Not teaching just trying not to look dumb in my SCA x Flashcards
Diarrhoea definition
3 or more loose stools in 24 hours
OR
Stools more frequent for that person >14days
OR
Stool weight >200g/day
Time course classification of diarrhoea
Acute <14 days
Persistent >14 days
Chronic >30 days
How much of the 10L of fluid entering the GIT that most people ingest/have from secretions is reabsorbed
99% so 100mL is excreted in faeces
Inflamm vs Non-Inflammatory diarrhoea
INFLAMMATORY:
- Bacteria, viral or parasite or IBD
- Mucoid or bloody stool
- Tenesmus
- Fever
- Crampy abdo pain
Infectious inflammatory:
- small vol, frequent, nil volume depletion
- C.diff, E.coli, shigella, salmonella
NON-INFLAMMATORY:
- Watery, large volume, frequent stool
- Volume depletion possible
- No tenesmus, blood, fever
A) Secretory:
- altered ion transport across mucosa so you have less absorption of fluids and electrolytes
- Enterotoxins (E.coli, rotavirus, V cholerae)
- Hormonal stuff
- Laxatives
B) Osmotic:
- Small stool volume
- From unabsorbed or poorly absorbed solute (magnesium, sorbitol, mannitol) so you have increased secretion of fluid into the gut lumen
- Improves or stops with fasting
- Maldigestion: impaired digestion in lumen or brush border e.g. lactase deficiency, pancreatic exocrine insufficiency
- Malabsorption: short bowel syndrome, mucosal disease like coeliac,
What are the most common causes of infectious diarrhoea
Watery:
- Norovirus
- Rotavirus
- E.coli
- Campylobacter
Inflamm:
- C.diff
- E.coli
- Shigella
- Salmonella
Astrovirus
RNA
Mostly causes diarrhoea in young children, immunocompromised, or older institutionalised patients
Can also cause encephalitis in humans
What meds can cause diarrhoea
Antibiotics
B-blockers
NSAIDs
PPIs
Colchicine
Laxative overuse
Anti-arrhythmics like quinidine
Diabetic meds e..g metformin
How does volume depletion present
Increased thirst
Reduced urine output
Dark urine
Lack of sweat
Orthostatic symptoms
When should you investigate diarrhoea
Dysentery
Total disability due to diarrhoea
Severe pain
Symptoms >7 days
What Ix do you do for diarrhoea
Usually just a clinical diagnosis!
Stool MCS + enteric PCR
- Do ova if persistent diarrhoea
Faecal calprotectin if ?IBD
FBC: anaemia, WCC
UECs: electrolyte disturbances, hypokalaemia, acidosis, renal dysfunction
CRP: systemic inflamm
Lactic acid: ischaemia
Antibody testing if ?AI
Abdo X-Ray/CT: good to identify complications (ileus, perforation, megacolon, obstruction)
Scope if IBD, pseudomembrane?, bleed
Viral vs Bacterial Diarrhoea
VIRAL:
- Self limiting <14 days
- Frequent symptoms: vomiting, diarrhoea, nausea
- May have fever, abdo pain and anorexia
BACTERIAL:
- High fever
- Blood
- Severe diarrhoea
- Probs faecal leucocytes and positive lactoferrin (neutrophil derived marker of intestinal inflamm) in stool = inflammation
Viral diarrhoea top causes
Norovirus
Rotavirus
Astrovirus
Enteric adenovirus
Why do these viruses cause diarrhoea
Damage the mucosa so impaired fluid absorption
Histology:
- Villous shortening
- Crypt hyperplasia
- Mononuclear inflammatory infiltrate
What is the usual mx of viral gastroenteritis
Oral (with Na, K and glucose is in the WHO one) or IV rehydration
Consider an anti-emetic but don’t routinely use (don’t want to mask symptoms)
- Ondansetron or cyclizine is first line
- Metoclopromide has neuro risks (EPS)
DO NOT routinely use anti-emetics (may prolong an inflammatory/infective disease or mask symptoms)
- Loperamide 1st line
What is a diverticular
herniation of colonic mucosa through the muscular wall of the colon at a weak point
- Usually between taenia coli where the vasa recta are
- Happen when there is sustained increased intraluminal pressure (low fibre diet, chronic constipation)
- Rectum is usually spared because no taenia coli
What are the complications of diverticulosis
Haemorrhage
Fistula
Perforation –> peritonitis or abscess
Diverticulitis !
Pathophys of diverticulitis
Neck of the diverticular become obstructed –> localised inflammation of mucosa –> ischaemia, bacterial translocation, trans-mural inflammation –> perforations –> abscess or peritonitis
diverticulitis RFs
Age
Lack of fibre
Obesity
Sedentary lifestyle
Diverticulitis presentation
LIF pain and tenderness
Anorexia, N, V
Diarrhoea or constipation
Can get LURT sx
Fever
Sometimes PR bleeding
Ex:
Reduced bowel sounds
Tender LIF
Gold standard diverticulitis Ix
CT! Best at confirming diagnosis and extent of the disease
- Colonic diverticulosis
- Pericolic fat stranding
- Bowel wall thickening
- Abscess?
Avoid colonoscopy initially due to perf risk
Diverticulitis Mx
Mild: oral ABx (Augmentin, maybe Taz) and liquid diet
Worse: IV Abx (Augmentin), IVH, NBM
Surgery:
- Hartmann’s procedure: sigmoid colectomy with end colostomy formation, reverse 3mo later
- Sigmoid resection with primary anastomosis and proximal defunctioning stoma )loop ileostomy) then later close the stoma
How do you judge which surgery you do for diverticulitis
Hinchey Classification so depending on abscess to peritonitis (either purulent or faecalent)
What are the fistulas you can get with diverticulitis
Colovesical: urinary sx, suprapubic pain, cystitis sx, gass in urine (more common in men)
Colovaginal: purulent discharge
LLQ Pain DDx
Acute diverticulitis
Ulcerative colitis > Crohns
Gastroenteritis (is more likely to be umbilical though)
Females: ectopic pregnancy, ovarian pathology, fallopian tube pathology
Explain jaundice
- From high levels of bilirubin in the blood
- Bilirubin is the breakdown product of haem so it comes from broken down RBCs
- Bilirubin is conjugated in the liver so it’s water soluble and excreted via the bile into the GI tract
- RBCs haem biliverdin unconjugated bilirubin conjugated in the liver
- Unconjugated bilirubin urobilinogen + stercobilinogen
- In jaundice, high levels of bilirubin are excreted by the kidneys (dark urine)
- Pale stool suggests an obstructive jaundice as stercobilinogen is absent from the stool (gives stool it’s colour)
Pathological effects of cholelithiasis
Silent
Cholecystitis
Mirrizi syndrome (cystic duct/hartmann’s pouch) –> compresses the common hepatic duct
Choledocolithiasis
Gallstone ileus
Cholecystitis on imaging
Thickened gb wall
pericholecystic fluid
CT can’t see which GB stone
cholesterol
MRCP is good for
CBD stones
Mx of cholecystitis
Cefazolin
Clear fluids only
Analgesia
Cholecystectomy within 72 hrs
Choledocolithiasis presentation
attacks of biliary colic with obstructive jaundice (pale stool, dark urine) which lasts hours or days
if not relieved you get back pressure and biliary cirrhosis or liver failure
Ix for choledocolithiasis
FBC: WCC
CRP
Lipase: pancreatitis
LFTs: cholestatic picture (ALP, GGT, BR) (can have increased ALT and AST if back-pressure)
Abdo USS
Abdo CT
If CBD then fo MRCP is great
Leave ERCP for therapy
Percutaneous transhepatic cholangiography (PTC) only in those who can’t have ERCP but need draining/stenting of bile duct
Mx of choledoclithiasis
Most are ABx (metronidazole) and pain relief and then cholecystectomy within 6 weeks
ERCP or PTC if need stent/draining
Complications of choledocolithiasis
Leakage of bile
Jaundice
Pancreatitis
Ascending cholangitis
Courvoisier’s Law
In the presence of jaundice, if the GB is palpable then the jaundice is unlikely to be stone
If obstruction causing jaundice then GB not usually distented so probably cancer
So if there’s jaundice and you feel the GB –> probs cancer oops unlucky
Ascending cholangitis presentation
Charcot’s triad: jaundice, fever RUQ pain
Reynold’s pentad: jaundice, fever, RUQ pain, hypotension, confusion
Can get obstructive symptoms
Ascending cholangitis mx
ERCP is gold standard
Will maybe need stent
Metronidazole
IV Fluids
Blood cultures
Analgesia
Causes of hypothyroidism
Hashimotos (anti-TPO, anti-TG)
Drugs: lithium, amiodarone, immune checkpoint inhibitors
Iodine deficiency
Sx of hypothyroidism
Dry skin
Bradycardia
Slow reflexes
Mental slowness
Thing hair
Tired
Weight gain
Depression
Reduced lipido
Goitre
Puffy eyes
Arthralgia
Cold intolerance
How can phenytoin (other anti-epilepsy drugs too) cause hypothyroidism
Induces hepatic CYP450 enzyme which breaks down thyroid enzymes
What are 1st line epilepsy drugs
Sodium valproate- all types
Lamotrigine (all but absent)
Carbamazepine (tonic-clonic only)
But don’t treat after just the 1st seizure as only 50% end up having another
Phenytoin
Anti-convulsant
Blocks voltage gated Na channels so takes a bigger signal to depolarise and cause AP
Good for tonic-clonic and simeple partial seizures/focal seizures but not absence
How can you see if someone had a seziure
Prolactin increases after a tonic-clonic
EEG
MRI HEad to see focal areas??
Tonic clonic seizure
A generalised seizure so impaired consciousness, distorted electrical activity in whole or big bit of brain
Tonic phase: tense muscles
Clonic phase: relax and contract lots so convulse
Post-ictal: altered consciousness
Simple partial/focal
Partial seizures only affect one part of brain
Simple don’t impair consciousness and they’re just one part so motor or sensory or autonomic
Omeprazole
Inhibits the H/K ATPase in gastric parietal cells so less H+ goes into the gastric lumen so you get less HCl and therefore less GORD
Another kind of drug for GORD is H2 receptor inhibitor as this activates the cAMP dependent pathway of the H/K ATPase
escitalopram
SSRI
MOA: inhibits the serotonin reuptake transporter (SERT) so you have more serotonin in the synapse –> monoamine theory of depression
For depression
SEs:
- QT prolongation
- GI side effects: esp N
- Headaches
- Dry mouth
- Insomnia
- Sexual dysfunction
- Serotonin syndrome
pravastatin
Inhibits HMG-CoA reductase in the biosynthesis pathway of cholesterol in the liver
SEs:
- Muscle pain
- N
- Lethargy
Budesonide/formaterol
Budesonide = corticosteroid
Formaterol = LABA (long acting beta agonist)
Salbutamol
SABA (short acting beta agonist)
