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MBBS VI Medicine > GI notes > Flashcards

GI notes Flashcards

1
Q

What is serology done for ulcerative colitis and results?

A

ANCA +ve, pANCA +ve, MPO ANCA negative

ASCA is not commonly tested

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2
Q

What can an AXR show in ulcerative colitis?

A

Absence of fecal matter (segmental manner of inflammation cannot hold the feces) hence presenting with diarrhea (doesnt necessarily need bowel prep due to diarrhea)
Dilatation of the bowel (worry about toxic megacolon): >9cm for caecum and >6cm transverse colon
Free gas in the peritoneum due to perforation as a complication of toxic megacolon

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3
Q

Indications in suspected ulcerative colitis for doing colonoscopy?
What is the bowel prep required for colonoscopy?
Is it always indicated in ulcerative colitis?
What are it’s complications?

A

To do biopsy to make histological dx and endoscopic dx + rule out concomitant infection

Bowel prep
* Low residue diet for 2 days
* Fluid diet 1 day before
* Split dose for bowel prep: needs to be drunk fast (not in sips) 1L in 1 hour
Requires sedatives (consious sedation not anaesthesia) and analgesics

RIsks: colonic perforation (1/1000) is higher as there is thinning of the mucosal wall (insufflation will cause rupture)
Bleeding from polypectomy
Vasovagal reaction: normally due to inadequate analgesics

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4
Q

In ulcerative colitis apart from colonoscopy what alternative can be used to visualize extent of lesion?

A

If safe can do flexible sigmoidoscopy and not under full sedation
Bowel will not be holding any faeces (inflamed mucosa cannot retain the faeces)
Ensure do not overinsufflate the bowel to avoid barotrauma causing perforation

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5
Q

What are the AE of azathioprine?
What genes needs to be checked?

A

It is an immunomodulator

  • Myelosuppression
  • Hepatotoxicity
  • Pancreatitis
  • Alopecia (totalis) will appear in a few months (rare)

Chinese prevalence of TPMT mutation is low (being phased out)
If TPMT mutation (low TPMT activity): higher 6TG and increased risk of myelosuppression

NUDT15 c.415C deficiency (increased chance of myelosuppression.

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6
Q

What method of administration of iron in ulcerative colitis and why?

A

2 reasons its IV
* Iron will cause mucosal toxicity (increased inflammatory cytokines) provoking ulcerative colitis
* Inflammatory state (IBD) causes increased hepcidin production which down regulates ferroportin 1 transporter in basolateral membrane of enterocytes thereby decreasing uptake of iron in the enterocytes

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7
Q

What are the 2 oppurtunistic infections linked with IBD that must be checked?

A

Clostridium difficile toxin by PCR (antibiotic associated)
CMV colitis (requires mucosal biopsy)

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8
Q

Compare the use of budesonide and prednisolone in IBD

A

Budesonide (synthetic steroid with high 1st pass effect (metabolized in intestine) so very little drug will escape into systemic circulation. Is an adv in UC as drug will stay in the intestine and not cause systemic toxicity.
But the effect is not as good as prednisolone (hence only used in mild cases)

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9
Q

Which liver enzymes are specific for hepatitis?
What enzymes for cholestatic pattern?

A

ALT is liver hepatic enzyme specific, AST is not used in some hospitals (not specific to liver)

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10
Q

What 2 parameters are used to monitor liver function in chronic failing liver?
Why dont use liver enzymes?

A

Bilirubin
INR

ALT initially will be increased due to parenchymal destruction. However after being released will go on a downward trend (not due to healing) due to dead hepatocytes until most are dead. No more ALT to release.

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11
Q

How can you tell from CBC and LFT of alcoholic liver disease?

A

AST>ALT (normally ALT is elevated in liver diseases)
Increased GGT

CBC
Macrocytosis: increased MCV

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12
Q

In hep B patient what are the 2 main reasons for increase in HBV DNA?

A
  • Non compliance of drug
  • Development of resistance strain (L180M, M204V)
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13
Q

What are the main antivirals used for HBV?

A

Lamivudine if prior to 2005 starting treatment (high level of resistance now)
Entecavir if starting treatment after 2005

If develops resistance –> transition to TAF (tenofovir) (less AE than TDF: nephrotoxicity and osteoporosis

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14
Q

What is ddx of fever and RUQ pain?

A
  • hepatitis of any cause
  • Acute cholangitis
  • Acute cholecystitis
  • RLZ pneumonia
  • Amoebic liver abscess
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15
Q

What further Ix to do if liver abscess shows klebsiella pneumoniae?

A
  • Consult eye for klebsiella pneumoniae endophthalmitis (urgent if has visual symptoms): 5-10% in klebsiella liver abscess patients esp DM
  • Colonoscopy for underlying colonic neoplasm esp if elderly >60y with DM
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16
Q

WHat are types of autoimmune hepatitis?

A

Type 1 (>95%): anti smooth muscle ab (anti-Sm Ab), ANA and anti-actin ab (AAA)
Type 2: anti liver kidney microsomal (LKM) Ab and anti-liver cytosol type 1 Ab (ALC-1)
Type 3: characterized by anti-soluble liver antigen (SLA Ab. Usually seen in adults, increased IgG.

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17
Q

Clinical features for autoimmune hepatitis?

A

Chronic hepatitis (majority)
* Asymptoamtic: incidental finding of increased transaminases
* Insidious onset of fatigue, anorexia, nausea, abd pain, arthralgia, non specific erythematous MP rash
* Jaundice
Acute hepatitis
* Transaminases in thousands but -ve for all viral hep markers
* May even cause acute liver failure

Associated extrahepatic disorders
* AI thyroidits, T1DM, UC, sjogrens syndrome, RA, SLE, psoriasis

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18
Q

Ix for suspected autoimmune hepatitis?

A

LFT: increased AST/ALT up to 10-20x ULN in acute setting
Ig: increased total gamma globulins, with isolated IgG
AutoAb: ANA (sens), anti-Sm for type 1, Anti-LKM for type 2, anti SLA for type 3
Histology: periportal plasma infiltration +/-fibrosis

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19
Q

How to make a dx of autoimmune hepatitis?

A
  • At least one elevated serum aminotransferases: AST/ALT >2xULN
  • At least 1 positive lab test: increased IgG or total Ig, ANA, ASMA, anti-LKM1, anti SLA

Exclusion of ddx
* PBC: AMA can occur in AIH but is seldom the sole ab present
* Overlap syndrome: may have features of both AIH and PBC or both AIH and PSC
* Viral hepatitis and drug induced liver injury

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20
Q

Mx of autoimmune hepatitis?

A

Induction with high dose steroids to damp down inflammation
Maintenance with tapering steroids to decreased S/E

1st line therapy: prednisone and azathioprine
Induction: prednisone 15-30mg/d + AZA 50-100mg/d
Maintenance (lower dosage): prednisone 5-10mg/d + AZA 50-150mg/d

Monitoring during tx: AST/ALT, bilirubuin, gamma globulin, IgG q3-6mo for decreased disease activity.

Salvage therapy as other options: cyclospoirne, tacrolimus, MMF, rapamycin

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21
Q

What must be tested before giving azathioprine?
What are its SE?

A

TPMT deficiency: absolute CI to AZA therapy –> TPMT is needed to break down 6-MP into inactive metabolites –> life threatening myelotoxicity.

SE
* BM myelosuppression
* Cholestatic hepatitis and venoocclusive disease
* Pancreatitis
* Skin rash
* Severe nausea and abd pain

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22
Q

What is overlap syndromes of autoimmune liver disorders?

A
  • AMA +ve autoimmune hepatitis: histological features of AIH, serological features of PBC, biochemical features of AIH e.g. increased transaminases
  • AMA -ve PBC : clinical, biochemical and histological features of PBC. Serological features of AIH i.e. ANA+, ASMA+, AMA-
  • AIH-PSC overlap: clinical and serological features of AIH with cholestatic features e.g. pruritisi, abnormal cholangiogram
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23
Q

Serology of PBC
Clinical features

A

AMA M2+

Clinical features: fatigue, pruritis, jaundice. skin findings: hyperpigmentation, cholesterol deposits: xanthomas, xanthelasmas. Excoriations and scratch marks. Fat malabsorption: steatorrhea, bone tenderness. Cirrhosis and portal hypertension in advanced stages.

Associated conditions: sjogren syndrome, scleroderma and thyroid disease. (not PSC which is bacterial immunology related to IBD)

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24
Q

dx criteria for PBC

A

at least 2 of
* Elevated ALP with a level of >1.5xULN
* Presence of AMA with titres at >1:40
* Histological evidence: non suppurative destructive cholangitis and destruction of interlobular bile duct

Consider PBC when increased ALP w/o extrahepatic biliary osbtruction
Unexplained itching, fatigue, jaundice or weight loss +/- RUQ discomfort

25
Q

What are features supportive of PBC or other ddx

A

Liver biopsy: only when dx in doubt , with features of AIH or refractory to UDCA

26
Q

Mx of PBC?

A

UDCA
Obeticholic acid: decreased ALP, GGT
Liver transplantation

Symptomatic treatment
* Pruritis: cholestyramine. Pregabalin (relieve pain)
* Steatorrhea: dietary fat restriction, MCT if caloric supplementation needed
* Deficiencies of fat soluble vitamins
* Hypercholesterolemia: UDCA alone, cholestyramine, statins
* Metabolic bone disease: vit D and Ca supplement

27
Q

Ix done for PSC

A
  • LFT: cholestatic pattern (increased ALP, bilirubin)
  • Serology: pANCA. AMA M2+ negative
  • USG: bile duct wall thickening, focal bile duct dilatation
  • Cholangiogram: intrahepatic and extrahepatic dilatation and strictures
  • liver biopsy: only reserved for suspected small duct PSC, suspected overlap syndrom with AIH
28
Q

ddx for PSC

A
  • Secondary sclerosing cholangitis
  • IgG4 associated cholangitis: usually occurs together wit htype 1 A/I pancreatitis
  • PSC-AIH overlap syndrome
29
Q

At what level of bilirubin is clinical jaundice?

A

50

30
Q

What is the cause of reversed de titis ratio in alcoholic hepatitis?

A
  • AST is in mitochondria (mAST) and cytosol (cAST), ALT in cytosol (represents cellular membrane damage)
  • Hepatic proportion of AST/ALT of 2.5:1 (AST is more essential) expected turnover of AST would be higher. However because AST is removed by the liver sinusoids twice as quickly (t1/2=18h) compared to ALT (t1/2=36h) –> AST and ALT are fairly similar
  • Patients are often tested within 24 hours of alcoholic exposure so the faster clearance of AST (t1/2 =18h) hasnt had time to take effect. In comparison to ALT which has t1/2 of 36h.
  • Decreased ALT activity due to B6 depletion in the livers of alcoholics and mitochondrial damage (AST) leading to increased release of mAST in serum.
31
Q

Resistance rate of lamivudine (used in old days)?
What new drug used for hep B?

A

50% resistance in 6 years. Lamivudine and entecavir shared the same YMDD resistance.
Swapped to TAF

32
Q

Varices in stomach

A

Portal hypertensive gastropathy

33
Q

What is MELD score?
Will patient be on antiviral after liver transplant?
How to manage the liver transplant?
Side effects of e.g. CsA

A

MELD score: bilirubin, creatinine and PT
Yes in case of occult infection (requires HBsAg and anti HBc as it can be HBsAg -ve but anti HBc+ve)
Put on steroids and immunosuppression to avoid acute rejection e.g. cyclosporin A, azathioprine, MMF
AE of CsA: infection, gum hypertrophy, new onset DM, hyperlipidemia

34
Q

Mechanism of NSBB for esophageal varices (used to reduce recurrence)?

A
  • Decrease portal venous inflow
  • Block adrenergic dilatory tone in mesenteric arterioles, resulting in unopposed alpha adrenergic mediated vasoconstriction and therefore a decrease in portal flow
35
Q

Would acute UGIB cause reduced Hb?

A

No as it has to be chronic bleeding so that the patient loses enough Fe and then BM produces RBC with reduced Hb, giving rise to Fe deficiency anemia

36
Q

If you suspect hep B drug not working, why?
How to check if antivirals not effective?

A

YMDD mutation (both in entecavir and lamivudine)
Check the viral titre: HBV DNA

37
Q

Liver abscess cause?
Route/source of infection of liver abscess?
Mx?

A

Bacterial: e.coli, k. pneumoniae (consult opthal for endophthalmitis)
Parasitic: entamoeba histolytica

Route of infection
* Ascending infection from biliary tract e.g. acute cholangitis
* Intraabd spread from GIT e.g. appendicitis, diverticulitis, pelvic abscess
* Direct spread from urinary tract
* Haematogenous spread from any part of body esp in newly dx DM patient that has poor BG control and immunocompromised

Mx: Ceftriaxone + metronidazole

Only extended spectrum B lactam are active against gram-ve bacteria e.g. tazocin

38
Q

Immunosuppressants used for liver transplant?
AE of these immunosuppressants?

A

Cyclosporine: nephrotoxicity, gum hyperplasia, HT, DM, hyperlipidemia, hirsutism, tremor
Azathioprine: hepatotoxicity, myelosuppression, pancreatitis
Tacrolimus: nephrotoxicity, neurotoxicity, HT, DM, hyperlipidemia

39
Q

How to treat HCV infection?

A
  • Identify genotype of HCV first
  • Direct acting antivirals: eclupsa (sofosbuvir + vepatasvir)
40
Q

What is included in Child pughs score

A

Symptoms (subjective): hepatic encephalopathy and ascites
Lab results: albumin, bilirubin and PT/INR

41
Q

Alcohol what neurological disease is common?

A

Cerebellar degeneration

Neuropsychiatric
* Alcoholic hallucinosis
* Delirium tremens
* Alcoholic dependence
* Morbid jealousy
* Depression

Organic
* Cerebellar degeneration
* Cerebral degeneration
* Alcoholic related myopathy
* Alcoholic seizure disorder
* Central pontine myelinolysis

Nitrutional deficiency: vit B1
* Wernickes encephalopathy
* Korsakoffs psychosis
* Beriberi

42
Q

Precipitating factors of HE

A
  • Increased N2 products: diet (protein), sepsis, GIB, transfusion, renal failure, constipation
  • Decreased vascular volume: GIB, overdiuresis, excess paracentesis with inadequate albumin replacement, diarrhoea and vomiting
43
Q

Initial Mx of HE and how does it work?

A

Lactulose

  • As an osmotic laxative in small bowel, treats constipation and decreases absorption of nitrogen compounds
  • Converted to lactic acid by lactobacilli, decreases pH in gut
  • inhibits urease-producing bacteria
  • Converts ammonia to ammonium in gut and traps it for excretion
  • brings ammonia from blood to gut
44
Q

How would you demonstrate the difference between IVC obstruction and caput medusae?

A
  • Direction of venous flow below umbilicus
  • Flow downward indicates caput medusae
  • Flow upwards indicates IVC obstruction
45
Q

Alcoholic cirrhosis with ascites patients presents to AE with sudden abd pain, ddx?

A
  • Acute pancreatitis due to alcoholism
  • SBP and complication of tapping like infection
  • Peptic ulcer in alcoholism
46
Q

In alcoholic cirrhosis what do you look for in clotting profile and why?
What is seen in albumin in globulin? What is this called? Why is AG ratio affected?

A

PT because F7 has a short half life of 24 hours
Reversed A/G ratio (decreased albumin and increased globulin)
Portosystemic shunting of gut antigens, inability of liver to degrade gut antigens, cirrhotic liver produces antigens which stimulates B cells to produce globulin (Ig)

47
Q

Viral serology negative jaundice what other tests?

A

Ig pattern: IgG (autoimmune hepatitis), IgA in alcoholic hepatitis, IgM in PBC
AI markers
* ANA
* Anti smooth muscle for AIH type 1
* If negative can check anti LKM1 for type 2 and anti SLA for type 3
* AMA M2+ for PBC
* Anti dsDNA, C3/4, anti ENA for SLE

48
Q

Pathology of autoimmune hepatitis?

A
  • Lymphocytic/plasma cell infiltration
49
Q

Osteoporosis mx?

A
  • DEXA scan –> then vit D, calcium and bisphosphonates initially
  • Bisphosphonates AE: esophagitis, atypical fractures, osteonecrosis of jaw
50
Q

Causes of liver parenchymal enzymes >1000

A
  • Viruses: Hep A-E, VZV, CMV, HSV
  • Toxins: drugs, alcohol, TCM
  • Ischemia: sepsis, hypotension, budd chiari syndrome
  • Autoimmune hepatitis
  • Acute biliary obstruction
  • Wilsons disease: especially in young patient
51
Q

ddx of raised AST/ALT in chronic hep B

A
  • E seroconersion
  • Spontaneous reactivation of hep B
  • Resistance to antiviral tx (YMDD variant: tyrosine methionine aspartate aspartate)
  • Chemo/steroid withdrawal (restored immune system starts to attack infected hepatocytes)
  • Steroids initiation: increased viral replication due to stimulation of GRE. Withdrawal of steroids would cause the immune system to attack infected liver cells –> fulminant hepatitis)
  • Rituximab (anti CD20) and alemtuzumab (anti CD52): causes B cell depletion –> 12-18 weeks for B cell recovery. Leading to fulminant hep B reactivation.
52
Q

Hep B serology

A

Viral tolerance: HBsAg+ve, HBeAg+ve, anti HBe-
Viral clearance: HBsAg+ve, HBeAg+ve, anti HBe-ve
Residual phase if seroconversion: HBeAg-ve, anti HBe+ve
Occult disease: HBsAg-ve and anti HBc +ve

53
Q

Pancreas CA chemo regimen, what common agent causing peripheral neuropathy?

A

FOLFIRINOX: folinic acid, fluorouracil (antimetabolite: damages the DNA of rapidly dividing cells in oral mucosa –> mucositis), irinotecan hydrochloride (topoisomerase inhibitor), and oxaliplatin

Oxiplatin likely causes the peripheral neuropathy (platinum based are the culprit commonly)

54
Q

Tumor markers for HCC vs cholangiocarcinoma
What imaging for HCC?

A
  • HCC: AFP
  • Cholangiocarcinoma: CA19-9, CEA

Triphasic CT scan: arterial enhancing lesion and delayed washout in portal venous phase.

55
Q

RF for cholangiocarcinoma

A
  • Recurrent inflammation from liver flukes (clonorchis sinensis)
  • Primary sclerosing cholangitis
56
Q

Stomach cancer chemo regimen?
Targeted therapy?

A

FOLFOX: oxaliplatin + 5-FU (fluorouracil)/leucovorin

HER2+ve: trastuzumab

57
Q

Hepatitis serology?

A

Disease status: HBsAg, anti HBs (been exposued before), anti HBc (occult infection)
Disease activity: HBeAg, anti HBe (after e-seroconversion), HBV DNA
Co-infection: anti HCV, anti HDC, +/-anti HIV

58
Q

Indications for starting hep B treatment?

A

Immune active hepatitis
* Active disease: ALT >2ULN or evidence of significant histologic disease
* Active viral replication: HBV DNA >20000 (HBeAg+) or >2000IU/mL (HBeAg-)
Presence of cirrhosis providede that HBV DNA is detectable
Use of immunosuppressants e.g. steroids, rituximab (potent)
Pregnnacy if HBV DNA is high: usually cover from 8w before delivery to 3 months afterwards

59
Q
A

MBBS VI Medicine (92 decks)

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