Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Yr 3 Medicine > Gastrointestinal Medicine > Flashcards

Gastrointestinal Medicine Flashcards

1
Q

A 19 year-old man presents with diarrhoea and abdominal pain. He is passing motions up to 10 times a day. He has lost 3 kg weight in the last week. What other symptoms would you ask about?

A

Gastroenteritis:
Any fever?
Any nausea+vomiting?
Any recent Abx use?
Any mucus in stools?
Any recent travel/food?

IBD:
Any extra-intestinal manifestations (arthritis, mouth ulcers, skin changes)
Any blood in stools?
Familial history?
WEIGHT LOSS?
Any urgency? (INDICATES LOWER BOWEL INFLAMMATION)
Smoking History?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

A 19 year-old man presents with diarrhoea and abdominal pain. He is passing motions up to 10 times a day. He has lost 3 kg weight in the last week.
What are you looking for on examination?

A

On examination:
DRE (Crohn’s bottom)
E.I.M (arthritis, mouth ulcers)
Generalised abdo pain?
Look thin?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What conditions can Faecal Calprotectin be raised?

A

IBD
Infection
Drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How can the nutritional status of a patient be assessed in a history and what dietary measures should be used?

A

Food intake charts

Ask the patient:
Appetite?
Diet history?
Weight changes?
Oral intake changes?
BMI?

If concerned:
Refer to dietitian
1) Fortisips and don’t interrupt meal time
2) NG tube
3) PEG/RIG/PEGJ/RIGJ (more long term then NG)
4) Parenteral Nutrition (into veins - if GI tract is blocked or diseased massively)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What’s important when putting a NG tube in?

A

Ensure the tip is in the stomach and not in the lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

A 19 year-old man presents with diarrhoea and abdominal pain. He is passing motions up to 10 times a day. He has lost 3 kg weight in the last week.
What investigations should you complete?

A

Investigations:
FBC (aneamic, high platelets)
U&Es (AKI/Abnormal electrolytes - GI Losses)
CRP (raised, but can’t exclude IBD if not)

Stool Cultures (exclude infective colitis)
Stool Faecal Calprotectin (raised, but not specific)

Flexible Sigmoidoscopy (most distal but safest with bloody diarrhoea)
Colonoscopy (can visualise large bowel)
Capsule Endoscopy (Views small bowel - Chron’s)

MRI + MRI Rectum (Chron’s small bowel/fistulas + Perianal Disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What features might help differentiate between Crohn’s and ulcerative colitis?

A

Chrons:
Familial
Affects anywhere in GI system
Skip Lesions
Transmural Inflammation
Increased Incidence in smokers
Perianal Disease

Ulcerative Colitis:
Not familial
Affects rectum + continues
Continuous pattern
Mucosal/Sub-mucosal Inflammation
Decreased Incidence in smokers
No perianal disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the differential diagnosis of patients with bloody stools?

A

Gastroenteritis
Haemorrhoids
IBD
Diverticulitis
Colorectal Cancer
Recent NSAID use?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which IBD gives you more weight loss?

A

Chron’s (as small bowels effected)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What’s important to consider with IBD?

A

PRO-THROMBOTIC STATE
(^risk of DVT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How do you treat acute IBD flare up?

A

IV Hydrocortisone/Methylprednisolone
PO Prednisolone

Mesalazine

LMWH (DVT Risk)

AVOID OPIATES (reduce colonic movement - ^perforation risk)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is steroid resistant acute IBD and how do you treat it?

A

Acute IBD that hasn’t reacted to steroids within 5 days (1 in 5)

1) Ciclosporin
2) Biologics (Infliximab)
3) Surgical Referral (Colectomy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the long term treatment of IBD?

A

1) Azathioprine (takes 3/12 to act) (FBC-lymphocytopenia + ^MCV)
2) Methotrexate (Chron’s) (Teratogenic + liver/lung fibrosis)
2) Mesalazine (UC)
3) Infliximab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the acute + chronic complications of IBD?

A

Acute:
Anaemia
AKI
Toxic Megacolon
DVT/Infection/HAP

Chronic:
Colorectal Cancer (UC > CD)
Primary Sclerosing Colitis (Cirrhosis + Cholangocarcinoma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the complication of the treatment of IBD? (steroids & biologics)

A

Steroids:
Mood change
Hypertension
Infection Risk
HYPERGLYCEMIA

Biologics:
Reduce Sperm count so need counciling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the common causes for GI bleeding?

A

Medications (NSAIDs/antiplatelets/anticoagulants)
Peptic Ulcers
Mallory-Weiss Tear (Oesophageal mucosa tear)
GI Cancers
Varices/Chronic Liver Disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are important clinical examination findings to document when a patient comes to you with GI bleeding?

A

Is it haematemesis (fresh blood)?
Is it coffee ground vomit (vomiting digested blood)?
Is there Malaena (black, smelly stools indicate an upper GI bleed)
Is there fresh PR bleeding (lower GI bleed, but a haemodynamically unstable patient may have a GI bleed with this)?
Any signs of liver disease peripheral stigmata? (ascites, fluid retention, jaundice, alcohol intake, splenomegaly)?
Weight loss (CANCER)?
Tachy or hypotensive (HAEMODYNAMICALY UNSTABLE/SHOCK)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What investigations would you recommend with someone with a GI bleed?

A

FBC (Low Hb - GI BLEED) (Thrombocytopenia - CLD, will need to give platelets if low anyway)
U&Es (^Urea - GI BLEED)
Clotting factors (abnormal clotting needs to be corrected to control bleeding)
Crossmatch 2 units of blood if become haemodynamically unstable
LFTs (to see for liver disease)
VBG - can see Hb quicker

URGENT ENDOSCOPY!!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Explain the ROCKALL score

A

Used after endoscopy to estimate the risk of GI rebleeding/mortality

Age
Features of Shock (tachy/hypo)
Co-morbidities (CHF, CKD, IHD, Cancer)
Cause of bleeding (M-W tear or malignancy)
Endoscopic stigmata of recent GI bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the management for an upper GI bleed? Pre endoscopy, non-variceal and variceal?

A

Pre-endoscopy:
IV Fluids
Blood transfusion (if unstable)
Platelet transfusion (if thrombocytopenic and active bleeding)
Prothrombin Complex Concentrate if on warfarin
Hold relevant meds

Non-variceal bleeds:
1) Endoscopy w/in 24hrs (clips)
2) Thermal Regulation
3) Refer to GI Surgeons
NO PPI BEFORE ENDOSCOPY

Variceal Bleeds:
1) IV Terlipressin (unless IHD OR peripheral VD)
2) IV Abx
3) Variceal Band Ligation, Linton Tube or TIPSS (transjugular intrahepatic portosystemic shunts) if not controlled

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How should you manage GI bleeds with patients taking aspirin/NSAIDs/clopidogrel?

A

Hold the meds while active bleeding.
Once stable, start these again!

Can discuss with patient and MDT (e.g. cardiology w/ aspirin) afterwards

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What monitoring would the nurses need to do post GI bleed?

A

Hourly HR,BP,JVP,Urine Output
Check vomit/stools for blood
NBM if high risk of rebleed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the long term management post GI-bleed?

A

FBC (Hb, platelets)
PPI (if non-variceal)
Repeat endoscopy if feel will rebleed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the pathophysiology of oesophageal varices?

A

Cirrhosis/ALD (usually causes) portal hypertension
Causes distention/dilation of veins at the site of porto-systemic anastomoses (oesophagus,ano-rectal, umbilical)
This veins can rupture causing bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the pathophysiology of peptic ulcer disease?

A

Defect in the gastric or duodenal mucosa that extends through the muscularis mucosa

RFs: H-Pylori, NSAIDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the Glasgow-Blatchford Bleeding score?

A

Used to see the likelihood of a GI bleed

High Urea
Low Hb
Low systolic BP
Tachycardiac
Syncope
Malaena
Hepatic Disease
HF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

A man presents with jaundice and abdominal bloating. What else do you want to ask him?

A

Alcohol intake?
Diet?
Any bleeding?
Appear confused (build up of urea)?
Any RUQ pain?
N+V?
Fever? (Hep infection)
Paracetamol OD?
Seizures/tremors? (Wilson’s)
Itchiness (bile under skin?)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What signs on clinical examination will you look for in liver disease?

A

Hands:
Palmar Erythema
Dupuytren’s contracture
Clubbing
Terry’s Nails (Leukonychia)
Asterixis (liver flap)?

Skin:
Spider naevi
Caput medusae
Gynecomastia
Ascites
Jaundice
Oedema
Bruising

Splenomegaly
Hepatomegaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are some important investigations for decompensated chronic liver disease?

A

LFTs
FBC + CRP
U+Es (hepato-renal)
Clotting
Hep Serology
USS liver?
DEXA scan (osteoporosis risk)
Endoscopy (if suspect varices)
Liver CT/MRI?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the differential diagnoses for individuals presenting with jaundice?

A

Pre Hepatic:
Haemoglobinopathies (sickle cell…)
Haemolysis

Hepatic:
Viral (Hep/EBV/CMV)
Hepatic Cancer (painless)
Gilbert’s
Alcoholic Liver Disease/Cirrhosis
Wilsons
Drug-Induced
PBC/PSC

Post-Hepatic:
Cholangiocarcinoma
Biliary Stricture
Gallstones
Pancreatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the key investigations for patients with jaundice?

A

LFTs + ALP
FBC
U+Es (hepato-renal)
Clotting
ERCP or liver USS
Bilirubin in urine
Hep Serology
Malaria blood film (if indicated)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Why might a patient with CLD be malnourished?

A

Reduced glycogen storage/gluconeogenesis
Reduced vitamin storage
Early satiety
Low bile salts available
Reduced protein metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How do we manage nutrition in liver disease?

A

Reduce salt intake
High protein intake
Vit D supplements (osteoporosis risk)
Graze (little and often)
Supplemets (if poor appetite)
Multivitamins
Avoiding Alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How should alcohol withdrawal be managed in patients admitted to hospital?

A

Chlordiazepoxide (benzodiazepine)

+ vitamin B (IM/IV)
+ thiamine (oral)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What services and treatments are available to help patients with alcohol addiction?

A

Disulfarim
AA
Rehabilitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What long-term complications of cirrhosis should be monitored?

A

Hepato-renal syndrome
Splenomegaly
Portal HTN/Varcices
Ascites/Oedema in legs
Ascites > Spontaneous Bacterial Peritonitis
Hepatic Encephalopathy (ammonia build up)
Malnutrition
Hepatocellular carcinoma risk?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is NASH? What are the risk factors and how do we diagnose it?

A

Non-Alcoholic Steatohepatitis
(Hepatomegaly w/ inflammation and fatty liver)

Found by USS

Increased risk in:
- obesity
- diabetes
- metabolic syndrome (HTN,DMII,Obesity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How do we treat NASH?

A

Weight loss
Mediterranean diet
Exercise
Smoking cessation/reduce alcohol
Control diabetes, BP, cholesterol

Bariatric surgery/liver transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How can you screen for harmful alcohol use?

A

Cut down (do you think you should)?
Annoyed at others for talking about your drinking?
Guilty feeling about drinking?
Eye opener (ever drink in the morning for nerves or cure a hangover)?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What does alcohol withdrawal appear and what time frames after you’ve stopped drinking?

A

6-12hrs: tremor, sweating, headache, craving, anxiety
12-24hrs: hallucinations
24-48hrs: seizures
24hrs+: delirium tremens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What’s Wernicke-Korsakoff Syndrome?

A

THIAMINE (B1) DEFICIENCY

Wernicke’s encephalopathy:
- confusion
- oculomotor disturbances
- ataxia

Korsakoff syndrome:
- memory impairment
- behavioural changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are the causes of cirrhosis?

A

1) ALD
2) NAFLD
3) Hep B/C

Wilson’s
CF
Haemochroamtosis
PBC
Autoimmune hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What will you find in your investigations for liver cirrhosis?

A

Raised LFTs (ALT/AST/ALP/Bilirubin)
Low albumin
Increased PT
Thrombocytopenia
Hyponatraemia (fluid retention)
High urea

Raised ELF (Enhanced Liver Fibrosis) blood test
+ve FibroScan (Transient Elastography)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are the key features of decompensated liver disease?

A

Ascites
Hepatic Encephalopathy (confusion, lethargy)
Oesophageal Varices bleeding
Yellow (jaundice)

AHOY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are the common symptoms associated with paracetamol OD?

A

Can be asymptomatic
N+V
RUQ pain
Jaundice
Reduced consciousness/coma (if w/ alcohol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What investigations would you arrange with a patient with a paracetamol overdose?

A

LFTs
Serum Paracetamol Conc
Glucose
FBC
INR
ABG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What clinical guidance/tool would you use to determine specific treatment for paracetamol overdose?

A

Paracetamol overdose treatment nomogram

Takes time since overdose and plasma paracetamol concentration into account

Maximal conc at 4 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is the management for paracetamol overdose and how does it work?

A

1) Activated charcoal (within first hr) - absorbs the toxins
2) Aceylcystiene IV (replenishes glutathione to prevent build up of toxic NAPQI)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

How would you conduct a Mental State Examination?

A

1) Observe (signs of neglect, self harm, weight)
2) Can patient hold normal conversation
3) Eye contact too intense or not there?
4) Body language? (threatening, withdrawn or restless)
5) Speech? (rate, tone, volume, fluency/rhythm)
6) Mood? (Low or manic)
7) Thought form? (Flow of conversation, trail of thought)
8) Perception? (hallucinations etc)
9) Cognition? (understand what’s going on)
10) Insight? (do they know what’s wrong with them)
11) Hold normal judgement?
12) Risk to themselves or others?

50
Q

What would be the criteria for safely discharging a patient after a paracetamol overdose?

A

Physically fit for discharge
Psych review and risk assessed for future overdose attempts
Need to be linked with outpatient mental health/addiction services

51
Q

A young man presents with pneumonia. He has a BMI of 17 kg/m2, what further info would you like to know about this guys weight?

A

Appetite?
Oral intake?
Diet history?
Weight changes?

Was this was recent weight loss? If so was it planned or not?
How long has it took to lose this weight?
Any mental health conditions for this?
Any physical reasons why he is unable to eat?

52
Q

What is the MUST (Malnutrition Universal Score Tour) and how is it calculated?

A

Calculates overall risk of malnutrition. 1 = medium risk, 2+ = high risk

BMI:
18.5-20 = 1
<18.5 = 2

Unexplained weight loss in last 3-6 months:
5-10% = 1
>10% = 2

Acutely ill patient/no nutritional intake for 5+ days = 2

53
Q

What are the possible causes of malnutrition?

A

Acutely ill = loss of appetite
Mental health conditions = depression
Mental conditions = stroke, dementia
Poor dental health/dentures
Dysphagia
GI causes = chron’s
Cancer
Social isolation/Loss of mobility

54
Q

How is malnutrition best managed?

A

Has to be individualised to that patient (try and solve the cause)

1) Encouragement with food (don’t interrupt meal times, make sure teeth/dentures are ok)
2) Food supplements (e.g. fortisips)

If unable to meet nutritional demands, unsafe swallow or non-functioning GI tract:

3) NG Tube (short-term) - look at pH to see if it is in stomach and not the lungs
4) PEG (Percutaneous Endoscopic Gastrostomy tube) - tube placed directly in stomach
Can be placed in jejunum too
5) Parenteral Nutrition (into veins)

55
Q

What is refeeding syndrome? What factors predispose someone to it? How can it be prevented?

A

Potentially fatal shifts in fluids and electrolytes in malnourished patients on refeeding following a period of starvation.

Low BMI
Unintentional weight loss (15%+ in last 3-6 months)
Little or no nutritional intake for >10 days
Low levels of potassium, phosphate, or magnesium before feeding
Hx of alcohol misuse
Drugs (insulin, chemo, antacids, diuretics)

Start on 10Kcal/kg/day and slowly raise
Restore circulating volume (monitor fluid balance)
Ensure daily multivitamin + thiamine/B12
Provide Mg, K and phosphate supplements (oral/IV)

56
Q

How many types of autoimmune hepatitis are there and what are the typical presentation of these?

A

Type 1 - middle-aged women around or after menopause with fatigue/liver disease signs

Type 2 - Acute hepatitis presentation (jaundice) with children/YA

57
Q
A
58
Q

What investigations are key in autoimmune hepatitis?

A

Raised ALT/AST (slight ^ALP)
High IgG

Type 1: Anti-nuclear antibodies (ANA)
Type 2: Anti-LKM1

+ve liver biopsy

58
Q

How do we manage autoimmune hepatitis?

A

Azathioprine
Prednisolone
Liver transplant

59
Q

What are the genetics behind hameochromatosis?

A

Autosomal recessive
C282Y mutation in HFE gene

60
Q

How does haemochromatosis present?

A
  • 40yrs + (later in females due to menstruation)
  • chronic tiredness
  • joint pain
  • bronze skin
  • testicular atrophy
  • erectile dysfunction/amenorrhea
  • memory/mood disturbance
  • hepatomegaly
61
Q

What investigations are needed to diagnose haemochromatosis?

A

Raised serum ferritin
Raised transferrin saturation
HFE Gene testing
Liver biopsy (Perl’s stain - iron conc in liver)
MRI (can see iron conc in liver)

62
Q

What are the complications of haemochromatosis?

A

Secondary diabetes
Liver cirrhosis/Hepatocellular carcinoma
Cardiomyopathy
Hypothyroidism
Chondrocalcinosis (Ca in joints)
Endocrine/Sexual issues (hypogonadism, infertility)

63
Q

How do we manage haemochromatosis?

A

Venesection
Monitor serum ferritin
Monitor and then treat complications

64
Q

What’s the genetics behind Wilson’s disease?

A

Autosomal recessive on chromosome 13

65
Q

How does Wilson’s disease present?

A

Teenagers/YAs

Hepatic Symptoms:
RUQ pain
Jaundice
Fatigue

Neurological Symptoms:
Tremor
Dysarthria
Dystonia
Parkinsonism

Psychiatric Symptoms:
Abnormal Behaviour
Depression/Psychosis
Cognitive Impairment

Eyes:
Kayser-Fleischer Rings (green-brown circles around iris)

66
Q

How can we diagnose Wilson’s disease?

A

Low serum caeruloplasmin (protein that carries copper)
24hr urine copper assay
Kayser-Fleischer Rings on slit lamp exam
MRI brain (double panda sign)
Low Hb

67
Q

How do we treat Wilson’s disease?

A

Penicillamine/Trientine (copper chelation)
Zinc salts (inhibit copper absorption in GI tract)
Liver transplantation

68
Q

What are the genetics behind alpha-1-antitrypsin deficiency? What is alpha-1 antitrypsin?

A

Autosomal co-dominant
Both gene copies are expressed and contribute to disease severity

Protease inhibitor

69
Q

What organs are affected in alpha-1 antitrypsin deficiency and how does it present?

A

Lungs:
- COPD
- ^protease enzymes attack connective tissues leading to elastic tissue destruction
- bronchiectasis + emphysema

Liver:
- cirrhosis
- A-1A produced in liver
- mutant version of A-1A builds up and is toxic to hepatocytes

70
Q

What investigations are needed for alpha-1 antitrypsin deficiency?

A

Low serum alpha-1 antitryspin
Genetic deficiency
CXR/HRCT thorax
Liver biopsy

71
Q

What is the management of alpha-a antitrypsin deficiency?

A

Smoking cessation
COPD treatment
Organ transplant
Monitor complications (hepatocellular carcinoma)
Family members screening

72
Q

What is the pathophysiology behind Primary Biliary Cholangitis (PBC)?

A

Autoimmune condition
Autoimmune inflamation of small bile ducts in liver (intrahepatic ducts)

Causes cholestasis (reduced flow of bile)
Bile/bilirubin/cholesterol unable to be excreted so levels in blood build up

73
Q

How does PBC present?

A

White woman 40-60 yrs
Can be asymptomatic

Symptoms:
- Fatigue
- Pruritis (^bile)
- GI symptoms (^bile)
- Abdo pain (^bile)
- Jaundice (^bilirubin)
- Pale stools (^bilirubin)
- Dark urine (^bilirubin)

Signs:
- Xanthoma/Xanthelasma
- Excoriations (scratches on skin due to itching)
- Liver cirrhosis/portal hypertension signs (end stage)

74
Q

What investigations are needed for PBC? (blood investigations + imaging)

A

LFTs (^ALP) (All LFTs^ in later disease)
Anti-mitochondral Antibodies (AMA)
Anti-nuclear Antibodies (ANA)
Raised IgM
USS (excludes differentials)

75
Q

How can we treat PBC?

A

Ursodeoxycholic Acid (makes the bile less harmful to epithelial cells)

Colestyramine (pruritus)
Replacement of fat-soluble vitamins
Immunosupression with steroids (potentially)

76
Q

How does PBC progress and what are the potential complications?

A

LIVER CIRRHOSIS > portal HTN + hepatocellular carcinoma

Sjogren’s
Hyperlipidaemia
Vit A,D,E,K deficiency
Osteoporosis
Thyroid disease

77
Q

What is Primary Sclerosing Cholangitis (PSC)?

A

Intrahepatic ducts and extra hepatic bile ducts become inflamed and damaged

Strictures form causing cholestasis

Combined genetic + environmental factors? Still Unclear

78
Q

How does PSC usually present?

A

Male
30-40s
Family Hx
ULCERATIVE COLITIS (could still have w/ chron’s but less likely)

RUQ Pain
Prutitis
Fatigue
Jaundice
Hepatomegaly
Splenomegaly

79
Q

What investigations are needed for PSC?

A

LFTs (^ALP) (All LFTs^ in late disease)

MRCP (Magnetic Resonance Cholangiopancreatography) will show bile duct strictures

Colonoscopy (UC Dgx?)

80
Q

What is the management for PSC?

A

Endoscopic Retrograde Cholangio-Pancreatography (ERCP):
- endoscopy to dilate strictures using stents.
- Abx given also to reduce bacterial cholangitis

Colestyramine (pruritis)
Fat-soluble vitamin replacement
Complications monitoring

81
Q

What are the complications of PSC?

A

Biliary strictures
Acute Bacterial Cholangitis
Cholangiocarcinoma
Cirrhosis (+ portal HTN/varices)
A,D,E,K deficiency
Osteoporosis

82
Q

What’s the pathophysiology behind GORD?

A

Gastro-oesophageal reflux disease
Acid flows through LOS
Oesophagus squamous epithelium more sensitive to acid then stomachs columnar epithelium

83
Q

What factors can worsen GORD symptoms?

A

Greasy/spicy foods
Coffee/tea
Alcohol
NSAIDs
Smoking
Obesity
Hiatus hernia

84
Q

What is the typical presentation of GORD?

A

Epigastric pain worse on eating
Heartrburn
Acid taste in mouth
Cough

85
Q

What is the management of GORD?

A

Lifestyle changes:
- Reduce tea, coffee, alcohol
- Weight loss
- Smoking cessation
- Smaller, lighter meals
- Avoid meals before bed

Medical management:
- Antacids (short-term)
- PPIs
- Stop NSAIDs

Surgery - laparoscopic fundoplication

86
Q

What is the pathophysiology behind coeliac disease?

A

Autoimmune condition triggered by eating gluten
Causes inflammation affecting the jejunum (small bowel)
Atrophy of intestinal villi cause malnutrition

87
Q

How does coeliac disease present?

A

Diarrhoea
Bloating
Fatigue
Weight Loss
Mouth ulcers

INFERTILITY

88
Q

What investigations are needed for coeliac disease?

A

Anti-tissue transglutaminase antibodies (Anti-EMA if this is borderline)
Total IgA levels (to exclude IgA deficiency) [if IgA low then this is the issue]
FBC (Hb - anemia)

If +ve Abs:
Endoscopy
Jejunal biopsy (crypt hyperplasia + villous atrophy/flattening)

89
Q

What is the management and potential complications of coeliac disease?

A

Lifelong gluten-free diet
Avoid:
Barley
Rye
Oat
Wheat

Nutritional Deficiencies
Anaemia
Osteoporosis
Small bowel adenocarcinoma
Ulcerative jejunitis
SMALL BOWEL LYMPHOMA

90
Q

What are the key features of IBS?

A

6/12 hx of:
Intestinal discomfort
Bowel habit abnormalities
Stool abnormalities

Abdo Pain
Diarrhoea
Constipation
Bloating
Worse after eating
Improved by opening bowels
Passing mucus

Worsened by:
anxiety/stress
sleep disturbances
illness

91
Q

What diagnoses are needed to be excluded before IBS and how?

A

Bowel Cancer
IBD
Coeliac disease
Ovarian cancer
Pancreatic cancer

FBC (Hb)
ESR/CRP
anti-TTG (coeliac)
Faecal calprotectin (IBD)
Ca125 (ovarian cancer)

92
Q

How do we manage IBS?

A

Drink fluids
Regular small meals
Adjust fibre dependent on diarrhoea/constipation
Limit caffeine, alcohol, fat

Loperamide (diarrhoea)
Bulk-forming laxative e.g. ispaghulxa husk (constipation)
Antispasmodics (cramps)

93
Q

What’s Peutz-Jeghers syndrome (PJS) and how does it present?

A

Polyp formation in GI tract

Freckles/brown spots in lips, mouth, fingers or toes
GI symptoms (pain, bleeding)

Increases risk of breast and GI cancers!

94
Q

What drugs increase the risk of bleeding from peptic ulcers?

A

NSAIDs + Aspirin
DOACS
Steroids
SSRI (antidepressants)

95
Q

How do peptic ulcers present?

A

Epigastric pain/discomfort
N+V
Dyspepsia (indigestion)

If bleed:
Haematemsis/coffee ground vomit
Melaena

96
Q

What investigations are needed if suspect peptic ulcer disease?

A

FBC (Hb drop?)
Endoscopy (can be seen)
Rapid Urease test (H.pylori?)
Biopsy (exclude malignancy?)

97
Q

How do we treat peptic ulcers?

A

Stop NSAIDs
Give PPI
Treat H. pylori:
Omeprazole
Amoxicillin
Clarithromycin/Metronidazol

Repeat endoscopy (4/8 weeks post bleed)

98
Q

What are the complications of peptic ulcer disease?

A

Bleed
Perforation > Peritonitis
Stricture/Pyloric stenosis

99
Q

What is Barrett’s Oesophagus? How is it managed?

A

Metaplasia where the lower oesophageal epithelium changes from squamous to colomnar epithelium
GORD the biggest risk factor

1) PPIs
2) Endoscopic monitoring to see if progresses to adenocarcinoma
3) Endoscopic ablation of cells

100
Q

What blood tests are seen in an upper GI bleed?

A

High Urea
Normal Creatinine
Low Hb

Cirrhosis/liver disease:
Normal Urea
High Ammonia (HEPATIC ENCEPHALOPATHY)
Low Hb

101
Q

What is Zollinger–Ellison Syndrome?

A

Duodenal/pancreatic tumour secreting gastrin causing dyspepsia

102
Q

What is the normal ranges for Hb & MCV?

A

Men Hb: 130 -180
Women Hb: 120 -170
MCV: 80-100

103
Q

Where is folate and B12 absorbed in the GI tract?

A

Folate: duodenum + proximal jejunum
B12: terminal ileum (Chron’s)

104
Q

What are some microcytic causes of anaemia?

A

Iron Deficiency:
Cancer
IBD
Coeliac
Dietary deficiency

Haemoglobinopathies

105
Q

What are some macrocytic causes of anaemia?

A

B12 deficiency
Folate deficiency
Alcohol (direct toxicity to bone marrow so have ^reticulocytes)
Hypothyroidism
Toxins/drugs (phenytoin, azathioprine)

106
Q

How long in duration are the B12 and folate stores?

A

B12: 2/3 years
Folate: 3 months

107
Q

What are some normocytic causes of anaemia?

A

Acute GI bleed (incl. angioectasia)
Urinary tract bleed
Anaemia of CD
Myeloma

Mixed deficiency (iron+folate)
Iron deficiency + iron tablets

108
Q

How would myeloma present?

A

AKI
Hypercalcaemia
High globulins
High IgG

109
Q

What will extra iron blood tests show if you suspect iron deficiency anaemia?

A

Low Fe
Low ferritin
Low transferrin saturation
High iron binding capacity

110
Q

How do you treat folate and B12 deficiency?

A

1) B12 (Im)
2) Folate first (p.o.)
3) (neurological issues - degeneration of cord - w/ low B12)

111
Q

What age groups/genders do we investigate anaemia in?

A

All Men
Women child bearing age - No (unless diarrhoea or symptomatic)
Older Women

112
Q

How do we see if there are haemoglobinopathies?

A

haemoglobin electrophoresis

113
Q

Who’s vulnerable to iron deficiency anaemia? What are some good sources?

A

Vegan/vegetarians

RED MEAT

114
Q

What are some cause of folate deficiency?

A

Dietary
Coeliac
Pregnancy
Methotrexate
Chrons

115
Q

What are some causes of B12 deficiency?

A

Chron’s
Pernicious anaemia
Chronic active gastritis (h.pylori)
Metformin

116
Q

What investigations should you order if somebody comes in with anaemia?

A

FBC
Iron studies
B12
Folate
Coeliac (anti TTG)
OGD/Colonoscopy

117
Q

What do you do if somebody comes to you with a previously corrected anaemia that now has returned after they have stopped taking iron tablets? (Hb: 90 > 140 - stopped tablets > 90)

A

Redo OGD/colonoscopy
Small bowel issue??? :
Small bowel MRI
Capsule endoscopy

118
Q

How do you treat normocytic anaemia?

A

Look for any deficiencies and replace them
Exclude myeloma
Transfuse
Do nothing

119
Q

How does gastroparesis present?

A

erratic blood glucose control, bloating and vomiting

Tx - metoclopromide

120
Q
A

Yr 3 Medicine (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions