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Medicine Y6 > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

Upper GI bleed: score for admission / intervention risk + parameters + use of score

A

Blatchford Score Parameters:

Blood urea nitrogen

Hb

Systolic BP

Other (HR>100, melena, syncope, hepatic pathology, HF)

Score: 0 = low risk, outpt 1-5 = admit 5< = high risk of intervention

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2
Q

Upper GI bleed: score for prognosis + parameters + use of score

A

Rockall Score (post-OGD)

Age

Shock (HR, BP)

Co-morbidities

Dx on OGD

Evidence of bleeding on OGD

Score gives % risk of mortality on rebleed

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3
Q

Upper GI bleed: DDx

A

PUD (40%, usually DU)

Gastritis (20%)

Mallory-Weiss

Varices

Oesophagitis

Ca stomach / oesophagus

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4
Q

Sepsis Six

A

Give 3 things:

  1. O2 high-flow (maintain >94%)
  2. IV fluids
  3. IV antibiotics

Take 3 things:

  1. blood cultures
  2. blood lactate
  3. urinary catheter (monitor output hourly)
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5
Q

Drug-induced liver disease: which drugs induce liver disease with a hepatocellular picture on LFTs?

A

SAM’S HEPATIC

Statins

Amiodarone

Methyldopa

Sodium valproate, phenytoin

Halothane (an anaesthetic)

ETOH

Paracetamol

Antibiotics: nitrofurantoin

TB drugs: isoniazid, rifampicin, pyrazinamide

Inhibitors of MAO

Cirrhosis-causing drugs (methotrexate, methyldopa, amiodarone)

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6
Q

Drug-induced liver disease: which drugs induce liver disease with a cholestatic picture on LFTs?

A

CAAPS

COCP

Antibiotics: flucloxacillin, co-amoxiclav, erythromycin

Anabolic steroids, testosterone

Phenothiazines: chlorpromazine, prochlorperazine

Sulphonylureas (gliclazide)

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7
Q

IBS: red flags for other causes

A
  • unexplained wt loss
  • rectal bleeding
  • FHx of bowel/ovarian Ca
  • >60y old + increasingly frequent/loose stools for the past 6w
  • anaemia
  • abdominal masses
  • rectal masses
  • inflammatory makers for IBD

(NICE)

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8
Q

IBS: diagnostic criteria

A

Rome IV Criteria (2016):

recurrent abdominal pain/discomfort on average +1d/w in the last 3m and associated with 2+ of

related to defecation

change of stool frequency

change of stool form

(UpToDate, BMJ)

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9
Q

Identify appropriate investigations for irritable bowel syndrome (IBS)

A

Bloods: FBC, ESR, CRP, anti-TTG or anti-endomysial Abs

Mainly to exclude other diagnoses (IBD, malignancy, coeliac)

(NICE)

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10
Q

Generate a management plan for irritable bowel syndrome (IBS)

A
  • Conservative
    • Education
      • reduce stress, increase exercise
      • dietary: regular meals, 8 cups of fluids /d, max 3 caffeinated drinks, reduce EToH, reduce intake ‘resistant starch’ (processed food), max 3 fresh fruit/d
      • if diarrhoea - avoid sorbitol (sweetener). If bloating - eat oats
      • try altering amount of fibre in diet (reduction), try exclusion diets (FODMAP)
      • Probiotics, alternative medicine
  • Medical
    • Antispasmodics PRN (eg dicyclomine)
    • If stool too loose: loperamide
    • If stool too hard: laxatives
      • 1st line: Movicol (avoid lactulose)
      • 2nd line: Linaclotide (if no response for 12m)
    • 2nd line: TCAs
    • 3rd line: SSRIs
  • Psychological
    • CBT - if not response to medical mx over 12m

(NICE)

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11
Q

What is the scoring system for the severity of pancreatitis

A

Modified Glasgow Imrie Score: PANCREAS

PaO2 <8kPa

Age >55

Neutrophils (WCC) >15x10^9

Calcium <2

Renal (Urea) >16 mmol/L

Enzymes: LDH>600, AST>200

Albumin <32 g/L

Sugars >10 mmol/L

Score calculates severity at 48h from admission. <3 = mild/moderate. 3+ = severe pancreatitis (consider HDU)

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12
Q

Explain the aetiology / risk factors of pancreatitis

A

GET SMASHED

Gallstones

EToH

Trauma

Steroids

Mumps

Autoimmune

Scorpion bite

Hypercalaemia, hyperlipidaemia

ERCP

Drugs (mesalazine, azathioprine, furosemide, sodium valproate)

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13
Q

Identify the possible complications of pancreatitis (acute and chronic)

A
  • Short:
    • Electrolyte / endocrine: hypocalcaemia, hypoglycaemia, hyperglycaemia
    • Pancreatic: pancreatic abscess/effusion/pseudocyst, necrotising pancreatitis
    • Systemic: AKI, ARDS, SIRS, DIC, haemorrhage (GI or intraperitoneal), MODS
  • Long: pancreatic insufficiency, chronic pancreatitis, portal vein thrombosis, enteric fistula, intestinal obstruction

(BMJ, UpToDate)

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14
Q

Generate a management plan for acute pancreatitis

A
  • Medical (ABCDE):Initial
    • IV fluids (normal saline, if fluids resus needed). Measure UO /h
    • High-flow O2 (if not saturating at 94%)
    • Analgaesia (WHO ladder, often IV opiates eg fentanyl)
    • IV Abx (if cholecystitis or infective)
    • Enteral feeding - if tolerated
  • Surgical
    • If gallstones:
      • ERCP w/i 72h onset of pain
      • Cholecystectomy (same admission, unless prolonged disease course)

(NICE, UpToDate)

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15
Q

How can the three types of AI hepatitis be differentiated on serology?

A

Type 1: ANA +ve and/or smooth-muscle Ab +ve, adults + children

Type 2: anti-liver/kidney microsomal type 1 Ab +ve, children only

Type 3: soluble liver-kidney antigen, middle-aged adults

(passmedicine)

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16
Q

What are the main risk factors for AI hepatitis?

A

RFs:

  • female
  • genetic: HLA B8, HLA DR3
  • PMHx: AI dx, hypergammaglobinaemia

(passmedicine)

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17
Q

Identify appropriate investigations for autoimmune hepatitis

A
  • Confirm diagnosis
    • Bloods: LFTs, ANA, SMA, anti liver/kidney microsomal type 1 Ab
    • Biopsy: piecemeal necrosis, bridging necrosis
  • Plan tx:
    • Bloods: FBC, UEs, clotting
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18
Q

Generate a management plan for autoimmune hepatitis

A
  • Medical
    • Steroids
    • Immunomodulators: azathioprine
  • Surgical
    • Liver transplant

(passmedicine)

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19
Q

Identify the possible complications of autoimmune hepatitis

A
  • Immediate: acute liver failure
  • Early: azathioprine-associated SEs (infections, neutropenia, pancreatitis)
  • Late: hepatocellular carcinoma, end-stage liver disease, steroid-associated SEs (DM, osteoperosis, obesity, HTN),

(BMJ)

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20
Q

Summarise the prognosis for patients with autoimmune hepatitis

A

Morbidity: 80% achieve remission w/i 3y. On long-term azathioprine, ~20% relapse.

Mortality: 10y survival >90%

(BMJ)

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21
Q

Define primary sclerosing cholangitis

A

Primary sclerosing cholangitis is a biliary disease of unknown aetiology characterised by inflammation and fibrosis of intra and extra-hepatic bile ducts

(passmedicine)

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22
Q

Explain the risk factors of primary sclerosing cholangitis

A
  • Female, 40s
  • PMH:
    • ulcerative colitis: 4% of patients with UC have PSC, 80% of patients with PSC have UC
    • Crohn’s (much less common association than UC)
    • HIV
  • ANCA +ve, anti-smooth muscle Ab +ve

(passmedicine)

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23
Q

Summarise the epidemiology of primary sclerosing cholangitis

A

13 / 100 000

F:M 2:1

Typically presents around 40y

(BMJ)

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24
Q

Generate a management plan for primary sclerosing cholangitis

A
  • Conservative: healthy diet + wt, limit ETOH
  • Medical
    • Symptom control
      • Pruritus relief: Colestyramine (or rifampicin, sertraline)
        • ergocalciferol + calcium carbonate if osteopenic OR bisphosphonates +/- HRT if osteoperotic
  • Interventional procedure
    • ERCP + stenting: if acutely ill + biliary stricture
  • Surgical
    • Liver transplant: if end-stage liver disease

(BMJ)

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25
Q

Identify the possible complications of primary sclerosing cholangitis

A

Immediate: acute liver failure (hepatic encephalopathy, bacterial cholangitis)

Early: fat soluble vitamin (ADEK) deficiencies

Late: chronic liver disease (ascites, oesophageal varices, choledocholithiasis)–> cirrhosis, cholangiocarcinoma (in 10%), HCC, increased risk of colorectal cancer

(passmedicine)

26
Q

Summarise the prognosis for patients with primary sclerosing cholangitis

A

Mortality: median survival 7-14y. After transplant 10y survival is 70%

Morbidity: up to 35% undergo liver transplant

(BMJ)

27
Q

Generate a management plan for ulcerative colitis

A
  • Remission induction (medical, depends on severity)
    • Mild/moderate 1st presentation or exacerbation of proctocolitis:
      • 1st: rectal and/or oral aminosalicylates (mesalazine)
      • +/- oral beclometasone diproprionate
      • 2nd: rectal and/or oral steroids (preferable if subacute)
      • No response at 4w: combine 1 + oral 2
      • Still no repsonse at 4w: consider oral tacrolimus
      • Last line: infliximab
    • Acute severe:
      • 1st: IV corticosteroids
      • 2nd: IV ciclosporin (if steroids CI, not tolerated)
      • 72h or progressing: 1 + 2 or surgery
    • Vaccinations (before starting immunosuppressants)
      • flu, pneumococcal, HepB, HPV, VZV (if seronegative)
  • Maintenance of remission
    • Mild/moderate: aminosalicylate (oral or rectal or both)
    • Extensive (left-sided): oral aminosalicylate
    • All extents (or acute severe, or 2 episodes/y requiring steroids):
      • 1st: oral azathioprine or oral mercaptopurine
      • 2nd: oral aminosalicylates (if 1 CI, not tolerated)
  • Monitor growth/bone health in children on steroids

(NICE)

28
Q

What are the risk factors for ulcerative colitis?

A

Strong RFs:

  • IBD FHx
  • HLA-B27
  • infection: enteritis is RF for relapse

Weak RFs:

  • NSAIDs
  • Non-smoker

(BMJ)

29
Q

Identify appropriate investigations for ulcerative colitis

A

Confirm diagnosis

  • Stool studies: cultures and faecal calprotectin (bowel inflammatory marker)
  • Bloods: CRP, ESR (at same time: FBC, LFTs (assoc w primary sclerosing cholangitis), UEs
  • Colonoscopy + biopsy
  • Consider: AXR, double-contrast barium enema

Screen for complications

  • Colonoscopy (Ca screening in long-standing cases)
  • (BMJ)*
30
Q

Identify the possible complications of ulcerative colitis

A
  • Early: inflammatory pseudopolyps, toxic megacolon, infection, perforation, lower GI bleed
  • Late: benign stricture, colonic adenocarcinoma, primary sclerosing cholangitis

(BMJ)

31
Q

Summarise the prognosis for patients with ulcerative colitis

A

Mortality: slightly higher overall mortality compared to general population. Toxic megacolon most common cause of death

Morbidity: 2/3 pts relapse w/i 10y of dx. 20-30% require colectomy.

(UpToDate, BMJ)

32
Q

Outline clinical features which may enable you to distinguish between Crohn’s disease and ulcerative colitis

A

(passmedicine)

33
Q

Ascending cholangitis: Charcot’s triad

A

Fever + RUQ pain + jaundice

34
Q

Summarise the epidemiology of ascending cholangitis

A

50-60y

M=F

(BMJ)

35
Q

Explain the aetiology of ascending cholangitis

A
  • Gallstones - most common cause. 1% risk
  • ERCP - 1% risk
  • Primary sclerosing cholangitis
  • Benign biliary stricture (chronic pancreatitis, chemoradiotherapy, post-surgical)
  • Malignant biliary stricture (cholangiocarcinoma, pacreatic ca, ampullary ca)

(BMJ)

36
Q

Generate a management plan for ascending cholangitis

A

Medical (ABCDE)

  • Sepsis six: including IV antibiotics (1st: tazocin or cef + met)
  • Analgaesia: IV opiates
  • Urgent biliary decompression (w/i 24-48h depending on severity)
    • ERCP + lithotripsy
    • Percutaneous transhepatic cholangiography (if ERCP CI)

Surgical (largely replaced by non-operative techniques)

  • Biliary decompression; or choledocotomy + T-tube insertion; or lap cholecystectomy
      • analgaesia + IV antibiotics

(BMJ)

37
Q

Identify the possible complications of ascending cholangitis

A

Early: sepsis, MODS, acute pancreatitis

Late: post-interventional impaired biliary drainage

(BMJ)

38
Q

Summarise the prognosis for patients with acute cholangitis

A

Rapid biliary decompression associated with good outcome

Poor prognostic factors: hyperbilirubinaemia, high fever, high WCC, elderly, hypoalbuminaemia, requiring surgical intervention

(BMJ)

39
Q

Identify appropriate investigations for ascending cholangitis

A

Confirm diagnosis

  • Bloods: CRP, ESR, FBC, LFTs, UEs, cultures
  • Imaging: USS abdo (90% show dilation of CBD)
  • ECRP is therapuetic

(passmedicine)

40
Q

GP: what are the recommendations for 2w-wait referral for ?colonic malignancy

A

Referral from GP - 2w wait

  • All pts with
    • >40 + unexplained wt loss + abdo pain
    • >50 + unexplained rectal bleeding
    • >60 + IDA or change in bowel habit
    • faecal occult blood +ve
  • Consider pts with
    • rectal / abdominal mass
    • unexplained anal mass / ulceration
    • <50 + rectal bleeding + abdo pain / wt loss / IDA / change in bowel habit

(passmedicine, NICE)

41
Q

Generate a management plan for haemorrhoids

A
  • Conservative:
    • Increase dietary fibre, increase fluid intake
  • Medical
    • Topical anaesthetics + topical steroids
    • Rubber band ligation: outpt
    • Doppler guided haemorrhoidal artery ligation
  • Surgical: only for large symptomatic haemorrhoids, not reponsive to previous tx
    • Stapled haemohorroidopexy

(passmedicine)

42
Q

What are the possible causes of ascites?

A

‘PINCH’

Portal HTN (esp cirrhosis)

Inferior vena cava obstruction

Neoplasms (ovarian malignancy, peritoneal mets)

Constrictive pericarditis

Hypoproteinaemia: nephrotic syndrome, liver failure, malabsorption

(Meeran)

43
Q

Give the common causes of hepatomegaly

A
  • Most common
    • Cirrhosis
    • Malignancy
    • R-sided HF
  • Less common
    • Infective: viral, bacterial (Weil’s)
    • Myoproliferative (leukaemia, myelofibrosis)
    • Biliary obstruction
44
Q

Generate a management plan for Crohn’s disease

A
  • Conservative: stop smoking, some evidence for avoiding NSAIDs + COCP, monitor wt gain (children)
  • Medical:
    • Acute - induce remission
      • 1st: steroids (oral/IV, topical in rectal disease)
        • if not tolerated, consider budesonide or enteral elemental feeding
      • 2nd: mesalazine
      • 3rd: + azathioprine or mercaptopurine or methotrexate
        • don’t use these as monotherapy
      • 4th: + infliximab (in refractory disease)
    • Long-term - maintain remission
      • 1st: azathioprine or mercaptopurine
      • 2nd: methotrexate
  • Surgical:eg limited ileocaecal resection
    • SEs: perforation, obstruction, toxic megacolon

(passmedicine)

45
Q

Give risk factors of Crohn’s disease

A

RFs: genetic (FHx), smoking, ?COCP , ?NSAIDs, diet rich in refined sugars

(BMJ)

46
Q

Identify the possible complications of Crohn’s disease

A

Early: fistulae, perianal abscess

Late: malabsorption, strictures, toxic dilatation

(AS)

47
Q

Summarise the prognosis for patients with Crohn’s disease

A

10-20% have prolonged remission after initial presentation

80% have surgery

(BMJ)

48
Q

Give potential causes of gynaecomastia

A
  • Physiological (puberty)
  • Congenital: Kleinfelter’s Syndrome (47XXY)
  • Failures: Cirrhosis and kidney failure
  • Endocrine: hypoandrogenism (orchidectomy, prostate ca tx), Addison’s, hyper/hypothyroidism
  • Drugs: spironolactone, digoxin, finasteride

(passmedicine, CfP)

49
Q

Give potential causes of dysphagia

A
  • Obstructive
    • Malignancy (oesophageal, gastric)
    • Stricture
    • Oesophageal web
    • External compression: goitre, largyngeal Ca
  • Motility disorder
    • Achalasia
    • Neurological: stroke, myasthenia gravis
    • Neurodegenerative: Parkinsons +, MND
  • Other: oesophagitis, phargngeal pouch, candida

(500 SBAs)

50
Q

Give potential causes of portal hypertension

A
  • Pre-hepatic: portal vein occlusion, splenic vein occlusion, nephrotic syndrome
  • Hepatic
    • Cirrhosis, sarcoidosis, myeloproliferative disorders, schistosomiasis
  • Post-hepatic: hepatic vein occlusion, R-sided HF, constrictive pericarditis

(path, 500 SBAs)

51
Q

Identify the possible complications of cirrhosis

A
  • Liver failure:
    • coagulopathy
    • encephelopathy
    • hypoalbuminism
    • hypoglycaemia
  • Portal hypertension:
    • splenomegaly
    • ascites (–> spontaneous bacterial peritonitis)
    • oesophageal varices (–> UGI bleed)
    • other portosystemic shunts
  • Increased risk malignancy: HCC

(500SBAs)

52
Q

Define cirrhosis

A

Irreversible liver damage. Histologically: loss of hepatic architecture + bridging fibrosis + nodular (micronodular <3mm, macronodular >3mm) regeneration. ‘Compensated’ = non-symptomatic. ‘Decompensated’ = at least one of ascites, bleeding (variceal), consciousness level drop.

(Y3 notes)

53
Q

Give causes of cirrhosis

A
  • Most common
    • Alcohol liver disease
    • Viral hepatitis (HCV, HBV)
    • Non-alcoholic fatty liver disease
  • Congenital: hereditary haemocromotosis, Wilson’s, alpha1 ATD, CF
  • AI: autoimmune hepatitis, PBC, PSC
  • Drugs: methotrexate, amiodarone, isoniazid
  • Neoplasm: HCC, mets

(AS)

54
Q

How is the severity of cirrhosis graded?

A

Modified Child Pugh Score

  • Ascites: mild = 2, moderate+ = 3
  • Encephelopathy: mild = 2, marked = 3
  • Bilirubin: <34 = 1, 34-50 = 2, 50+ = 3
  • Albumin: >35 = 1, 28-35 = 2, <28 = 3
  • PTT(s): <4 = 1, 4-6 = 2, >6 = 3

Total Score <7 = A = 45% 5y survival

Total Score 7-9 = B = 20% 5y survival

Total Score 10+ = C = <20% 5y survival

55
Q

Identify appropriate investigations for cirrhosis

A

Confirm diagnosis:

  • Bloods: FBC, UEs, clotting, LFTs, glucose, albumin
  • Ascitic tap: chemistry, cytology, MC&S, SAAG
  • Imaging: USS abdo

Screen causes:

  • Viral: HBV, HCV
  • NAFLD: lipids
  • AI: AutoAbs (AMA, ANA, SMA, pANCA)
  • Genetic: caeruloplasmin, ferritin
  • Neoplasm: AFP, Ca199

(AS)

56
Q

Generate a management plan for cirrhosis

A
  • Conservative: Good nutrition (Ensure), ETOH abstinence, avoid NSAIDs/sedatives/opiates
  • Medical:
    • Symptomatic:
      • cholestyramine (pruritus)
      • Ascites – fluid restriction (<1.5L/d), low-salt diet (40-100mmol/d), diuretics (spironolactone PO counters deranged renin-angiotensin system. +/- furosemide PO, watch Na), regular weights, target <0.5kg/d
    • Manage cause
      • Antivirals (HCV, HBV)
      • Primary biliary cirrhosis – high dose ursodeoxycholic acid
      • Wilson’s disease – penicillamine
  • Manage complications
    • Portal hypertension/varices – β-blockers, regular endoscopy
    • Laxatives, phosphate enema – remove toxins to reduce confusion
  • Surgical
    • Transplantation – only definitive Tx. Increase 5yr survival from ~20% in end-stage to ~70%

(Y3 notes)

57
Q

Outline the potential causes of jaundice

A
  • Pre-hepatic = haemolytic = unconjugated
    • Inherited: eg sickle cell, G6PD
    • Acquired:
      • Immune: AIHA (warm/cold, drug induced (penicillin))
      • Non-immune
        • Infections: malaria
        • MAHA: DIC
        • Mechanical: valves
  • Hepatic:
    • Unconjugated: Gilberts, Crigler-Najjar (impared conjugation)
    • Conjugated:
      • Infective: viral (HBV, HCV, CMV, EBV), syphilis, Weils
      • Inflammatory: alcoholic, AI, drugs (methotrexate, amiodarone, methyldopa)
      • Malignancy: HCC, mets
      • Metabolic: HH, Wilson’s, alpha1ATD
  • Post-hepatic = obstructive = conjugated
    • Drugs: CAAPS
    • Inflammatory: PSC, PBC
    • Malignant: cholangiocarcinoma, pancreatic Ca

(Y3 notes)

58
Q

How can you determine whether ascites is due to portal hypertension?

A

Serum Ascites Albumin Gradient (SAAG)

  • SAAG >= 1.1g/dL = transudative = Portal HTN (esp cirrhosis)
  • SAAG <1.1g/dL = exudative
    • Infection: TB peritonitis
    • Inflammation: pancreatitis
    • Malignancy: peritoneal mets, ovarian Ca
    • Nephrotic syndrome

(AS)

59
Q

Identify appropriate investigations for Crohn’s disease

A
  • Confirm diagnosis:
    • Bloods: ESR, CRP
    • Stool: faecal calprotectin
    • Imaging: colonoscopy (diagnostic) + biopsy
      • Small bowel barium enema: rose-thorns, apple-core, Kantor’s sign (string = stricture)

(passmedicine)

60
Q

Define achalasia

A

failure of relaxation of the lower oesophageal spincter due to loss of ganglionic cells in myenteric plexus. Leads to dilation of upper oesophagus (‘birds beak’ appearance)

61
Q

Generate a management plan for achalasia

A
  • Medical:
    • Nifedipine
    • Botulinum toxin injecton
  • Surgical:
    • 1st lineHeller’s myotomy: incise outer muscle layers of lower oesophagus
      • +/- fundoplication (for reflux)

(250 SBAs)

Medicine Y6 (14 decks)

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