Not teaching just trying not to look dumb in my SCA x Flashcards

1
Q

Diarrhoea definition

A

3 or more loose stools in 24 hours
OR
Stools more frequent for that person >14days
OR
Stool weight >200g/day

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2
Q

Time course classification of diarrhoea

A

Acute <14 days
Persistent >14 days
Chronic >30 days

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3
Q

How much of the 10L of fluid entering the GIT that most people ingest/have from secretions is reabsorbed

A

99% so 100mL is excreted in faeces

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4
Q

Inflamm vs Non-Inflammatory diarrhoea

A

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,

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5
Q

What are the most common causes of infectious diarrhoea

A

Watery:
- Norovirus
- Rotavirus
- E.coli
- Campylobacter

Inflamm:
- C.diff
- E.coli
- Shigella
- Salmonella

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6
Q

Astrovirus

A

RNA

Mostly causes diarrhoea in young children, immunocompromised, or older institutionalised patients

Can also cause encephalitis in humans

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7
Q

What meds can cause diarrhoea

A

Antibiotics
B-blockers
NSAIDs
PPIs
Colchicine
Laxative overuse
Anti-arrhythmics like quinidine
Diabetic meds e..g metformin

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8
Q

How does volume depletion present

A

Increased thirst
Reduced urine output
Dark urine
Lack of sweat
Orthostatic symptoms

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9
Q

When should you investigate diarrhoea

A

Dysentery
Total disability due to diarrhoea
Severe pain
Symptoms >7 days

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10
Q

What Ix do you do for diarrhoea

A

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

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11
Q

Viral vs Bacterial Diarrhoea

A

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

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12
Q

Viral diarrhoea top causes

A

Norovirus
Rotavirus
Astrovirus
Enteric adenovirus

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13
Q

Why do these viruses cause diarrhoea

A

Damage the mucosa so impaired fluid absorption

Histology:
- Villous shortening
- Crypt hyperplasia
- Mononuclear inflammatory infiltrate

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14
Q

What is the usual mx of viral gastroenteritis

A

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

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15
Q

What is a diverticular

A

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

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16
Q

What are the complications of diverticulosis

A

Haemorrhage
Fistula
Perforation –> peritonitis or abscess
Diverticulitis !

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17
Q

Pathophys of diverticulitis

A

Neck of the diverticular become obstructed –> localised inflammation of mucosa –> ischaemia, bacterial translocation, trans-mural inflammation –> perforations –> abscess or peritonitis

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18
Q

diverticulitis RFs

A

Age
Lack of fibre
Obesity
Sedentary lifestyle

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19
Q

Diverticulitis presentation

A

LIF pain and tenderness
Anorexia, N, V
Diarrhoea or constipation
Can get LURT sx
Fever
Sometimes PR bleeding

Ex:
Reduced bowel sounds
Tender LIF

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20
Q

Gold standard diverticulitis Ix

A

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

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21
Q

Diverticulitis Mx

A

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

22
Q

How do you judge which surgery you do for diverticulitis

A

Hinchey Classification so depending on abscess to peritonitis (either purulent or faecalent)

23
Q

What are the fistulas you can get with diverticulitis

A

Colovesical: urinary sx, suprapubic pain, cystitis sx, gass in urine (more common in men)

Colovaginal: purulent discharge

24
Q

LLQ Pain DDx

A

Acute diverticulitis
Ulcerative colitis > Crohns
Gastroenteritis (is more likely to be umbilical though)

Females: ectopic pregnancy, ovarian pathology, fallopian tube pathology

25
Q

Explain jaundice

A
  • 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)
26
Q

Pathological effects of cholelithiasis

A

Silent
Cholecystitis
Mirrizi syndrome (cystic duct/hartmann’s pouch) –> compresses the common hepatic duct
Choledocolithiasis
Gallstone ileus

27
Q

Cholecystitis on imaging

A

Thickened gb wall
pericholecystic fluid

28
Q

CT can’t see which GB stone

A

cholesterol

29
Q

MRCP is good for

A

CBD stones

30
Q

Mx of cholecystitis

A

Cefazolin
Clear fluids only
Analgesia
Cholecystectomy within 72 hrs

31
Q

Choledocolithiasis presentation

A

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

32
Q

Ix for choledocolithiasis

A

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

33
Q

Mx of choledoclithiasis

A

Most are ABx (metronidazole) and pain relief and then cholecystectomy within 6 weeks

ERCP or PTC if need stent/draining

34
Q

Complications of choledocolithiasis

A

Leakage of bile
Jaundice
Pancreatitis
Ascending cholangitis

35
Q

Courvoisier’s Law

A

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

36
Q

Ascending cholangitis presentation

A

Charcot’s triad: jaundice, fever RUQ pain

Reynold’s pentad: jaundice, fever, RUQ pain, hypotension, confusion

Can get obstructive symptoms

37
Q

Ascending cholangitis mx

A

ERCP is gold standard
Will maybe need stent

Metronidazole
IV Fluids
Blood cultures
Analgesia

38
Q

Causes of hypothyroidism

A

Hashimotos (anti-TPO, anti-TG)

Drugs: lithium, amiodarone, immune checkpoint inhibitors

Iodine deficiency

39
Q

Sx of hypothyroidism

A

Dry skin
Bradycardia
Slow reflexes
Mental slowness
Thing hair
Tired
Weight gain
Depression
Reduced lipido
Goitre
Puffy eyes
Arthralgia
Cold intolerance

40
Q

How can phenytoin (other anti-epilepsy drugs too) cause hypothyroidism

A

Induces hepatic CYP450 enzyme which breaks down thyroid enzymes

41
Q

What are 1st line epilepsy drugs

A

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

42
Q

Phenytoin

A

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

43
Q

How can you see if someone had a seziure

A

Prolactin increases after a tonic-clonic
EEG
MRI HEad to see focal areas??

44
Q

Tonic clonic seizure

A

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

45
Q

Simple partial/focal

A

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

46
Q

Omeprazole

A

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

47
Q

escitalopram

A

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

48
Q

pravastatin

A

Inhibits HMG-CoA reductase in the biosynthesis pathway of cholesterol in the liver

SEs:
- Muscle pain
- N
- Lethargy

49
Q

Budesonide/formaterol

A

Budesonide = corticosteroid
Formaterol = LABA (long acting beta agonist)

50
Q

Salbutamol

A

SABA (short acting beta agonist)