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Medicine > GI > Flashcards

GI Flashcards

1
Q

Name 5 predisposing factors for Diverticular Disease

A

Age
Developed country
Low fibre diet
Constipation
Small faecal volume

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2
Q

Why dont diverticulae form in the rectum?

A

it has an outer longitudinal layer that completely surrounds the diameter of the rectum

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3
Q

How would you manage Diverticulosis?

A

Increased fibre
Bulk-forming laxatives (e.g. Ispaghula husk)

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4
Q

How would you manage uncomplicated diverticulitis

A

Oral co-amoxiclav (5 days)

Analgesia

Clear fluids until symptoms improve

Follow up in 2 days

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5
Q

Name 6 complications of acute diverticulitis

A

Perforation
Peritonitis
Peridiverticular abscess
Harmorrhage
Fistula (colon to bladder or vagina)
Ileus / obstruction

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6
Q

Name 3 Abs related to coeliac disease

A

anti-TTG
anti-EMA
anti-DGP

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7
Q

What are the main histological features of coeliac disease?

A

Crypt hypertrophy of the small bowel

Villous atrophy

Intra-epithelial WBCs

Chronic inflammation of the lamina propria

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8
Q

Which HLA genotypes are associated with Coeliac disease?

A

HLA-DQ2 (95%)
HLA-DQ8

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9
Q

Which dermatological finding is associated with coeliac disease?

A

Dermatitis herpetiformis

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10
Q

What first line blood tests are indicated in coeliac disease?

A

FBC - anaemia
Irodn studies
B12 / folate
Total IgA levels
anti-TTG

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11
Q

How do you manage coeliac disease?

A

gluten-free diet

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12
Q

Who are most likely to be affected by IBS?

A

Younger women

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13
Q

What are the 3 main symptoms of IBS?

A

IBS

Intenstinal discomfort
Bowel havit abnormalities
Stool abnormalities

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14
Q

How do you diagnose IBS?

A

Exclude red flags

Rome III criteria (>6 months of abdo pain / discomfort + one of the following);

Pain relieved by opening bowels
Bowel habit abnormalities
Stool abnormalities

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15
Q

What are the subtypes of IBS?

A

IBS-D (diarrhoea)
IBS-C (constipation)
IBS-M (mixed)

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16
Q

What dietary changes are suggested for those with IBS?

A

FODMAP

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17
Q

How might you pharmacologically manage IBS?

A

Loperamide - diarrhoea

Ispaghula husk

Antispasmodics for cramps

Linaclotide - when 1st line laxatices fail

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18
Q

What are the key features differentiating Crohn’s and UC?

A

Crohn’s - weight loss, RIF mass

UC - bloody diarrhoea, LLQ pain

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19
Q

How do you classify UC?

A

Mild - intermittent bleeding, mild diarrhoea (<4 stools/day)

Moderate - up to 10 bloody stools daily

Severe - >10 bloody stols a day, weight loss, anaemia

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20
Q

What are the most common extra-intestinal manifestations specific to Crohn’s?

A

Gallstones
Oxalate renal stones

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21
Q

What are the most common extra-intestinal manifestations specific to UC?

A

PSC

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22
Q

What extra-intestinal manifestations are common to both Crohn’s and UC?

A

Erythema nodosum
Pyoderma gangrenosum
Enteropathic arthritis
Red eye

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23
Q

How does Crohn’s and UC affect the length of the bowel?

A

Crohn’s - skip lesions, mouth to anus

UC - rectum, never beyond ileocaecal valve

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24
Q

What are the histological findings of Crohn’s?

A

Inflammation of all layers

Increased goblet cells

Non-caseating granuloma

Skip lesions, ulcerations, cobblestoning

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25
Q

What are the histological findings of UC?

A

No inflammation beyond submucosa

Neutrophilic infiltration of crypt abscesses

Depletion of goblet cells

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26
Q

Which types of enema would you use to image IBD?

A

Crohn’s - Small bowel enema

UC - barium enema

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27
Q

How would you manage Crohn’s?

A

Induce remission - steroids / enteral nutrition

(if steroids don’t work then azathrioprine, methotrexate…)

Maintain remission - azathioprine / mercaptopurine

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28
Q

How would you manage UC?

A

MIld-moderate
1) - aminosalicylate
2) - corticosteroids

Severe - IV hydrocortisone

Maintain remission - aminosalicylate, azathioprine, mercaptopurine

Surgery

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29
Q

How would you manage an acute severe attack of UC?

A

IV hydrocortisone cyclosporin

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30
Q

How would you manage UC surgically?

A

Panproctocolectomy
Ileostomy / J-pouch

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31
Q

How would you classify haemorrhoids?

A

1) no prolapse

2) prolapse when straining, returns on relaxing

3) prolapse when straining, does not return on relaxing

4) prolapse permanently

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32
Q

Name 4 topical treatments for haemorrhoids

A

Anusol (shrinks haemorrhoids)

Anusol HC (short term, has hydrocortisone)

Germoloids (LA)

Proctosedyl (short term, steroids)

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33
Q

Name 4 non-surgical treatments for haemorrhoids

A

Band ligation

Injection sclerotherapy

IR coagulation

Bipolar diathermy

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34
Q

Name 3 surgical options for haemorrhoids

A

Haemorrhoidal artery ligation

Haemorrhoidectomy

Stapled haemorrhoidectomy

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35
Q

How would you manage a patient with intractable rectal prolapse who is unfit for surgery?

A

Circumanal rubber ring

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36
Q

Who tends to have malabsorption due to bacterial overgrowth?

A

Elderly patients, those with structural problems

e.g. surgery, diverticula, crohn’s, SB dysmotility

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37
Q

What investigations would you perform on someone with suspected bacterial overgrowth?

A

Bloods (low B12)
Breath test
SB aspirate
Barium test radiology

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38
Q

How would you treat bacterial overgrowth?

A

Abx 2 weeks
Abx free period

Repeat cycle

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39
Q

How is Giardia Lamblia transmitted?

A

faeco-orally

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40
Q

What will giardia lamblia show on bloods?

A

Low B12
Low iron

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41
Q

How would you treat Giardia Lamblia infection?

A

Metronidazole

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42
Q

What pathogen causes whipple’s disease?

A

Tropherym Whipplei

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43
Q

How does Whipple’s disease present?

A

Fever
Arthralgia
Weight loss
Malabsorption
Neurological signs (foot drop)

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44
Q

What disease does Tropical Sprue mimic?

A

Giardia Lamblia infection

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45
Q

How would you manage Tropical sprue?

A

Tetracycline
Folic acid

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46
Q

What is the main post-mucosal factor contributing to malabsorption?

What causes this?

A

Lymphangiectasia

May be primary (pt born without lymphatics)

Secondary - radiotherapy / cancer

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47
Q

How would you confirm the diagnosis of lymphangiectasia?

A

Signs - oedema, steatorrhoea

Bloods - low albumin, lymphocytes, and gamma globuline

Duodenal biopsy (stranded fat)

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48
Q

What is the most common cause of SBO?

A

adhesions

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49
Q

What is the most common cause of LBO?

A

malignancy

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50
Q

What sort of vomiting is expected in someone with BO?

A

Green bilious

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51
Q

How do you manage BO?

A

DRIP and SUCK

(NBM, fluids)
Prepare for surgery

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52
Q

What is ‘third spacing’ in BO?

A

Bowel secretes fluid which is absorbed in the colon

In BO, this can’t be reabsorbed. The further up the obstruction, the more fluid accumulates, leading to hypovolaemia and shock

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53
Q

How would you differentiate SBO from LBO on AXR?

A

SBO - valvulae conniventes, central

LBO - haustra, peripheral

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54
Q

How would you differentiate peritonitis from ischaemia in bowel perforation?

A

Peritonitis - rigid abdomen

Ischaemia - soft abdomen

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55
Q

What areas of the bowel are particularly susceptible to ischaemic colitis?

A

Watershed areas;
- splenic flexure
- rectosigmoid junction

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56
Q

Name all of the causes of pancreatitis

A

I GET SMASHED

Idiopathic
Gallstones
Ethanol
Trauma
steroids
Mumps
AI
Scoprion sting
Hyperlipidaemia
ERCP
Drugs (furosemide, thiazide-diuretics, azathioprine)

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57
Q

What are the 3 most common causes of pancreatitis?

A

Gallstones
Ethanol
ERCP

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58
Q

How would acute pancretitis affect serum amylase levels?

A

> 3x upper limit

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59
Q

An increase in what enzyme is considered more sensitive and specific compared to amylase?

A

Lipase

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60
Q

Which scoring system is used to classify pancreatitis?

A

0-1 - mild
2 - moderate
3+ - severe

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61
Q

How would you manage chronic pancreatitis?

A

Abstinence from smoking / alcohol

Analgesia
Creon

SC insulin
ERCP with stenting

Surgery

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62
Q

What is the definition of acute gastritis?

A

Gastric mucosal infiltration by neutrophils

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63
Q

What is the definition of chronic gastritis?

A

Gastric mucosal infiltration by lymphocytes and plasma cells (+ maybe neutrophils)

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64
Q

What are the causes of chronic gastritis?

A

H. pylori
AI
Reactive (chronic bile reflux, NSAIDs)

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65
Q

What other condition is AI gastritis associated with?

A

Pernicious anaemia

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66
Q

What are the 4 consequences of gastritis?

A

Acute peptic ulceration

Peptic ulcer disease

Intestinal metaplasia

Gastric cancer

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67
Q

What are the causes of acute peptid ulceration?

A

NSAIDs
Stress ulcers (sepsis/shock/trauma)
Curling ulcers (severe burns)
Cushing ulcers (intracranial disease)

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68
Q

What are the 3 main causes of peptic ulcer disease?

A

H.pylori infection
NSAIDs
Zollinger-Elison syndrome

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69
Q

What is Zollinger-Ellison syndrome?

A

Uncontrolled gastrin production by tumour cells -> hyperacidity

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70
Q

What is the greatest RF for development of gastric cancer?

What is the most common type of gastric cancer?

A

H.pylori

Adenocarcinoma

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71
Q

How might you differentiate Appendicitis and Mesenteric Adenitis?

A

MA - maintains appetite, high grade fever (>39), normal WCC + CRP, improves after 24 hours

A - No appetite, low grade fever, ^ WCC+CRP, pt deteriorates

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72
Q

Where is McBurney’s point?

A

1/3 distance from ASIS to umbilicus

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73
Q

What is Robsing’s sign?

A

Appendicitis

Palpation of LIF -> RIF pain

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74
Q

What is the Cope sign?

A

Retrocaecal appendix, slides over obturator internus

Pain on flexion and internal rotation of R hip

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75
Q

What are the 2 types of oesophageal cancer?

Which infections are RF for these cancers?

Where in the oesophagus do they occur?

A

SCC - HPV, upper

Adenocarcinoma - H.pylori, lower

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76
Q

What is the main mode of diagnosis of oesophageal cancer?

A

Endoscopy

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77
Q

How would you manage a superficial oesophageal or gastric cancer?

A

Endoscopic mucosal resection

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78
Q

In pancreatic cancer, what is the most common type and where do they occur?

A

Adenocarcinoma

Head

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79
Q

What is the average survival of pancreatic cancer from diagnosis?

A

6 months

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80
Q

What is the key presenting feature of pancreatic cancer?

A

Painless obstructive jaundice

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81
Q

What metabolic sign might be an indication of pancreatic cancer?

A

New onset DM
Rapid worsening of glycaemic control of T2DM

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82
Q

Who gets a 2WW for suspected pancreatic cancer?

Who gets a direct access CT abdomen?

A

> 40 jaundice

> 60 weight loss + additional symptom

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83
Q

What is Courvoisier’s law?

A

A palpable gallbladder along with jaundice is unlikely to be gallstones.

The cause is usualy cholangiocarcinoma or pancreatic cancer

84
Q

What is Trousseau’s sign?

A

Migratory thrombophlebitis as a sign of malignancy, particularly pancreatic adenocarcinoma

85
Q

Which tumour marker is raised in pancreatic cancer?

A

CA 19-9

86
Q

What is the technical name for the Whipple procedure?

How is a modified Whipple procedure different?

A

pancreaticoduodenectomy

Leaves the pylorus in place (PPPD, pylorus-preserving pancreaticoduodenectomy)

87
Q

What common drug reduces the incidence and mortality of colorectal cancer?

A

Aspirin 75mg ODN

88
Q

When should you refer to a specialist for investigation of genetic colorectal cancer?

A

2x 1st degree relatives w/ colorectal cancer at average <60years

Criteria for AD colorectal cancer syndrome met

89
Q

Name 3 AD colorectal cancer syndromes

A

Lynch syndrome (HNPCC)

Familial adenomatous polyposis (FAP)

Peutz-Jegher’s syndrome

90
Q

What are the 3 most common cancers in Lynch syndrome?

A

Colorectal cancer
Endometrial cancer
Ovarian cancer

91
Q

What criteria is used to diagnose Lynch syndrome?

A

Amsterdam criteria

92
Q

Which mutations are associated with Lynch syndrome?

A

MLH1
MSH2
MSH6
PMS2

93
Q

How are those with Lynch syndrome screened for colorectal cancer?

A

2 yearly colonoscopy from 25-75 years

94
Q

What mutation is associated with FAP?

A

APC gene mutation

95
Q

At what age are those with FAP initiated in colorectal cancer screening?

A

12 years

96
Q

What oral clinical sign is associated with Peutz-Jeghers syndrome?

A

hyper-pigmented macules on the tongue

97
Q

what gene mutation is associated with Peutz-Jeghers syndrome?

A

STK11

(TSG)

98
Q

How is colorectal cancer staged?

A

TNM

Duke’s still commonly used but technically outdated

99
Q

How would you differentiate HSV and CMV oesophagitis?

A

HSV - fewer ulcers, 2mm shallow, volcano-like

CMV - deeper and wider

100
Q

What must you test for in someone with oesophagitis?

A

HIV

101
Q

How would you treat oesophagitis?

A

Ganciclovir

102
Q

What pathogen causes gastritis?

A

H.pylori

103
Q

How would you diagnose gastritis?

A

Urea breath test
Rapid urease test (CLO test)

104
Q

What can untreated H.pylori gastritis lead to?

A

Stomach cancer
Gastric MALT lymphoma

105
Q

How do you treat H.pylori gastritis?

A

1 week triple therapy

PPI
Clarithromycin
Amoxicillin

106
Q

What area of the bowel is affected by watery and bloody diarrhoea?

A

Watery - small bowel
Bloody - large bowel

107
Q

What is the main diarrhoeal illness requiring treatment?

A

C.Diff

108
Q

Name 5 causes of watery diarrhoea

A

Staph aureus

C.perfringens

C.Diff

Bacillus cereus

Vibrio cholera

109
Q

How does staph aureus look down the microscope?

A

Gram + cocci

110
Q

How might you differentiate C.perfringens and staph aureus infection?

A

C. perfringens no vomiting as it produces it’s toxin once ingested

111
Q

What are the main complications associated with C.Diff?

A

Toxic megacolon
Bowel perforation

112
Q

How would you treat C.Diff infection?

A

mild - metronidazole
moderate / severe - vancomycin
Recurrent - findaxomicin

Consider FMT

113
Q

What 2 types of toxins are produced by bacillus cereus?

A

Emetic - vomiting within 1-5 hours
Diarroheal - diarrhoea within 8-16 hours

114
Q

What sign sugests vibrio cholera infection?

A

Rice-water stool

115
Q

How would you manage vibrio cholera?

A

Ciprofloxacin
Rehydration

116
Q

How would C.perfringens look down the microscope?

A

Gram + bacilli

117
Q

What sort of bacteria cause bloody diarrhoea?

A

Gram - bacilli

118
Q

Name 4 bacterial causes of bloody diarrhoea

A

Salmonella enteritidis
Salmonella typhi
Shigella
Campylobacter jejuni
E.coli

119
Q

How long can diarrhoea last for in with salmonella enteritidis?

A

7 days

120
Q

What is the pathophysiology of salmonella typhi?

A

travel shits

enteric fevers, invade peyer’s patches, disseminates

121
Q

How do you manage salmonella typhi?

A

Azithromycin
Ceftriaxone
Meropenem

122
Q

What complications are associated with Shigella infection?

A

RA
conjunctivitis
HUS

123
Q

What is the most common serotype of E.coli?

How do you treat them? why?

A

0157:H7

DON’T GIVE ABX - ^toxin release, making it worse

124
Q

Name 3 parasitis causes of bloody diarrhoea

A

Giardia
Worms
Schistosomiasis

125
Q

Where might you catch schistosomiasis?

A

Lake MalawiW

126
Q

What is Cirrhosis?

A

Liver insult over many years causing fibrosis and vascular remodelling

127
Q

What is liver Fibrosis?

A

Damage to hepatocytes stimulating Kupffer cells to produce chemical mediators activating perisinusoidal stellate cells

128
Q

What is involved in vascular remodelling of the liver?

A

Capillarisation of sinusoidal endothelium due to loss of fenestrations and perisinusoidal fibrosis

129
Q

What are the 3 main clinical consequences of Cirrhosis?

A

Hepatocellular failure
Portal HTN
Hepatocellular carcinoma

130
Q

How would you define chronic hepatitis?

A

Inflammation of the liver continuing without improvement for at least 6 months

131
Q

How is the morphology of acute hepatitis different to portal hepatitis?

A

Acute - lobular inflammation
Portal - portal inflammation

132
Q

What are the 3 AI liver diseases?

A

AIH
PSC
PBC

133
Q

What are the 2 types of AIH?

A

1 - women, 40-50s, after menopause, more acute

2 - children, girls, jaundice

134
Q

Which antibodies are associated with AIH?

A

1 - ANA, anti-SM, anti-SLA/LP

2 - anti-LKM1, anti-LC1

135
Q

How would you confirm a diagnosis of AIH?

A

LIver biopsy

136
Q

How would you manage AIH?

A

Steroids
Azathioprine
Liver transplant

137
Q

Who is at higher risk of PBC?

A

Females

138
Q

What is the most common AI liver disease?

A

PBC

139
Q

How do you treat PBC and PSC?

A

Ursodeoxycholic acid (UDCA)

140
Q

Who is at higher risk of PSC?

A

Males

141
Q

How do you investigate PSC?

A

MRCP

142
Q

What are the 3 extra-hepatic manifestations of PSC?

A

Pyoderma gangrenosum
Erythema nodosum
Episcleritis

143
Q

What proportion of adults are estimated to have NAFLD?

A

25%

144
Q

What are the 4 stages of NAFLD?

A

NAFLD
NASH
Fibrosis
Cirrhosis

145
Q

What score is used to assess liver fibrosis in NAFLD?

A

Fibrosis 4

146
Q

What are the management options for NAFLD?

A

Lots of lifestyle stuff

Lose 10% of bosy weight
Control DM

147
Q

What is the stepwise progression of ALD?

A

Alcoholic fatty liver
Alcoholic hepatitis
Cirrhosis

148
Q

What is the definition of binge-drinking?

A

6 units for women and 8 for men in a single session

149
Q

How would you manage ALD?

A

Stop drinking
Nutritional support (thiamine)

150
Q

When should you suspect Portal HTN?

A

Chronic liver disease
Thrombocytopenia
Splenomegaly

151
Q

What is the main cause of pre-hepatic Portal HTN?

A

Portal vein thrombosis

152
Q

Name 2 causes of intra-hepatic Portal HTN

A

Cirrhosis (developed world)

Schistosomiasis (developing world)

153
Q

Name 3 causes of post-hepatic Portal HTN

A

Budd Chiari syndrome
IVC obstruction
HF

154
Q

What is Budd-Chiari syndrome?

A

Hepatic vein obstruction

155
Q

What are the 3 main consequences of Portal HTN to be aware of?

A

Ascites
Variceal Haemorrhage
Hepatic Encephalopathy

156
Q

How would you manage Portal HTN?

A

NSBBs (propranolol or nadolol)

Carvedilol

Endoscopy

Variceal band ligation

157
Q

How would you know if ascites is caused by Portal HTN?

A

SAAD >1.1 g/dL

158
Q

How would you manage Ascites?

A

Spironolactone

Consider paracentesis, liver transplant, or TIPSS if resistance to diuretics

159
Q

What is TIPSS?

A

Trans-jugular intra-hepatic, porto systemic shunt

Way of reducing portal pressure quickly, shunting blood fro the portal vein directly to the hepatic vein

160
Q

How might you reduce the risk of SBP in those with ascites?

A

Ciprofloxacin

161
Q

What are the key features of hepatorenal syndrome?

A

Ascites
Hyponatraemia
Hepatorenal syndrome

162
Q

What are the 2 types of hepato renal syndrome?

A

Acute - sepsis
Chronic - end stage liver disease

163
Q

How would you manage hepatorenal syndrome?

A

AKI stuff
Sepsis screen
Terlipressin

164
Q

What are the 4 key sources of upper GI bleeds?

A

Peptic ulcers
Mallory-Weiss tears
Oesophageal varices
Stomach ulcers

165
Q

What is used to estimate the risk of a patient having an upper GI bleed?

A

Glasglow-Blatchford Bleeding Score

166
Q

What is the association between urea and upper GI bleeding?

A

High urea

Acids + enzymes break down blood from bleed -> urea absorbed in intestines

167
Q

What is used to estimate the risk of bleeding and mortality after endoscopy for upper GI bleed?

A

Rochall score

168
Q

What primary prevention is there for variceal bleeding?

A

Small - carvedilol
Medium-large - band ligation + NSBBs

If oesophageal varices - terlipressin, Abx

169
Q

How would you manage acute variceal bleed?

A

Terlipressin -> supportive -> endoscopy (ligation) -> 5 days -> 2nd endoscopy if indicated -> TIPSS if indicated

170
Q

What secondary prevention is available for variceal bleeding?

A

Terlipressin (wean off)
Abx 7 days
Lactulose
Sucralfate

171
Q

Why is lactulose offered to those with oesophageal varices?

A

Encephalopathy risk

172
Q

Why is Sucralfate offered to those with oesophageal varices?

A

May reduce rate of banding induced oesophageal ulceration

173
Q

How would you differentiate cholecystitis from cholangitis?

A

Cholecystitis - no jaundice

Cholangitis - jaundice

174
Q

What are most gallstones made of?

A

Cholesterol

175
Q

What would you call a biliary stone in the common hepatic duct?

A

Hepatolithiasis

176
Q

What would you call a biliary stone in the CBD?

A

Choledocolithiasis

177
Q

What are the 4 RF’s for developing gallstones?

A

4F’s
Fat
Fair
Female
Fourty

178
Q

Why are patients with gallstones encouraged to reduce their fat intake?

A

reduces CCK secretion and hence gallbladder contraction

179
Q

What sign is suggestive of acute cholecystitis?

A

Murphy’s sign

180
Q

What is the first line imaging for acute cholecystitis?

A

Abdo US

181
Q

What is gallbladder empyema?

A

infected tissue and pus in the gallbladder

182
Q

How would you manage gallbladder empyema?

A

IV Abx

One of;
Cholecystectomy
Cholecystostomy

183
Q

What are the 2 main causes of Acute Cholangitis?

A

Obstruction in bile ducts (gallstones)
Infection from ERCP

184
Q

What is the most common pathogen causing acute cholangitis?

A

E.coli

185
Q

What is the presentation of acute cholangitis?

A

Charcot’s Triad
RUQ pain
Fever
Jaundice

186
Q

What is the most common type of primary liver cancer?

A

Hepatocellular carcinoma

187
Q

Name 4 established RFs for HCC

A

ALD
NAFLD
Hep B
Hep C

188
Q

Who is screened for HCC and how is this done?

A

Liver cirrhosis

Every 6 months - US, AFP

189
Q

What interventional radiology procedure may be used to treat HCC?

A

Transarterial chemoembolisation

190
Q

What is the most common type of cholangiocarcioma?

A

Adenocarcinoma

191
Q

What is the most commo site for cholangiocarcinoma?

A

Perihilar region

192
Q

What form of AI liver disease is associated with cholangiocarcinoma?

A

PSC

193
Q

What tumour marker is associated with cholangiocarcinoma?

A

CA19-9

194
Q

Name 2 benign liver tumours

A

Haemangioma
Focal Nodular Hyperplasia

195
Q

Who is more at risk of Focal Nodular Hyperplasia?

A

women, those on OCP

(related to oestrogen)

196
Q

Which 2 LFTs are associated with hepatic pathology?

A

ALT
AST

197
Q

Which 2 LFTs are associated with biliary pathology?

A

ALP
GGT

198
Q

What other 2 tests are essential alongside LFTs?

A

Coagulation screen
BGL

199
Q

What would an isolated rise in ALP suggest?

A

Bone pathology

200
Q

What would an isolated rise in GGT suggest?

A

Alcohol XS

201
Q

What would a rise in both ALP and GGT suggest?

A

Cholestasis

202
Q

What might cause an isolated ^Bilirubin?

A

Gilbert’s syndrome (glucosyltransferase deficiency)

203
Q

What might cause decreased production of albumin?

A

Malnutrition
Severe liver disease

204
Q

What might cause increased loss of Albumin?

A

Protein-losing enteropathies
Nephrotic syndrome

205
Q

Why is albumin not the best marker of liver function?

A

It has a 1/2 life of 20 days so takes some time to decrease

206
Q

How would severe liver disease affect a coagulation screen?

A

Decreased clotting factors
^PT / INR

Medicine (20 decks)

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