elderly," which then goes on to influence behavior. But the principle is the same.

Slow walking is only the half the story, though. Ap Dijskerhuis and Ad van Knippenberg² performed similar experiments. Instead of influencing their subjects with an "elderly" stereotype, they set up an experiment in which participants had to spend 5 minutes describing either professors or secretaries. (The subjects, again, were undergraduates.)

This time the experiment measured general knowledge, so the next stage of the experiment had the subjects answering Trivial Pursuit questions. They weren't aware the two stages were connected.

What happened is almost unbelievable: subjects who had previously described professorsknown for their perceived intelligenceattained, on average, 60% correct answers, against 46% for the people who had to describe secretaries.

It could be that people who have been considering the professor stereotype are more likely to trust their own judgment; the particular attribute of this stereotype that is causing the response isn't really known. The people exposed to the secretary stereotype didn't do any worse than they should have done: compared to people who hadn't been primed at all, they got about the same number of questions correct and worked their way through the questionnaire in only 6 minutes (compared to an 8-minute average). So in this case it turns out that both stereotypes have good qualities going for them. Secretaries are efficient. But it isn't always the case that stereotypes are positive.

People who identify with groups commonly stereotyped to be poor at math tend to do worse at math tests when their membership in that group is made relevant immediately before the test, as with a checkbox at the top of the test that asks them to indicate their ethnic identity or gender.³

Fortunately, it is possible to counteract this kind of exemplar activation. If you were in this situation, the activation can be overridden by reasserting yourself against the stereotype. Women who have been explicitly told that the math test they are about to do shows no gender bias don't underperformit's the subtle, nonconscious stereotyping that has a real effect (like having to tick a box at the top of the page), causing people who identify with a commonly stereotyped group to take on the stereotype assumption, even if incorrect. Once thinking about the stereotype and the effects it might have is made conscious, the bias disappears.

These exemplar activation experiments are as challenging as any you'll find in psychology. Word puzzles about the elderly slow your walking speed (and actually your reaction time too); just focusing on the stereotype of a professor for 5 minutes makes you better at general knowledge. But it also reinforces the stereotype: people who already hold that identity are pushed into their pigeonholes. Our need to conform runs deep, even when it's against our best interests. But in those cases, concentrating on your individuality is all you need to push back.

Make Yourself Happy

2008-09-14T23:04:00.000-07:00

Find yourself a pen, preferably a nontoxic, nonleaky one. We're going to use this little item to improve your quality of life and give you a little pleasure.

HOW??

Put the pen between your teeth, in far enough so that it's stretching the edges if your mouth back without being uncomfortable. Feeling weird? Just hold it there for a little, and appraise your level of mood. You should find that you end up feeling just a little happier.

If you want to go for the reverse effect, remove the pen (maybe give it a wipe), then trap it between your upper lip and nose like a mustache. If you're feeling anything, it's likely to be a touch of gloom, particularly in contrast to when you had the pen in your mouth.

Alternatively, if you're pen-averse, refer to the pictures in and scrutinize the smiling face for a while. You should find yourself perked upwhile the unhappy photo will likely send you downhill if you stare at it a little.

WHY

Emotional expressions are much more than just by-products of our affective system, the system that deals with emotions. Expressions serve as agents that transmit emotions to other individuals and are crucial in creating and maintaining our own emotional experience. And while aspects of this may be conscious and deliberatemy girlfriend may throw me a grin to let me know she's not mad that I've been glued to the computer all evening, and that reassurance will make me happythere is a deeply automatic component. This is termed primitive contagion and is characterized as a three-stage process: it begins with perception, which triggers mimicry, which itself produces emotion. deals with how we perceive emotions, so here we`ll unpack the other two stages: mimicry and resulting emotion.

eye attention

2008-09-14T22:58:00.000-07:00

What are you paying attention to? These words? In a minute it could switch to a friend or to making coffee or to the person on the bus who just stood up and you noticed out of the corner of your eye. We don't pay attention to everything we see or experience. Following two conversations at the same time is hard, even though we hear both perfectly well, and, likewise, it's simply not possible to read every word on the page of a book simultaneously, although they're all in plain view.

While your senses work overtime to provide as much input as possible, there's a bottleneck in the brain's limited capacity for attention. So we consciously decide which line of text to focus on and read across and down the page, line by line. And this happens at the expense of all the other stimuli we could have attended to, such as the color of the walls or the traffic noise from the road outside.

Choosing what to give attention to is voluntary...mostly. But attention can also be captured.

After visual information leaves the eye, it doesn't just go to one place for processing; the signal divides. Our conscious appreciation of visual information is provided by processing done in the visual cortex. It sits at the back of the brain in the area called the occipital lobe and performs what we typically associate with the job of vision: figuring out exactly what shape the thing you're looking at is, what color, if it's moving, then in what direction and how fast, what it means, and so onproviding the raw information needed to put names to faces and avoid stepping in front of a car while crossing a road.

Attention capture, on the other hand, relies on processing done by a region of the brain called the superior colliculus. It gets a copy of the same visual information the visual cortex does from the retina, but processes it in a different way. This region is evolutionarily ancient, which means the basic structure was established and refined in brains far simpler than our own, through many species of animals. (Rather than relegating it to second place, fish and amphibians do most of their visual processing with their equivalent of the superior colliculus, called the optic lobe.) So as one might expect, it's not particularly sophisticated, compared to the visual cortex. And it doesn't use much of the information it receives; the superior colliculus looks at a black-and-white world through frosted glass. Then again, it doesn't need much. This processing is for rapid response, when it appears something potentially dangerous is happening and urgent action is needed quicker than the complex visual cortex can respond. It's just useful enough to guide reflex movements, tell the head and body to orient in a particular direction, and force attention to snap to important-seeming events.

The visual cortex and superior colliculus aren't the only regions of the brain that process signals from the eye; there are about 10 in total. Basic visual information also informs pupil size for different light levels, influences our day-night cycle, and influences head and eye movement.

That's what's going on when attention is captured. There's a sudden movement and the rapid response bit of your brain says, "Hey, I don't know what that was, but pay it some attention and figure out what to do in case it attacks us." Looking at the crowd, your attention darts around automatically because this bit of your brain feels startled enough to interrupt consciousness every time somebody waves suddenly.

When you're sitting in a darkened theater, absorbed in the dialog on stage, think about what happens when a door opens at the side of the room. The sudden appearance of light grabs your attention. If it happens again, despite the fact that you know you're not interested, it still grabs your attention and demands a response. It's distracting. That's the automatic nature of attention capture coming into play.

On the upside, that bright light flashing in the corner of your eye could well be a ray of sunlight being revealed as a large dangerous something lumbering out of the shadows toward you. The automatic capture of attention serves to orient conscious perception in important directions.

Automatic responses can go further than just grabbing your attention. This part of the brain is also responsible for the looming instinct, which, given a growing dark shadow anywhere in the field of vision, can trigger not just attention but a physical flinch.

Events that capture attention include the two already mentioned: sudden light (actually, a sudden change in contrast) and sudden movement. In keeping with the purpose of facilitating rapid response, it's only new movement that captures attention. Ongoing motion, like a moving car or a walking person, doesn't trigger the automatic shift in attention.

Two other triggers provide hints as to what else our brains regard as so critical to survival that they deserve a rapid response. One is an object appearing abruptly. In general, our brains give special treatment to objectsas opposed to backgrounds and shadows, which are given less attention. This makes sense, as objects such as other people, animals or food usually require a response of some kind. There are even dedicated routines to object tracking. An extra person, rock, or car in the sceneespecially if it appears suddenlyis likely to be a big deal, so attentional capture is triggered.1

John Eastwood and his colleagues also suggest another trigger that is worth mentioning as it shows just how deep our social nature goes. The trigger here is facial expression.² Eastwood's team made simple line-drawing faces, happy and sad ones, and asked people to count certain of the lines that made up the drawings. When the drawings were upside-down, so they were unrecognizable as faces, people did the counting exercise easily. But when the drawings were the right way up, counting took longer for drawings of faces that displayed negative emotions rather than for drawings of positive expressions. Why? The team's conclusion is that negative expressionssad or angry facesdistract you, in just the same way as light through a theater door grabs your attention away from the main action.

Fool Others into Feeling Better

2008-09-14T22:52:00.000-07:00

Injury or infection triggers a coordinated suite of physiological responses involving the brain, hormones, and immune system. The brain generates pain and fever, stress hormones mobilize energy from fat, and immune cells cause local swelling and redness. These processes are collectively known as the acute phase response because they occur rapidly and tend to subside after a few days. Medical assistance can help these unpleasant signs and symptoms to subside more quickly, even when that assistance is completely bogussuch as a witch doctor waving a rattle at you or a quack prescribing a sugar pill. This is known as the placebo effect.

Nobody knows for sure yet how the placebo effect works, but one theory is that the brain is very sensitive to the presence of social support during the process of recovery from injury and infection. The various components of the acute phase response are all designed to promote recovery and prevent further injury while recovery is taking place. Pain, for example, makes you guard the wounded area. But these measures also have costs; high levels of pain, for example, can actually lengthen the healing process. The brain makes a trade-off between the risks of further damage to the injured area and the delay to the healing process. The presence of social support during recovery shifts the balance between these competing risks because some of the burden of preventing further damage is transferred from the sick person to those around them. The sick person can therefore reduce his own costly self-protective measures, such as pain, and allow the healing process to progress more rapidly.

Another suggestion is that the placebo effect works by means of conditioning Conditioning is a very general kind of learning process in which one stimulus is substituted for another. The classic example is Pavlov's dogs, which learned to salivate on hearing a bell after Pavlov had trained them to associate the sound of the bell with the arrival of food. In technical terms, an unconditioned stimulus (the sight of the meat), which leads naturally to a certain unconditioned response (salivating at the sight of the meat), is repeatedly paired with a conditioned stimulus (the sound of the bell). Eventually, the dogs learn the conditioned response of salivating at the sound of the bell. Pavlov's students showed that immune responses can also be conditioned, and others have gone on to suggest that this is what lies behind the placebo response. The unconditioned stimulus is a real drug or some other medical treatment that works even if you have never tried it before and don't believe in it. The unconditioned response is the improvement you feel after receiving the treatment. The conditioned stimuli are all the things that are repeatedly paired with the treatmentthe size, shape, and color of the pill, for example. If you then take a pill that has the same size, shape, and color as the real one, but which lacks the active ingredient, you may still experience some improvement because your immune system has been conditioned to respond to such stimuli.

Placebos won't cure the vast majority of medical conditions. It is much easier and quicker to list the things that placebos can influencepain, swelling, stomach ulcers, some skin conditions, low mood, and anxietythan the things they don't. Everything else is probably not placebo-responsive. That said, placebos are able to help in the management of nearly all illnesses because nearly all illnesses involve pain, low mood, and/or anxiety.

Abbreviations

2008-09-14T22:42:00.000-07:00

You might find these abbreviation within some posts,

OHCM

Oxford Handbook of Clinical Medicine, sixth edition

OHCS

Oxford Handbook of Clinical Specialties, seventh edition

Â±

with/without

+ve

positive

-ve

negative

â†‘

increased

â†“

decreased

Â°

degrees

greater than

less than

1Â°

primary

2Â°

secondary

5-HIAA

5-hydroxyindole acetic acid

A&E

accident and emergency

AAU

accident unit

ABG/s

arterial blood gas/gases

AFB

acid-fast bacillus

ALT

alanine transaminase

ANA

anti-nuclear antibody

ANCA

anti-neutrophil cytoplasmic antibody

A-P

anterior to posterior

ARDS

acute respiratory distress syndrome

aortic stenosis

ASOT

anti-streptolysin O titre

AST

asparate transaminase

atrioventricular

Î²-hCG

Î²-human chorionic gonadotrophin

bone marrow

BMI

body mass index

blood pressure

bpm

beats per minute

cANCA

cytoplasmic anti-neutrophil cytoplasmic antibody

CAPD

continuous ambulatory peritoneal dialysis

CCF

congestive cardiac failure

CK-MB

creatine kinase MB isoenzyme

CNS

central nervous system

COPD

chronic obstructive pulmonary disease

CPK

creatine phosphokinase

CRP

C-reactive protein

CSF

cerebrospinal fluid

computerised tomography

CTPA

computerised tomography pulmonary angiogram

CVA

cerebrovascular accident

CVS

cardiovascular system

CXR

chest X-ray

direct current

DIC

disseminated intravascular coagulation

D-dimer

dextrorotatory dimer

drug history

decilitre

DOB

date of birth

DVT

deep vein thrombosis

ECG

electrocardiogram

ECT

electroconvulsive treatment

EEG

electroencephalogram

ELISA

enzyme-linked immunosorbent assay

ERCP

endoscopic retrograde cholangiopancreatography

ESR

erythrocyte sedimentation rate

FBC

full blood count

FDP/s

fibrogen degredation product/s

FEV₁

forced expiratory volume (1 second)

family history

Fluorescence

FSH

follicular stimulating hormone

FT3

free T3

FT4

free T4

FVC

forced vital capacity

G6PD

glucose-6-phosphate dehydrogenase

GALS

Gait, Arms, Legs, Spine

Î³GT

Î³ glutamyl transpeptidase

GCS

Glasgow Coma Scale

gastrointestinal

general practitioner

Gr/g

gram

Grm/dL

grams/decilitre

GTT

glucose tolerance test

genitourinary

haemoglobin

HBsAG

hepatitis B surface antigen

hCG

human chorionic gonadotrophin

HCV

hepatitis C virus

mercury

HIV

human immunodeficiency virus

HLA-B27

human lymphocyte antigen B27

HOCM

hypertrophic cardiomyopathy

HPC

history of each presenting complaint

HR-CT

high resolution computerised tomography

IgM

immunoglobin M

IHD

ischaemic heart disease

intramuscular

I-P

inter-phalangeal

intravenous

IVU

intravenous urography

JVP

jugular venous pressure

potassium

litre

LFT

liver function test

luteinizing hormone

LIF

left iliac fossa

LMN

lower motor neurone

LRT

lower respiratory tract

left ventricle

MCP

metacarpophalangeal

myocardial infarction

mmHg

millimetres of mercury

mmol

millimoles

multiple sclerosis

MSU

midstream urine

sodium

NAD

no abnormality detected

NSAIDS

non-steroidal anti-inflammatory drugs

NSAP

non-specific abdominal pain

omni die (once daily)

OGD

oesophagogastroduodenoscopy

OHCD

Oxford Handbook of Clinical Diagnosis

pulmonary component of 2^nd heart sound

P-A

posterior to anterior

pernicious anaemia

PAS

periodic acid Schiff

presenting complaints

PCR

polymerase chain reaction

pulmonary embolism

PEFR

peak expiratory flow rate

PMH

past medical history

PND

paroxysmal nocturnal dyspnoea

per os (by mouth)

per rectum (by the rectum)

PSA

Prostatic-specific antigen

PUO

pyrexia of unknown origin

per vaginam (by the vagina)

qds

quater die sumendus (to be taken 4 times a day)

factor rheumatoid factor

rheumatoid arthritis

RBB

right bundle branch

RBC

red blood cells

RLQ

right lower quadrant

respiratory system

RUQ

right upper quadrant

right ventricle

social history

SLE

systemic lupus erythematosus

STEMI

ST elevated myocardial infarction

SVC

superior vena cava

SVT

supraventricular tachycardia

triiodothyronine

thyroxine

tuberculosis

tds

ter die sumendus (to be taken 3 times a day)

TFT

thyroid function test

TSH

thyroid stimulating hormone

TURP

transurethral resection of prostate

U&E

urea and electrolytes

UMN

upper motor neurone

URT

upper respiratory tract

URTI

upper respiratory tract infection

USS

ultrasound scan

V/Q

ventilation/perfusion

VSD

ventriculoseptal defect

WBC

white blood cell

WCC

white cell count

WHO

World Health Organization

weight

Ziehl-Neelsen

Postural fall in blood pressure

2008-09-14T22:35:00.000-07:00

To be significant the blood pressure must fall >30mmHg and stay down for at least 1 minute and be accompanied by dizziness.

Main differential diagnoses and typical outline evidence

Drug induced due to excessive dose of hypotensive agent, L-dopa, carbidopa, phenothiazines, antidepressants	Suggested by: drug history.
	Confirmed by: by resolution or improvement after stopping or reducing drug.
Autonomic neuropathy due to diabetes mellitus or tabes dorsalis (rarely)	Suggested by: history of long standing diabetes (common) or tabes dorsalis (rare). Also, diarrhoea, abdominal distension and vomiting (gastroparesis), impotence, urine frequency.
	Confirmed by: *ECG monitor of beat to beat variation:* <10>
	Management: OHCM p298.
Idiopathic orthostatic hypotension	Suggested by: no other features except elderly.
	Confirmed by: isolated phenomenon.

Pulse irregular

2008-09-14T22:34:00.002-07:00

Main differential diagnoses and typical outline evidence

Atrial fibrillation caused by ischaemic heart disease, thyrotoxicosis, etc.	Suggested by: irregularly irregular pulse.
	Confirmed by: *ECG* showing no P waves, and irregularly irregular normal QRS complexes.
	Management: OHCM p130.
Atrial flutter with variable heart block caused by ischaemic heart disease, etc.	Suggested by: irregularly irregular pulse.
	Confirmed by: *ECG* showing â€˜saw toothâ€™ F waves, and irregularly irregular normal QRS complexes.
	Management: OHCM p130.
Atrial or ventricular ectopics caused by ischaemic heart disease, etc.	Suggested by: regular rate with irregular dropped beat.
	Confirmed by: *ECG* showing normal sinus rhythm with irregular QRS complexes not preceded by P wave, and then compensatory absence of subsequent QRS.
	Management: OHCM p132.
Wenkenbach heart block caused by ischaemic heart disease, etc.	Suggested by: regular rate with regular dropped beat.
	Confirmed by: *ECG* showing progressive prolongation of P-R interval with normal QRS complex followed by an absent QRS complex.

Bradycardia (<60bpm)

2008-09-14T22:34:00.001-07:00

Main differential diagnoses and typical outline evidence

Athletic heart	Suggested by: young/fit, asymptomatic.
Athletic heart	Confirmed by: above clinical findings.
Drugs	Suggested by: history e.g. beta blockers.
Drugs	Confirmed by: improvement when drug withdrawn.
Sinoatrial disease	Suggested by: elderly, ischaemic heart disease.
	Confirmed by: *ECG*: abnormal P wave or P-R interval.
	Management: OHCM p127.
Ventricular or supraventricular begemini	Suggested by: known ischaemic heart disease.
	Confirmed by: *ECG:* premature ectopics with compensatory pause.
	Management: OHCM p126.
Myocardial infarction	Suggested by: central, crushing chest pain (can be atypical pain).
	Confirmed by: *ECG:* Q waves, raised ST segments, and inverted T waves. â†‘*CPK* and *troponin*.
	Management: OHCM pp120â€“124.
Hypothyroid	Suggested by: constipation, weight gain, dry skin, dry hair, slow relaxing reflexes.
	Confirmed by: â†‘*TSH*, â†“T4.
	Management: OHCM p306.
Hypothermia	Suggested by: history of exposure to cold temperature and immobility.
	Confirmed by: Core temperature <35(c.
	Management: OHCM p836.

Red eye

2008-09-14T22:28:00.000-07:00

Gritty pain suggests external cause. Aching pain suggests internal cause. Light sensitivity always accompanies inflammation in the eye. Fluoresceine (Fl) yellow dye glows green with a blue examination light and stains all epithelial breaks.

Some differential diagnoses and typical outline evidence

Spontaneous sub-conjunctival haemorrhage	Suggested by: painless bright red area on conjunctiva (oxygenated blood) and no light sensitivity.
	Confirmed by: clinical appearance and resolution over days. No Fl staining of cornea (not done often).
	Management: OHCS p432.
Conjunctivitis due to bacterial infection	Suggested by: red eyes, dilated blood vessels on the eyeball and the tarsal (lid) conjunctiva with a purulent discharge Â± bilateral Â± gritty pain.
	Confirmed by: above clinical appearance. Not light sensitive and no Fl stain of cornea.
	Management: OHCS p432.
Conjunctivitis due to viral infection	Suggested by: red eyes with dilated vessels on the eyeball only, sometimes in one quadrant around the cornea with a watery â€˜tap runningâ€™ discharge. Gritty pain Â± impaired vision.
	Confirmed by: Fl stain showing dendritic (branching) pattern and resolution with topical antiviral.
	Management: OHCS p432.
Conjunctivitis due to allergy	Suggested by: red eyes with pink swollen conjunctiva and white stringy mucoid discharge.
	Confirmed by: no Fl stain and no visual loss and resolution with chromoglycate (over six weeks) or steroid eye drops.
	Management: OHCS p432.
Corneal ulcer (ulcerative keratitis) due to abrasion or Herpes simplex, Pseudomonas, Candida, Aspergillus, protozoa	Suggested by: painful, light-sensitive, deeply red eye with yellowish abscess in the cornea. Purulent discharge.
	Confirmed by: slit lamp examination after *fluorescein instillation showing* hypopyon (pus in the eye).
	Management: OHCS p432.
Episcleritis	Suggested by: localised red eye with superficial vessel dilatation. Mild pain. No visual loss or light sensitivity.
	Confirmed by: Instillation of one drop of phenylephrine 2.5% causing a blanching of the lesion.
	Management: OHCS p432.
Scleritis	Suggested by: localised area of dark red dilated superficial and deep vessel on the sclera with aching pain and tenderness.
	Confirmed by: failure to blanche with one drop of 2.5% phenylephrine.
	Management: OHCS p432.
Acute closed-angle glaucoma (emergency)	Suggested by: severely painful red eyeball with marked visual loss, accompanied by nausea and vomiting Â± history of haloes around lights and severe headache with blurred vision.
	Confirmed by: dull grey cornea, non reacting and irregular pupil with raised ocular pressures.
	Management: OHCS p430.
Iritis or uveitis (see page 264)	Suggested by: redness around cornea and haze in front of iris and severe light sensitivity (photophobia).
	Confirmed by: small non-reacting and irregular pupil. Slit lamp examination showing flare, cells and hypopyon (pus in eye).
	Management: OHCS p430.

Gynaecomastia

2008-09-14T22:24:00.000-07:00

These findings should have been discovered during the general examination. Breast swelling in male with disc of firm tissue. If there is no disc, it is fatty tissue only

Some differential diagnoses and typical outline evidence

Immature testis	Suggested by: adolescence and no testicular lump.
Immature testis	Confirmed by: normal testosterone, estrogen and LH levels normal ultrasound scan of testis.
Digoxin, Spironolactone	Suggested by: taking of drug and no testicular lump.
Digoxin, Spironolactone	Confirmed by: improvement when drug stopped.
High alcohol intake	Suggested by: high alcohol intake and no testicular lump.
High alcohol intake	Confirmed by: improvement when alcohol stopped.
Hepatic cirrhosis	Suggested by: long history of high alcohol intake (usually), spider naevi, abnormal liver size (large or small) and consistency (fatty or hard).
	Confirmed by: very abnormal biochemical liver function tests, â†“LH, â†‘*oestrogens, â†“testosterone*.
	Management: OHCM p232.
Testicular tumours	Suggested by: scrotal mass Â± pain, tenderness if haemorrhage occurs. (Sometimes arising in undescended testis).
	Confirmed by: testicular ultrasound, inguinal exploration, â†‘*Î±-fetoprotein, â†‘Î²-hCG*.
	Management: OHCM 512.
Hypogonadism (primary to testicular disease, or secondary to low LH from pituitary defect or tumour)	Suggested by: sparse pubic hair, no drug or alcohol history, poor libido.
	Confirmed by: *Testosterone*â†“, LHâ†‘ (in primary testicular disease), LHâ†“ or normal (when secondary to pituitary diseases).
	Management: OHCM pp316, 318.
Bronchial carcinoma	Suggested by: smoking history, haemoptysis, weight loss, clubbing.
	Confirmed by: *CXR, bronchoscopy* with biopsy.
	Management: OHCM p182.
Klinefelter's syndrome	Suggested by: poor sexual development, infertility, eunuchoid.
Klinefelter's syndrome	Confirmed by: 47, XXY *karyotype*.
Obesity	Suggested by: no breast tissue, only mammary fat.
	Confirmed by: improvement with weight loss.
	Management: OHCM p208.

Cough with sputum

2008-09-14T21:56:00.000-07:00

The majority of patients presenting with a productive cough will have a short history of days or weeks but many will have a background of a chronic cough.

Some differential diagnoses and typical outline evidence

Chronic bronchitis	Suggested by: grey sputum, slow progression over years and a smoker (nearly always).
	Confirmed by: grey sputum >3 months over two consecutive years.
	Management: OHCM p188.
Acute viral bronchitis	Suggested by: onset over hours or days. Fever, white/yellow sputum.
Acute viral bronchitis	Confirmed by: no consolidation on *CXR*, quick spontaneous resolution.
Acute bacterial bronchitis	Suggested by: onset over hours or days. Fever, mucopurulent sputum, dyspnoea.
	Confirmed by: *sputum culture* and sensitivities, response to appropriate antibiotics.
	Management: OHCM p188.
Pneumonia	Suggested by: onset over hours or days. Rusty brown sputum (i.e. purulent sputum tinged with blood). Sharp chest pain worse on inspiration, pleural rub, fever, cough, consolidation etc.
	Confirmed by: patchy shadowing on *CXR* and sputum/blood culture.
	Management: OHCM pp173â€“6.
Bronchiectasis	Suggested by: progression over months or years. Finger clubbing, cupful(s) of pus-like sputum per day. Coarse late inspiratory crepitations.
	Confirmed by: *CXR:* cystic shadowing; high resolution *CT chest:* honeycombing and thickened dilated bronchi.
	Management: OHCM pp178, 179.
Lung abscess	Suggested by: copious amount of foul smelling pus/brown sputum, haemoptysis, high swinging fever, chest pain over weeks, usually preceded by a prior significant respiratory infection (e.g. pneumonia).
	Confirmed by: fluid level in cavity on *CXR, CT chest*, response to physiotherapy, antibiotics and aspiration.
	Management: OHCM pp176, 618.

Cough and pink frothy sputum

2008-09-14T21:48:00.000-07:00

Some differential diagnoses and typical outline evidence

Acute pulmonary oedema	Suggested by: onset over minutes or hours of shortness of breath, orthopnoea, displaced apex, loud 3^rd heart sound, fine crackles at lung base.
	Confirmed by: CXR appearance (see 640) poor LV function on echocardiogram.
	Management: OHCM pp136â€“8, 786.
Mitral stenosis	Suggested by: months or years of orthopnoea, mitral facies, tapping, displaced apex, loud 1^st heart sound, diastolic murmur, fine crackles at lung base. Enlarged left atrial shadow (behind heart) and splayed carina on CXR.
	Confirmed by: large left atrium and mitral stenosis on echocardiogram.
	Management: OHCM p146.

Sudden breathlessness, onset over seconds

2008-09-14T21:45:00.000-07:00

This situation may be life-threatening; the severity of the underlying condition often creates helpful diagnostic information.

Pulmonary embolus
arising from DVT in leg, pelvic vein or right atrium
Suggested by: central chest pain also with abrupt shortness of breath, cyanosis, tachycardia, loud second sound in pulmonary area, associated DVT or risk factors of silent DVT. PO2 low, CO2 normal or low.

Confirmed by: V/Q scan ventilation/perfusion mismatch. Spiral CT scan: clot in artery, pulmonary angiogram shows filling defect (see above).
Management: OHCM pp96, 194, 802.

Pneumothorax
Suggested by: pain in centre or side of chest with abrupt breathlessness. Resonance to percussion over same side especially lung apex.

Confirmed by: expiration CXR showing loss of lung markings outside sharp line.
Management: OHCM pp194, 750, 798.

Anaphylaxis
Suggested by: dramatic onset over minutes, history of prior allergen exposure, acute bronchospasm with wheeze and dyspnoea, flushing, sweating and a feeling of dread, facial oedema, urticaria and warm but clammy extremities. Tachycardia and hypotension.

Confirmed by: clinical presentation and by controlled allergen exposure and examination. Response to adrenaline IM.
Management: OHCM p780, OHCS p237.

Inhalation foreign body
Suggested by: history of putting an object in mouth e.g. peanut. Sudden stridor, severe cough, low pitched, monophonic wheeze.

Confirmed by: relief in extremis by performing Heimlich manoeuvre etc. or if not in extremis, foreign body seen on CXR/CT or bronchoscopy.

Glasgow Coma Scale

2008-09-14T21:36:00.000-07:00

Eye opening

Spontaneous 4

To speech 3

To pain 2

No response 1

Verbal response

Orientated 5

Confused: talks in sentences but disorientated 4

Verbalizes: words not sentences 3

Vocalizes: sounds (groans or grunts) not words 2

No vocalization 1

Motor response

Obeys commands 6

Localizes to pain: e.g. brings hand up beyond chin to supraorbital pain 5

Flexion withdrawal to pain: no localization to supraorbital pain but flexes elbow to nail bed pressure 4

Abnormal flexion to pain 3

Extension to pain: extends elbow to nail bed pressure 2

No response 1

How long will you have?

2008-09-14T21:27:00.000-07:00

Consultation length varies. In general practice in the UK the average length is 10 minutes. This is usually adequate as the doctor may have seen the patient on several occasions and know the family and social background. In hospital 5-10 minutes may be adequate for return outpatients, but for new and complex problems much longer - 20-30 minutes - may be needed. If you are a student learning to talk with and examine patients allow 30 minutes at least. Plan your time around how long you expect your patients to take so that others are not kept waiting, and be prepared to be flexible.

Starting the consultation

2008-09-14T21:19:00.000-07:00

Before starting, make sure you are talking to the correct patient. Introduce yourself, as your patients should know who you are and what you do. If you are in training, tell them, as patients are usually eager to help. It helps to create a good impression if you appear to have prepared to see them. Look at the patient records and at any transfer or admission letters before the consultation. It is easier to give your patient your attention if you do not write notes during the consultation, but you may have to write some things, e.g. blood pressure readings or family trees, which are easily forgotten. If you are going to take notes let your patient know. Throughout this part of the chapter there are examples of a doctor and a patient talking with each other. These are only illustrations, not hard and fast rules. Remember that it is the principles of communication that are important. If you get the principles right, then the words you use will change depending on the situation. To begin with, here are a few ideas on how to get an interview going.
Good morning Mrs Jones, I have got the right person haven't I? I am Mr Brown. I
am a fourth year medical student. I've been asked if I could come and talk to you
and examine you as you have just come into the ward today. Is that OK?
It might take me 20-30 minutes if that is alright with you.
I would like you to tell me what has been happening and then I'll want to ask a few
questions and examine you.
I see that you can't really get out of bed so I am afraid we'll need to talk here. I'll
pull the screens round, but I'm sorry it is not that private, so if I ask you anything
that you don't want to tell me in case others hear then just say so.
Because I'll have to get quite a bit of information from you, I'll need to make a few
notes. I hope that is alright because I'll forget otherwise. Now if I am writing things
down it doesn't mean I'm not listening to you, I still will be.
Are you happy with all that?

TALKING WITH PATIENTS

2008-09-14T21:15:00.000-07:00

People visit doctors for many reasons. Sometimes it is because something unexpected and catastrophic has happened to them, but usually it is because of an ongoing problem, a relatively minor complaint or because something 'isn't right'. Before coming to the doctor they may have spoken to family or friends, tried remedies suggested by them, spoken to other health professionals, e.g. pharmacists, or complementary practitioners, or may have found information on the internet and brought this with them. Their decision to go to a doctor may only have been made after these attempts to explain or heal their illness or problem have been unsuccessful. By the time they have reached a doctor most patients have formed some idea of what might be wrong with them and will have worries or concerns that they need to talk about.
The general practitioner (GP) or family doctor is usually the first point of contact. Even a straightforward visit can be a big event for patients. They have to decide to go, usually make an appointment, work out what they are going to say and may have to arrange time off work or for child care. They then have to sit in a waiting room. This is an almost universal human experience; think about how it affected you the last time you had to do this. Things can become even more perplexing if the visit is to a hospital outpatient department or part of a hospital admission when their anxiety and apprehension can get worse as this is where 'serious' things happen. Whatever the cause, patients are seeking explanation and meaning for their symptoms. Whatever the setting, the doctor needs to try to work out why patients are there, what they are most concerned about and to agree with them the best course of action. The first and major part of that is talking with the patient (Table 1.1). If you listen carefully they will probably tell you what is wrong with them, will certainly tell you what is concerning them, and the physical examination will help you to confirm this or not. Communication is integral to the clinical examination and is most important at the beginning to gather information, and at the end to share information and engage your patients in their management. Effective communication skills positively influence health outcomes::
-Active listening helps the doctor recognize what is wrong
-Patient satisfaction is improved if patients understand what is wrong and what they can do to help
-When a doctor and patient agree on mutual goals health outcomes are improved
-Positive support and empathy improve health outcomes and enhance the relationship between the doctor and the patient
-Medicine taking is improved by clear information about what a medicine is meant to do