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Clinical Medicine > GI > Flashcards

GI Flashcards

1
Q

Recommended Alcohol Consumption

A

No more than 14 units per week , spaced evenly over 3 or more days with no more than 5 units in a day

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2
Q

CAGE Questioning for alchoholic?

A

Cut down (Ever thought you should?)

Annoyed (Annoyed by others commenting on your drinking)

Guilty (Guilty about drinking)

Eye Opener (Morning drink to help hangover/nerves)

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3
Q

Signs of Liver Disease?

A

Jaundice

Hepatomegally

Spider Naevi

Palmar Erytema

Gyencomastia

Brusing (Adbnormal Clotting)

Ascites

Caput Medusae

Asterixis

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4
Q

Progression of alchohol withdrawl?

Management?

A

Progression

  • 6-12 hours: tremor, sweating, headache, craving and anxiety
  • 12-24 hours: hallucinations
  • 24-48 hours: Seizures
  • 24-72 hours: Delirium tremens (Mortality 35%. Due to chronically upregulated GABA system and downregulated Glutamate (NMDA) => extreme excitability of the brain

Management
- Chlordiazepoxide (benzo)
- Diazepam (less common)
- IV vitamin B (thiamine) followed with low dose oral to prevent Wernike-Korsakoff

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5
Q

Features of Werkicke-Korsakoff?

A

Wernikes’ Encephlopathy
- COnfusion
- Occulomotor
- Ataxia

Korsakoff’s Syndrome
- Memory impairment (retrograde and anterograde)
- Behaviorial changes

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6
Q

Causes of Liver Chirosis

A

Common
- Alcoholic LIver DSiease
- Non-Alchoholic Fatty liver diseae
- Hep B
- Hep C

Less common:
- Autoimuine Heaptiotis
- PBC
- Heamachhromatosis
- Wilsons
- Alpha-1 antitrypsin deficiency
- Cystif FIbrosis
- Drugs (Ambiodarone, methotraxatre, sodium valproate)

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7
Q

Investigations for Liver Chirosis?

A

Bloods
* Albumin/Prothrombin times derranges
* Hyponatremia due to fluid retention
* Urea/Creatinine in hepatorenal syndrome
* Alphafetoprotein (Tumor marker for heppatocellular carciinoma checked every 6 month sin those w/ chirosis)

Ultrasound
- Nodularity
- Corkscrew Apearance
- Enlarged portal veins
- Ascites
- Splenomegally

Fibroscan (Checks elasticity of the liver w. high frequency sounds waves)

Endoscopy (espogeal Varcies)

MRI/CT Scan (Malignancy)

Biopsy (Confirmatory of Chirosis)

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8
Q

Classification system for Chirosis?

A

Child-Pugh Score

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9
Q

How does chirossis lead to malnutrition/muscle wasting?

A

Increased use of muscle tissue as fuel and reduction in protein available in body for muscle growth. Also disrupts ability of liver to store glucose as glycogen and release when requirted => body uses muscle as fuel

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10
Q

Common locations for varices?

A

Gastroesophogeal junction
Illeocecal junction
Rectum
Umbilical Vein (caput Medusae)

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11
Q

Treatment of stable varices?

A

Proplanolol

Elastic band ligation

Transjugular intra-hepatic portosystemic shunt (TIPS): IR sends wire down jugular vein into liver via hepatic vein, make a connection between hepatic vein and portal vein and place a stent. Allows blood to flow directly from portatl vein to hepatic relieveing pressur ein the portal system and thus reducing varcieal formation. Used if endoscopic treatments dail or uncontrolled bleeding varices

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12
Q

Treatment of bleeding esophogeal varices?

A

Resucitation
- Vasopressin Analogues (Terlipressin) => vascoconstriction
- Coagulopathy correction (Vitamin K + FFP)
- Prophylactic Broad Spectrum Antibiotics

Urgent Endoscopy
- Injection of sclerosant into varices can be used to cause inflamatory obliteration of teh vessel
- Elasttic band ligation

Sengstaken-Blakemore Tube (Inflatable tube to tamponade bleeding esophogeal varices when endoscopy fails)

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13
Q

Management of Ascites?

A

Low sodium diet

Anti-aldosterone diuretics (Spirolactone)

Parecentesis

Prophylactic antibiotics (Ciprofloxacin) in those w/ less than 15g/L protien in ascitic fluid

Consider TIPS in refractory ascites (IR sends wire down jugular vein into liver via hepatic vein, make a connection between hepatic vein and portal vein and place a stent. Allows blood to flow directly from portatl vein to hepatic relieveing pressur ein the portal system and thus reducing varcieal formation)

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14
Q

What is spontaneous bacterial periotnitis secondary to?

Most common organisms?

Managment?

A

10% of pts w/ ascited secondary to chirosis develop SBP

Most commonly:
- E. Coli
- Klebsialla
- Gram Postive Cocci (Staph/Enterococcus)

Management: Cefotaxime

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15
Q

Pathophysiology/Management of Hepatorenal syndrome?

Management?

A

Pathophysiology: Occurs in liver chirosis. Hypertension in portal sytem => stretching of portal vessels => loss of blood volume in other areas of circulation including kidneys => renin-andiotensin system => renal vasoconstriction which combined with low circualtion leads to starvation of blood to kidneys

Fatal within a week unless liver transplant performed!!

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16
Q

Pathophysiology of Hepatic Encephalopathy?

Management?

A

Ammonia is produced by intestinal bacteria and absorbed by gut. Build up occurs in HE for two reasons:
- Functional impairment of liver cells prevent metabolism of ammonia
- Collateral vessel formation between portal and systemic circualtions mean ammonia byupasses the liver altogether

Preciptating Factors:
- Constipation
- Infection
- GI Bleeding
- High protein diet
- Sedatives

Managmeent:
- laxatives clear amonia from gut before it is absorbed (Lacutlose)
- antibiotics reduced # of ammonia producing gut bacteria (Rifaximin used as poorly absorbed so remains in GI tract)

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17
Q

Investigating Abnormal Liver Function Tests?

A

Ultrasound Liver

Enhances liver fibrosis (ELF) Blood test (First line for assesing liver fibrosis)

Fibroscan

Hep B/C Serology

Autoantibodies (Autoimmune hepatitits, PBC, PSC)

Ceroplasmin (WIlson’s Disease)

Alpha 1 antitryupsin levels

Ferritin/Transferrin Saturation (Heriditary Hemochromatosis)

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18
Q

Causes of Hepatitis?

A

Alchoholic Hepatitis

Non-Alchoholic Fatty liver dsiease

Viral Hepatitis

Autoimmune Hepatitis

Drug Induced Hepatitis (Parecetamol Overdose)

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19
Q

Typical LFT derrangements in Hepatitis?

A

Hepatitic Picture: High Transaminases (AST/ALT) w/ less of a rise in ALP

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20
Q

Most common viral hepatitis worldwide?

A

Hep A

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21
Q

Hepatitis A
- RNA/DNA?
- Transmission?
- Pathology?
- Resolution?

A

RNA Virus

Fecal/Oral Route

Causes cholestasis => Dark urine, pale stools, moderate hepatomegaly

Resolved without treatment in 1-3 months

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22
Q

Hepatitis B
- RNA/DNA?
- Transmission?
- Resolution?
- Screening?

A

DNA Virus

Contact w/ blood/bodily fluids (Verticle Transmission mother to child)

Most spontaneouslyt recover, 10-15% go on to become chronic hepatitis in which the viral DNA is integrated into pts. DNA

When screening test HBcAb (previous infection) and HBsAg (active Infection). If positive then do further testing for HBeAg and viral load (HBV DNA)
- HBsAg- active infection
- HBeAg- viral replicaiton (high infectivity)
- HBcAb- IgM high= ACTIVE, IgM low= CHRONIC; IgG = PAST (if HBsAg Negative)
- HBsAb- Vaccination or Past/Current Infection
- HBV DNA- Viral Load

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23
Q

Hepatitis C
- RNA/DNA?
- Transmission?
- Complications?
- Resolution?

A

RNA Virus

Spread by blood/bosdily fluids (no Vaccine avialable). Curable with direct acting anti-virals

Complications (Liver Chirossis, Hepatocellular Carcinoma)

1/4 recover spontaenously, rest becomes chronic

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24
Q

Autoimmune Hepatitis
- Types?
- Antibodies?
- Treatment?

A

Type 1 (Women in late 40’s/50’s with fatigue/liver disease)
- ANA
- Anti-Actin
- Anti-SLA/LP

Type 2 ( Teenage years acute presentation w/high transaminases and jaundice)
- Anti-LKM1
- anti-LC1

Treatment:
- High dose prednisolne (Tapering)
- Azathioprine (Life-Long)

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25
Q

Hemachromatosis Pathophysiology

A

Pathophysiology
- Iron storage disorder => excdess total body iron adn deposition in tissues
- Caused by HFE gene chr 6 (AR)
- Usually presnets >40 when iron overload becomes symptomatic (Later in females due to mentruation eliminating iron)

26
Q

Hemachromatosis Symptoms

A

Symptoms
- Chronic tiredness
- Joint pain
- Pigmentation (Bronze)
- Hair Loss
- ED
- Amenorrhea
- Cognitive (memory/mood)

27
Q

Hemachromatosis Diagnosis?

`

A

Diagnosis
- Serum Ferritin (Acute phase reactant, goes up w/ inflamatory conditions)
- Transferrin Saturration helps differentiate high ferritin from Iron Overload
- Serum ferritin and Transferrin Sats high => genetic test to confirm Hemochromatosis
- Liver Biopsy and Perls stain of iron in Parencymal cells(Supplanted by genetic testing)
- MRI show iron deposits in liver/heart

28
Q

Complications of Hemachromatosis?

A

Type 1 Diabetes (Iron effects pancreas functioning)

Liver Chirrosis

Iron deposits in pituitary/gonads => endocrine and sexual problems

Cardiomyopathy (Iron Deposits in Heart)

Hepatoceullar Carcinoma

Hypothyroidism (Iron Deposits in Thyroid)

Chrondocalcinosis (Calcium deposits in joints => Arthritis)

29
Q

Managment of Hemachromatosis

A

Venesection (weekly removal of iron)

Monitoring Serum Ferritin

30
Q

Pathophysiology/Features of Wilson’s Diseases

A

Excessive copper acumulation in the body caused by mutation on Chr 13 (AR)

Features:
- Heaptitis => Cirrhosis
- Neurological: (Dysarthria and Dystonia) Copper in Basal Ganglia => SYMETRICAL Parkinsonism (Tremor bradynkinesia and Rigidity) differentiated from UNILATERAL parkinsonism in Parkinson Disease
- Pscyhiatric (Depresion to psychosis)
- Kayser-Fleischer Rings
- Hemolytic anemia
- Renal Tubular Acidosis
- Osteopenia

31
Q

Diagnosis of Wilson’s Disease

A

Serum Caeruloplasmin
- Initial investigation
- Protein that carries copper in blood
- Not specificic can be falsely elevaed in cancer/inflamatory conditions

Liver Biopsy to check copper content (GOLD STANDARD)

24 hour urine copper assay

Kayser-Fleischer Rings

32
Q

Management of Wilson’s Disease

A

Pencillamine/Trientene (Copper Chelation)

33
Q

Alpha 1 Anti-Trypsin Deficiency
- Pathophysiology
- Diagnosis
- Management

A

Pathophysiology: Inherited deficiency of protease inhibiotor => excess protease enzyme that attacks liver and lung tissues
- Liver Cirrhosis (>50yo)
- Pulmonary Basal EMphysema (>30 yo)

Diagonsis
- LOW Serum alpha 1 antitrypsan
- Liver biopsy (Cirrhosis + Acid-Schiff Positive Globules (Breakdown products of proteases in hepatocytes)
- Genetic Testing for A1AT Gene
- High resolution CT Thorxa (Pulmonary Emphysema)

Management
- STOP Smoking
- Organ Transplant
- Monitor for HCC

34
Q

Primary Billary Cirrhosis
- Pathophysiology/Associations
- Presentation
- Diagnosis
- Treatment

`

A

Pathophys/Assc
- Immune system attacks small bile ducts of liver=> obstrcution (Cholestasis)=> FIbrosis, Cirrhosis, Liver Failure
- Middle Ages Women, Other Autoimune diseases

Presentation
- Pruritis
- GI pain/Fatigue
- Jaundice + Pale, Greezy Stools
- Xanthomata + Xantholasma
- Sigsn of Chirrosis (Ascited, Splenomegaly, spider nevi)

Diagnosis
- LFTs: Alkaline Phosphatase first to be raised (as with most obstructive pathology)
- Autoantibodies: Anti-mitochondrial antibodies most specific, Anti-nuclear Antibodies (35%)
- LIver Biopsy used to diagnose/stage

Treatment:
- Ursodeoxycholic Acid (Reduces intestinal absorption of cholesterol)
- Colestyramine (Bile Acid Sequesterant. Binds bile acids preventing absorbtion in gut, helps with pruritis)
- Liver Transplant

35
Q

Primary Sclerosing Cholangitis
- Pathophysiology/Associations
- Presentation
- Diagnosis
- Complications
- Treatment

A

Pathophys/Assc
- Intraheaptic/extrahepatic ducts become strictured and fibrotic => obstruction => Hepatitis, Fibrosis, Cirrhosis
- Sclerosis (Hardening of bile ducts)
- Cholangitis (Inflamation of Bile ducts)
- Associated with Ulcerative Collitis , Male, Age 30-40

Presentation
- Pruritis
- Chronic URQ Pain
- Jaundice
- Fatigue
- Hepatomegaly

Diagnosis
- LFTs: Cholestatic picture w/ rasies Alkaline Phosphatase (as with most obstructive pathology)
- Gold Standard Diagnosis: Magnetic Reso nance Cholangiopancreatography (MRCP)

Complications
- Acute bacterial cholangitis
- Cholangiocarcinoma
- Colorectal Cancer
- Cirrhosis/Liver Failure
- Billiary Stricutre

Treatment:
- Liver transplant curative
- Endoscopic Retrograde Cholangio-Pancreatography (ERCP): endoscope through person’s esophgus, stomach, duodenum entering the sphincter of Odi and into ampula of Vater where they are able to enter the bile ducts and inject contrast agent. XRAY is then used to identify any strictures which can be dialated and stented during the procedure
- Ursodeoxycholic Acid (Reduces intestinal absorption of cholesterol)
- Colestyramine (Bile Acid Sequesterant. Binds bile acids preventing absorbtion in gut, helps with pruritis)

36
Q

Types of Liver Cancer?

Risk factors?

Tumor Marker?

A

Hepatocelluar Carcinoma (80%)
- Viral Heapatitis
- Alcohol
- Non-Alchoholic fatty liver disease
- Alphafetoprotein

Cholangiocarcinoma (20%)
- Primary Scerlosing Colangitis
- CA19-9

37
Q

Risk factors for Primary Sclerosis Cholangitis (PSC)?

A

Ulcerative Collitis
Male (30-40)

38
Q

Investigations for Liver Cancer?

A

Tumor Markers
- Alpha-Fetoprotein- HCC
- CA19-9 Cholangiocarcinoma)

Liver Ultrasound

CT/MRI for diagnosis/staging

ERCP for biopsy of cholangiocarcinoma

39
Q

Treatment of Liver Cancer?

A

HCC
- Kinase inhibitors: Sorefinib
- Resection/Transplant when confined to liver

Cholangiocarcinoma
- ERCP to place a stent improves symptoms

40
Q

Barrett’s Esophogus Pathophysiology/Risks

A

Squamous => Columnar

Premalignany => risk of developing Adenocarcinoma

Pts require regular endoscopy to monitor

41
Q

Presentation of GORD?

A

Heartburn

Acid Regurgitation

Epigrastic pain

Bloating

Nocturnal Cough

Hoarse Voice

42
Q

Treatment of GORD?

A

Lifestyle Modificaiton

Acid Neutralizer (Gaviscon)

PPI (-Prazole)

Ranitidine (H2 recptor antagonist)

Laprosocpic fundoplication- Tying of fundus around lower esophogud to narrow the sphincter

43
Q

Tests for H Pylori?

A

Urea Breath Test
Stool Antigen Test
Rapid Urease Test (CLO test)
- biopsy taken of stomach mucosa
- Urea added to sample
- If H. Pylori present then urease enzymes convert urea=> amonia making solution more alkalaine

44
Q

Treatment of H Pylori?

A

Triple Therapy (7 Days)
- PPI
- Amoxicillin
- Clarithromyocin

45
Q

Gastric Ulcers vs. Duoddenal Ulcer Pain?

A

Eating Worsens Gastric Ulcer Pain

Eating Improves Duodenal Pain

46
Q

Diagnosis/Management of Peptic Ulcers?

A

Diagnosed by Endocopy: Rapid Urease (CLO Test) performed to check for H. Pylori. Biopsy also to exclude malignancy

Managed w/ High Dose PPI and monitoring with endoscopy

47
Q

Causes of Upper GI Bleeding

A

Esophogeal Varices

Mallory-Weis Tears

Ulcers of Stomach/Duodenum

Cancers of Stomach/Duodenum

48
Q

Presentation of GI Bleeding?

A

Coffee Ground Vomit

Meleana (Black greesy stools)

Hemodynamic Instalility

49
Q

Management/Investigations of Upper GI Bleed?

A

ABATED
* ABCDE Resusitation
* Bloods
* Acess (2 large bore cannula)
* Transfuse
* Endoscopy (Oesophagogastrroduodenoscopy (OGD)- Varcieal banding/cauterization of bleeding vessel)
* Drugs (stop anticoags/NSAIDs

Send bloods for
* Hemoglobin (FBC)
* Urea (U/Es)
* Coagulation (INR, FBC platelets)
* Liver Disease (LFTs)
* Crossmatch 2 units blood

In pts suspected of oesophogeal varices (chronic liver disease):
- Terlipressin
- Broad Spectrum Antibiotics

50
Q

Scoring system to asses whether pt has an Upper GI bleed?

A

Glassgow-Blatchford score (Initial Presentation)

Rockall Score (Post-Endoscopy)

51
Q

Group/Save vs. Crossmatch?

A

Group/Save: lab checks pts. blood group and keeps smaple of blood saved in case needed

Crossmatch: Lab finds blood, tests that it is compatible and keeps it ready in fridge if necesary

52
Q

Transfusion Guidelines

A

Blood, platelets, FFP (clotting factors) to pts w/ massive hemorage

Platelets given in active bleeding and thrombocytopenia (platelets <50)

Prothrombin complex concentrate given to pts on warfarin actively bleeding

53
Q

Chron’s vs. Ulcerative Colitis?

A

Chron’s NESTTS:
- No blood or mucus
- Entire GI tract
- Skip lesions
- Terminal ileum most effected
- Transmurral Inflamation
- Smoking is a risk factor (don’t set nest on fire)
- Chron’s Also assc. w/ weight loss, strictrues and fistulas

Ulcerative Colitis (U-C CLOSEUP)
- Continuous inflamation
- Limited to colon/rectum
- Only superficial mucosa affected
- Smoking is PROTECTIVE
- Excrete blood/mucus
- Use Aminosalicilates
- Primary Sclerosiing Cholangitis

54
Q

Presentation/Diagnosis of IBD?

A

Presentation
- Diarrhea
- Abdominal Pain
- Passing Blood
- Weight Loss

Testing
- Routine bloods for anemia, infection, kidney/liver function
- CRP
- Fecal Calprotectin (90% sensitive/specific for IBD)
- Endoscopy (OGD/Colonoscopy) is diagnostic
- Imaging with ultrsound/CT/MRI for complications such as fistulas, abscesses and strcitures

55
Q

Management of Chron’s

A

Inducing remission: First line Steroids: Oral Prednisolone or IV Hydrocortisone

Maintaining Remission: Azathioprine, Mercaptopurine, Methotrexate, Infliximab, Adalimumab

Surgery when disease only affects distal ileum or if strictures/fistulas

56
Q

Managment of Ulcertaive Colitis

A

Inducing remission:
- First line: Aminosalicylate
- Second Line: Corticosteroids
- Severe Disease: IV Corticosteroids/IV Ciclosporin

Maintaining Remission:
- Aminosalicylate (Mesalazine)
- Azathioprine
- Mercaptopurine

Surgery:
- Panproctocolectomy will remove the disease
- Pt left with either a permament ileostomy or an** Ileo-anal anastomosis (J-pouch)**: this is where the ileum is folded back onto itself anf fasioned into a larger pouch that functions like a rectum. Atached to anus allowing normal bowel passing

57
Q

Diagnosis of IBS?

A

Normal FBC, ESR and CRP bloods

NEGATIVE Fecal Calproectin (Excluded IBD)

NEGATIVE anti-TTG Antibodies (Coeliac Serology)

And 2 of the following:
- Abnormal stool passage
- Boating
- Worse symptoms after eating
- Mucus w/ stools

58
Q

Management of IBS?

A

Lifestyle/Diet

Medication:
- Loperaminde for Diarrhea
- Laxatives for Constipation
- Tricyclic/SSRI antidepressents
- CBT

59
Q

Pathophysiology/ Presentation of Coeliac’s Disease?

A

Autoantibodies (anti-TTGand anti-EMA) created in response to gluten that target epithelial cells of the small bowel (Jejunum partcularly) => atrophy of the intestinal vili=> malabsorption and symptoms of diease:
- Diarrhea
- Fatigue/Weight Loss
- Mouth Ulcers
- Anemia (Iron/B12/Folate Deficiency)
- Dermatitis Herptiformis (Itchy blistering rash on abdomen)

60
Q

Genetic Associations of Coeliac’s?

A

HLA-DQ2

HLA DQ8

Test all new cases of type I diabetes for Coeliacs as often linked

61
Q

Diagnosis of Coeliac’s?

A

Investigations must be done while pt remains on gluten:

Auto-Antibodies:
- Check total IgA levels to exlcude IgA defficiency
- Raised anti-TTG
- Rasied anti-EMA

Endoscopy and Intestinal Biopsy:
- Crypt Hypertrophy
- Villous Atrophy

62
Q

Associations w/ Coeliacs?

A

Type 1 Diabetes

Thyroid Disease

Autoimune Hepatitis

PBC

PSC

Clinical Medicine (8 decks)

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