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PHASE 2A REVISION Qs > pts mock 2 > Flashcards

pts mock 2 Flashcards

1
Q

What is the imaging of choice for diverticulitis

A

CT ab/pelvis with contrast. Would demonstrate a thickened bowel wall

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2
Q

Diverticulitis management

A
  • Mild presentation: oral antibiotics, analgesia, low residue or liquid diet
  • Severe presentation:
    • Supportive management:NBM, IV fluids and analgesia
    • IV antibiotics:co-amoxiclav is typical but depends on local guidelines
    • Acute PR bleeding: transfuse blood products and arrange angiographic embolisation (blocks blood vessels) if available, otherwise, surgery is required
    • Surgery: if bleeding is not controlled or perforation is present, emergency surgical resection is required e.g. Hartmann’s procedure (removing the affected section of the bowel and creating an alternative path for faeces to be passed).
  • Diverticular abscess: radiological drainage or surgery
  • Recurrent diverticulitis: elective colonic resection
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3
Q

colonoscopy of crohn’s

A
  • Mucosal inflammation, deep ulcers, skip lesions and cobblestone mucosa
  • Histology: transmural inflammation, granulomas and goblet cells
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4
Q

Maintaining remission of Crohn’s

A

1st line: Azathioprine or Mercaptopurine

2nd line:Methotrexate, Infliximab, Adalimumab

Post-surgery: consider azathioprine, with or without methotrexate

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5
Q

Colonoscopy of UC

A
  • Red and raw mucosa with widespreadshallow ulceration
  • No inflammation beyond the submucosa, unless fulminant disease
  • Lamina propria inflammatory cell infiltrates
  • Pseudopolyps: mucosa adjacent to ulcers is preserved, which has the appearance of polyps
  • Crypt abscessesdue to neutrophil migration through gland walls
  • Goblet cell depletion, withinfrequent granulomas
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6
Q

What is the scoring system for ulcerative colitis

A

Truelove and Witts’ severity index

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7
Q

management for ulcerative colitis

A 
Mild = 1st line aminosalicylate and 2nd line corticosteroids
(if limited to the sigmoid flexure - proctosigmoiditis and left-sided colitis- use a topical aminosalicylate, for extensive - from proximal to the sigmoid - use topical and high dose oral)
Acute severe (any site) = 1st line IV corticosteroid and 2nd line IV ciclosporin
Maintenance = aminosalicylate, azathioprine, mercaptopurine
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8
Q

Surgery for people with ulcerative colitis

A
  • Colectomy may be required: leaves patient with J-pouch (can be reversed) or ileostomy.
    • J- pouch: ileoanal anastomosis, colon removed and rectum fused to ileum
    • Ileostomy: colon and rectum are removed and the ileum brought out on
      to the abdominal wall as a stoma
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9
Q

Tubulo-interstitial causes of AKI

A

usually due to acute tubular necrosis (ATN). Other tubulointerstitial causes include acute interstitial nephritis that can occur secondary to medications (e.g. NSAIDs, PPI’s, penicillins) and infections. This typically leads to damage to the renal parenchyma that can lead to scarring and fibrosis in the long-term.

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10
Q

what levels are assessed before starting azathioprine or mercaptopurine

A

Thiopurine methyltransferase (TPMT)

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11
Q

signs of nephritic syndrome in AKI

A

Nephritic syndrome: haematuria; proteinuria; oliguria and hypertension

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12
Q

signs of tubulo-interstitial disease in AKI

A

arthralgia, rashes and fever

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13
Q

complications of AKI

A

hyperkalaemia, fluid overload, metabolic acidosis, uraemia, Uraemic complications

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14
Q

how do you protect the myocardium with hyperkalaemia

A
  • Protection of the myocardium:10ml of 10% calcium gluconate.
  • Reduce extracellular potassium: aim is to drive potassium into the intracellular compartment. Insulin and beta agonists (e.g. 2.5mg nebulised salbutamol) are given.
  • Additional: stop or adjust potassium-sparing or potassium-containing medications. Resins can reduce potassium absorption but these takehours/days to have effect.
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15
Q

treatment of metabolic acidosis

A

sodium bicarbonate or dialysis

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16
Q

Give examples of nephrotoxic drugs

A

ACEi, NSAIDs, Spironolactone

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17
Q

Prostatitis (acute) medication

A
  • Antibiotics: courses typically 14 days
    • First line:Oral ciprofloxacinor ofloxacin
    • Second line:Oral levofloxacin or co-trimoxazole
    • IV antibiotics: for patients with significant infection under microbiology guidance.
  • TRUSS guided abscess drainage, if needed
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18
Q

reiter’s syndrome triad

A

Reactive Arthritis
urethritis, arthritis and conjunctivitis (might also get mouth ulcers)
Typically get acute, asymmetrical monoarthritis, typically in the lower leg

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19
Q

Budd-Chiari syndrome presentation

A

presents with abdominal pain, ascites and liver enlargement

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20
Q

Saint’s triad

A

hiatus hernia, cholelithiasis and colonic diverticulosis

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21
Q

What is dalteplarin

A

LMWH

22
Q

prophylaxis for dvt after hip replacement

A

Patients undergoing an elective hip replacement should be given
thromboprophylaxis with either a low molecular weight heparin administered for 10 days
followed by low-dose aspirin for a further 28 days, or a low molecular weight heparin
administered for 28 days in combination with anti-embolism stockings until discharge,
or rivaroxaban

23
Q

what is apixaban

A

an anticoagulant

24
Q

what is the target for rituximab

A

CD20

25
Q

First line for uncomplicated malaria

A

Artemether with lumefantrine (Riamet)

26
Q

First line for complicated malaria

A
  1. Artesunate- this is the most effective treatment but is not licensed.
  2. Quinine dihydrochloride
27
Q

What is the name for a malignant tumour of smooth muscle

A

Leiomyosarcoma

28
Q

What is the medication for paracetamol overdose

A

N-acetyl cystine

29
Q

What enzyme degrades trypsin

A

chymotrypsin C

30
Q

What are the causes of acute pancreatitis

A

I GET SMASHED, pregnancy, neoplasia

31
Q

Genetic link to pancreatitis

A

PRSS1

32
Q

Signs of Pancreatitis

A

Should be suspected in any person with:

  • Acute upper or generalised abdominal pain, particularly if they have a history or clinical features of gallstonesoralcohol misuse
  • Abdominal tenderness and guarding
  • Abdominal distension
  • Jaundice
  • Cullen’s sign - periumbilical bleeding, secondary to intraperitoneal haemorrhage
  • Grey Turner’s syndrome - flank bleeding secondary to retroperitoneal haemorrhage
  • Fox’s sign: bleeding over the inguinal ligament secondary to retroperitoneal haemorrhage
33
Q

symptom of pancreatitis

A

Poor urinary output: due to insensible fluid losses, third-spacing (movement of fluid from intravascular to interstitial spaces)

  • Nausea, vomiting and anorexia
  • Severe upper abdominal pain
  • Steatorrhoea
34
Q

the scoring of pancreatitis

A

Modified glasgow scoring

35
Q

Primary investigation of pancreatitis

A
  • Serum amylase: amylase rises faster than lipase but also levels fall faster within 24-48hrs; less specific than lipase; isnotof prognostic value. Serum amylase may be raised in other conditions such as renal failure, so is non-specific
  • Serum lipase: more specific for acute pancreatitis; levels rise slower than amylase but have a longer half-life. Amylase is tested more frequently in the UK
36
Q

Acute pancreatitis treatment

A

IV Fluid resuscitation…

  • ERCP
  • Cholecystectomy
  • Alcohol cessation and withdrawal management
37
Q

PBC key presentation

A

The classic presentation of PBC is with significant itching in a middle-aged female. (I think its just jaundice really from charcot’s triad)

38
Q

Signs of PBC

A
  • Skin hyperpigmentation: due to increased melanin
  • Clubbing
  • Mild hepatosplenomegaly
  • Xanthelasma and xanthomata (late sign) - due to leakage of cholesterol
  • Scleral icterus (late sign)
39
Q

Symptoms of PBC

A
  • Pruritis (itchy skin) - leakage of bile salts
  • Fatigue and weight loss
  • Dry eyes and dry mouth - Sjögren’s syndrome
  • Obstructive jaundice (late sign)
40
Q

Management of PBC

A
  • Ursodeoxycholic acid (A bile acid analogue which dampens the inflammatory response, acts as an anti-apoptotic agent, and improves cholestasis)
  • Fat-soluble vitamin supplementation: cholestasis impairs fat absorption
  • Cholestyramine
  • Codeine phosphate: for diarrhoea
  • Biphosphonates: for osteoporosis
41
Q

Gold standard investigation for acute cholecystitis

A

Abdominal ultrasound -

  • Pericholecystic fluid
  • Distended gallbladder
  • Thickened gallbladder wall (>3 mm)
  • Gallstones
  • Positive sonographic Murphy’s sign
42
Q

Gold standard for PSC

A

ERCP - but has been replaced by MRCP as MRCP is less invasive.

43
Q

empirical first line treatment for septic arthritis

A

flucloxacillin

44
Q

First line treatment for withdrawal seizures

A

chlordiazepoxide

45
Q

What is sjorgrens syndrome

A

Sjogren’s syndrome is the immune destruction of exocrine glands and often presents with arthritis,
dry eyes and dry mouth. The Schirmer test involves placing a small strip of paper in the eye to
measure tear production and is used in the diagnosis of Sjogren’s, alongside lacrimal gland biopsy
and antibody testing.

46
Q

treatment for ankylosing spondylitis (in order)

A
  • NSAID e.g. ibuprofen or naproxen (2-4 weeks. If no improvement, switch to another NSAID)
  • Steroid - used during flares (oral, IM or directly into joints)
  • Anti-TNF e.g. etanercept or monoclonal antibodies against TNF e.g. infliximab, adalimumab
  • Monoclonal antibodies targeting IL-7 - e.g. secukinumab
47
Q

What is pseudogout

A

Pseudogout is a form of inflammatory arthritis caused by deposition of calcium pyrophosphate crystals in the synovium.

48
Q

The greatest risk factor for pseudogout

A
  • increasing age (the greatest)
    • Previous joint trauma
  • Hyperparathyroidism
  • Haemochromatosis
49
Q

What is Reiter’s triad

A

Reactive arthritis secondary to a Chlamydia infection. This can cause Reiter’s
triad of conjunctivitis, urethritis and arthritis (can’t see, can’t pee, can’t climb tree) as well as
keratoderma blennorrhagium (the rash on his feet) and mouth ulcers

50
Q

Explain Amaurosis Fugax

A

Often described as a black curtain coming across the vision.
A classical syndrome of painless short-lived monocular blindness.
It is a term usually reserved for transient visual loss of ischaemic origin.
- Occurs due to the temporary reduction in the retinal, ophthalmic or ciliary blood flow leading to temporary retinal hypoxia.
- The principle cause of amaurosis fugax is transient obstruction e.g. due to emboli, of the ophthalmic artery, which is a branch of the internal carotid artery.
- However, other ischaemic causes to consider include giant cell arteritis (i.e. temporal arteritis) and central retinal artery occlusion.

51
Q

What is Polymyalgia rheumatica

A

is a condition that causes pain, stiffness and inflammation in the muscles around the shoulders, neck and hips.

PHASE 2A REVISION Qs (12 decks)

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