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Junior blocks > GI, renal and hepatic medicine > Flashcards

GI, renal and hepatic medicine Flashcards

1
Q

What is the distribution of UC?

A

Continuous
Mucosal only
Rectum to ileocaecal valve

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2
Q

What is the distribution of Crohn’s?

A

Patchy
Full thickness
Mouth to anus

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3
Q

What are the macroscopic changes seen in UC?

A

Continuous inflammation

Pseudopolyps

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4
Q

What are the macroscopic changes seen in Crohn’s?

A

Cobblestoning
Apthous ulcers
Serpiginous ulcers
Rose thorn ulcers

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5
Q

What are the microscopic changes seen in UC?

A

Crypt abcesses
Decreased goblet cells
Inflammatory infiltrate of the lamina propria

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6
Q

What are the microscopic changes seen in Crohn’s?

A

Granulomas with Langerhan’s giant

Increased goblet cells

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7
Q

What are the radiological changes seen in UC?

A

Lead pipe colon
Fat halo
Thumb printing

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8
Q

What are the radiological changes seen in Crohn’s?

A

Kantor’s string sign on barium xray

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9
Q

What surgical procedure is appropriate for an emergency presentation of UC?

A

Sub total colectomy, end ileostomy and a mucous fistula

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10
Q

Which surgical procedure is appropriate for an elective presentation of UC?

A

Pan proctocolectomy, an ileoanal pouch may be a selected option for some.
Although increased risk of colon cancer.

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11
Q

Which marker is often high in Crohns?

A

ASCA

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12
Q

What are the complications seen in UC?

A

Toxic megacolon

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13
Q

What are the complciations seen in Crohn’s?

A

Stricture - Obstruction
Fistula
Abcess

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14
Q

What are the extra-intestinal symptoms of IBD in general?

A

Skin - pyoderma gangrenosum, erythema nodosum
Eyes - Iritis, uveitis, episcleritis
Joints - Ank spond, sacroilitis, osteoporosis

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15
Q

What are the extra-intestinal symptoms specific to UC?

A

Primary sclerosing cholangitis

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16
Q

What are the extra-intestinal symptoms specific to Crohn’s?

A

Gallstones
Pancreatitis
Hepatic abcess

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17
Q

What are the extra-intestinal symptoms specific to Crohn’s?

A

Gallstones
Pancreatitis
Hepatic abcess
Oxalate renal stones

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18
Q

Does Crohn’s or UC have a higher risk of Ca?

A

UC

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19
Q

What are the symptoms of Crohn’s?

A

Diarrhoea usually non-bloody
Weight loss more prominent
Upper gastrointestinal symptoms, mouth ulcers, perianal disease
Abdominal mass palpable in the right iliac fossa

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20
Q

What are the symptoms of UC?

A

Bloody diarrhoea more common
Abdominal pain in the left lower quadrant
Tenesmus

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21
Q

What is the effect of smoking on Crohn’s and UC?

A

Eases UC

Causes Crohn’s flares

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22
Q

What is the workup for suspected IBD?

A 
Fbc - anaemia, prothrombotic state
U+E - hypokalaemia
CRP - tracking
LFTs- primary sclerosing cholangitis
B12 and folate - terminal ileum involvement
Stool cultures
Faecal calprotectin - inflammatory bowel marker
Abdo xray - obstruction, toxic megacolon
CXR - perforation
Endoscopy and biopsy
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23
Q

How would you manage an acute flare of IBD?

A 
Fluids
Electrolytes
Analgesia - avoid NSAIDs
Rectal mesalazine
then oral prednisolone if no effect
Avoid antibiotics unless severe or septic
Avoid loperamide - risk toxic megacolon
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24
Q

How would you manage IBD pharmacologically?

A
  1. Sulfasalazine
  2. Azathioprine or mesalazine
  3. Infliximab

Plus smoking cessation, b12/iron where possible, refer to surgeons in UC.

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25
Q

What are the indications for infliximab in IBD?

A

Failed with DMARDS
Severe active disease
Review every 12 months

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26
Q

What are the causes of portal hypertension?

A

Cirrhosis
Right heart failure
Budd-Chiari (hepatic vein thrombosis)
Schistosomiasis

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27
Q

What is the pathophysiology of portal hypertension?

A

Increased pressure in the portal vein increases back pressure on the gastric vein. This opens up embryonic channels eg between the gastric and azygous vein. They form varices as the pressure increases.

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28
Q

What are the complications of portal hypertension?

A

Ascites - spontaneous peritonitis

Varices

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29
Q

Where are the most common sites of varices?

A

Oesophageal
Rectal
Caput medusa

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30
Q

Describe the histopathology of cirrhosis?

A

Nodules of hepatocytes surrounded by bands of collagen

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31
Q

What are the complications of cirrhosis?

A

Hepatocellular carcinoma
Decompensation
Portal hyptension (and therefore ascites and varices)

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32
Q

Describe the metabolism of alcohol.

A

Alcohol dehydrogenase
Acetaldehyde (and Mallory’s hyaline)
Acetaldehyde dehydrogenase
Acetate

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33
Q

How does alcohol cause cirrhosis?

A 
Increased acetaldehyde
Inflammation
Increased cytokines
Increased fibroblasts
Fibrosis
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34
Q

What are the main metabolic causes of cirrhosis?

A

Alcohol
Fat (NASH)
Copper (Wilson’s)
Iron (Haemochromatosis)

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35
Q

What are the main inflammatory causes of cirrhosis?

A 
Hep B and C
Autoimmune
Primary biliary cirrhosis
Primary sclerosing cholangitis
Alpha 1 antitrypsin
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36
Q

What are the signs of cirrhosis?

A 
Jaundice
Ascites
Visible epigastric vessels
Spider naevi
Duypuytren's 
Parotidomegaly
Metabolic flap
Increased oestrogen - gynaecomastia, palmar erythema, decreased body hair
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37
Q

What are the signs of a decompensated cirrhosis?

A

Metabolic flap
Increased bilirubin, increased INR, decreased albumin

Encephalopathy:

  • decreased attention
  • insomnia
  • confusion
  • dyspraxia
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38
Q

Why does liver disease often cause renal disease?

A

Hepatorenal syndrome

Bilirubin is toxic to kidneys

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39
Q

What is the management for cirrhosis?

A

Beta blockers to prevent variceal bleeding
Spironolactone for ascites - consider paracentesis
Monitor alpha fetoprotein - HCC

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40
Q

What blood results indicate recent alcohol misuse?

A

Gamma GT

Increased MCV without anaemia

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41
Q

What blood results indicate haemochromatosis?

A

Very increased ferritin

Decreased total iron binding capacity

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42
Q

What are the 3 sequelae of haemochromatosis?

A

Iron deposits in the liver, pancreas and pituitary

Cirrhosis
Diabetes
Melananin

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43
Q

What is the sign of Wilson’s disease?

A

Kayser - Fleischer rings in the eyes

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44
Q

How does primary biliary cirrhosis present?

A

Middle aged woman
Fatigue
Sjogrens
Cholestasis - leads to pruritis, jaundice, steatorrhea and cirrhosis

Positive ANA, anti-mitochondrial

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45
Q

How does primary sclerosing cholangitis present?

A

Young with IBD
Cholestasis: jaundice and pruritus
Right upper quadrant pain
Fatigue

Abnormal LFTs and positive ANCA

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46
Q

Describe the 2 implications of a raised gamma GT.

A

Alcohol
Or
Distinguishes obstructive hepatic pathology, not bone related when raised with alk phos

47
Q

What does a raised alk phos indicate?

A

Cholestasis (especially if also raised gamma GT)
Bone remodelling
Preganancy

48
Q

What is the differential for raised unconjugated bilirubn?

A

Gilberts

Cirrhosis
Heart failure

Haemolysis
Hypothyroid

49
Q

What is the differential for raised conjugated bilirubin?

A

Obstruction - cholestasis, PBC, PSC, HCC

Infiltration - amyloid, sarcoid, TB, haemochromatosis

50
Q

What are the markers for synthetic liver function?

A

INR

Albumin

51
Q

What is the differential for low albumin?

A

If also proteinuria:
AKI and Sepsis

Otherwise:
Cirrhosis
Malignancy

52
Q

Which blood tests are included in the liver screen?

A 
Antibodies: 
Hep A, B, C (hepatitis)
ANA, anti-mitochondrial (pbc)
ANCA (psc)
dsDNA, SM (autoimmune hep)

Ferritin and TIBC (haemachromatosis)
Alpha 1 antitrypsin
Thyroid (hypo)
Glucose (diabetes)

53
Q

How does haemachromatosis present?

A

Fatigue
Arthralgia - hands and wrists
Anti-dsDNA positive

Very high ferritin
Low TIBC

54
Q

What are the most useful prognostic markers in paracetamol overdose?

A

arterial ph

creatinine
encephalopathy

55
Q

Which blood test indicates a significant upper GI bleed?

A

Urea

acts as a protein meal and temporarily increases

56
Q

Which blood test indicates coeliac?

A

positive anti-endomysial antibodies

57
Q

How does coeliac present?

A

Intermittent oily diarrhoea
Failure to thrive
Other unexplained GI symptoms
Unexplained anaemia

58
Q

What complications are associated with repeated exposure to gluten in coeliac?

A

Villous atrophy which in turn causes malabsorption

T-cell lymphoma

59
Q

What are the most common causes of CKD?

A

Diabetes
Hypertension
Polycystic kidney disease

60
Q

What are the indications for dialysis in?

A

eGFR<8-10
Uraemic symptoms
Refractory acidosis, fluid overload, hyperkalaemia

Nephrotoxins that can be removed - eg aspirin OD

61
Q

What are uraemic symptoms?

A

Pruritis
Jaundice
Uraemic pericarditis
Uraemic flapping tremor

Lethargy
Cramps
Thirst
N+V
Hiccups
Mental status changes - encephalopathy
62
Q

What is a nephritic presentation?

A

Haematuria, hypertension

63
Q

What is a nephrotic presentation?

A

Proteinuria, oedema, hyperlipidaemia

64
Q

Which glomerulonephritis present as nephritic?

A

Goodpasture’s,
ANCA positive vasculitis - eg Wegeners
IgA nephropathy
Polycystic kidney disease

65
Q

Which glomerulnephritis present as nephrotic?

A

Diabetic nephropathy
Minimal change
Focal segmental
Membranous

66
Q

What is the pathophysiology of membranous glomerulonephritis?

A

Thick BM due to IgG deposits

Therefore damage, allows protein out

67
Q

What is the pathophysiology of minimal change glomerulonephritis?

A 
Podocyte damage
(Allows protein out)
68
Q

What is the pathophysiology of focal segmental glomerulonephritis?

A 
Podocyte sclerosis
(Allows protein out)
69
Q

What is the pathophysiology of IgA nephropathy?

A

IgA deposits in the actual glomerulus (blood vessels)
(Inflammation and haematuria)
Particularly at the time of simple infection eg sore throat (when iga increases)

70
Q

What is the pathophysiology of Goodpastures vasculitis?

A

Anti BM antibodies attack BM (type 4 collagen)

Haematuria, also lung haemorrhage

71
Q

What is the pathophysiology of Wegeners granulomatosis? (granulomatosis with polyangitis)

A

ANCA attacks small and medium vessels

Visible haematuria, lung and URT

72
Q

What is tubulointerstitial nephritis?

A

Nephritic presentation usually triggered by a drug reaction or chronic pyelonephritis

73
Q

Which drugs are associated with tubulointerstitial nephritis?

A 
NSAIDs
Lithium
Penecillin
PPI
Lead

(Not ACE, they do reversible AKI)

74
Q

What are the symptoms of CKD?

A 
Fluid overload
Hypertension
Bleeding
Uraemia
Tertiary hyperparathyroid
Anaemia
Hyperkalaemia
Acidosis
75
Q

What are patients with CKD at high risk of?

A

IHD and stroke

76
Q

Why do patients with CKD get anaemia?

A

Anaemia of chronic disease

Reduced EPO production

77
Q

Why do patients with CKD get fluid overload?

A

Kidneys no longer managing the homeostasis of Na

78
Q

Why do patients with CKD get hyperparathyroid?

A

Tertiary
Because the kidney can’t get rid of phosphate, this increases
Therefore Ca is mopped up too much
Low Ca, precipitates high PTH

Also secondary
Where the kidney stops activating vit D
Therefore less Ca absorption

79
Q

Which drugs can make symptoms of CKD worse?

A

Steroids (uraemia)

K sparing diuretics (increase hyperkalaemia)

80
Q

Which drugs can worsen egfr in CKD and AKI?

A

ACE
NSAIDs
CT contrast
Ciclosporin

81
Q

Which drugs require a higher dose in CKD?

A

Furosemide

82
Q

Which drugs require a lower dose in CKD/are toxic to the kidney?

A 
Digoxin
Lithium
Morphine
Penicillin
Gentamicin
Vancomycin
Erythromicin
83
Q

How does the kidney normally compensate for hypoperfusion?

A

RAAS activation
Angiotensin constricts the efferent

Juxtaglomerular apparatus detect low sodium in the distal tubule
Prostaglandins relax the afferent

84
Q

What are the causes of prerenal AKI?

A 
Hypovolaemia
Sepsis
Decreased oncotic pressure - cirrhosis
HF
Renal artery stenosis
NSAIDs
ACE
85
Q

What is the name given to the condition when pre renal AKI becomes refractive to fluids?

A

Acute tubular necrosis

86
Q

What are the causes of acute tubular necrosis?

A

Pre renal AKI (refractive to fluid)
Nephrotoxins
Endotoxins - E coli

87
Q

What are the main nephrotoxins?

A 
Myoglobin (rhabdomyelisis)
Bilirubin (heptaorenal syndrome)
Urate (gout)
ACE 
NSAIDs
Gentamicin
88
Q

What are the causes of post renal AKI?

A

Within the lumen:
2 stones
2 clots
2 tumours

In wall:
TB strictures

Outside:
BPH
Prostate Ca
Blocked catheter
AAA
Other tumour - cervical, uterine, renal
89
Q

How would you differentiate between pre renal, post renal and intrinsic AKI?

A

Pre - low bp, sepsis, responds to fluid, fbc for infection

Intrinsic - nephrotoxic drugs? blood and protein in dip, red cell casts on microscopy

Post - ultrasound for hydronephrosis, palpable bladder, complete anuria

90
Q

Describe the workup for AKI

A

Careful fluids
Monitor input and output

U and E - extent
Fbc - sepsis?
LFT - Hepatorenal?

Urine dip - sepsis and intrinsic?
Urine microscopy - sepsis and intrinsic?

Ultrasound - obstruction?

Biopsy if considering intrinsic

91
Q

How do you manage hyperkalaemia?

A

Ca gluconate and ECG for the heart

Insulin and dextrose plus salbutamol neb to put insulin back into cells

92
Q

Describe the stages of CKD?

A

eGFR

1 . >90 ml/min, with some sign of kidney damage on dipstick or USS
2 60-90 ml/min, with some sign of kidney damage on dipstick or USS
3a 45-59 ml/min,
3b 30-44 ml/min,
4 15-29 ml/min,
5 Less than 15 ml/min - dialysis or a kidney transplant may be needed

93
Q

Spironolactone

94
Q

Furosemide

95
Q

What is Henoch-Schonlein purpura? How does it present?

A

IgA mediated small vessel vasculitis

Palpable, erythematous rash on the extensor surfaces of the arms and legs associated with abdominal pain. Haematuria and mild renal failure

96
Q

How does polycystic kidney disease present?

A

Hypertension and subarachnoid haemorrhage
Recurrent UTIs and episodic haematuria
Nephritic

97
Q

Describe the genetic profile of polycytic kidney diease.

A

Autosomal dominant

98
Q

What feature of nephrotic syndrome makes it prone to VTE?

A

Loss of antithrombin-III, proteins C and S

99
Q

What are the main causes of intrinsic AKI?

A 
Acute tubular necrosis
Acute on chronic glomerulonephritis
Nephrotoxins
Tumour lysis syndrome
Rhabdomyolysis
100
Q

What are the stages of AKI?

A

Stage 1, 2 and 3

1.5-2 x baseline creatinine
2-3
3+

101
Q

Why are egfr and creatinine poor markers of kidney function? What is a better measure?

A

If they are not in a steady state the markers will be 1 step behind the actual function as they take time to build up.

Albumin: Creatinine is better

102
Q

What is the most common cause of nephrotic syndrome in young people?

A

Minimal change

103
Q

How do you minimise the risk of CT contrast in a patient with CKD?

A

Give saline pre and post procedure

104
Q

How can you differentiate between acute tubular necrosis and prerenal AKI?

A

Prerenal can lead to ATN but..

  1. It responds to fluid challenge
  2. It has low URINE Na because the kidneys are still trying to hold on to it to maintain volume
    In ATN they can’t do this so high urine Na (both have low serum Na)
105
Q

What are the symptoms of hypernatraemia?

A 
Irritability
restlessness
muscle twitching
spasticity
hyperreflexia
106
Q

What is the main risk in hypernatraemia?

107
Q

What is the main risk in hyponatraemia?

108
Q

How do you treat hyponatraemia?

A

Hypovolaemic - Slowly give saline
Euvolaemic - Treat underlying cause
Hypervolaemic - loop diuresis and fluid restriction

109
Q

Why do you have to treat hyponatraemia slowly?

A

Risk of pontine demyelination if you increase sodium too quickly

110
Q

What are the causes of hypovolaemic hyponatraemia?

A

Na loss

Diarrhoea
Vomiting

Diuretics
ACE
Nephropathies

111
Q

What are the causes of hypervolaemic hyponatraemia?

A

Dilution

Heart failure
Cirrhosis
Nephrotic syndrome
CKD

112
Q

In hypovolaemic hyponatraemia, how do you know whether there is an intrinsic renal loss of Na or an extra renal loss?

A

Urinary Na

If high (>20) Intrinsic
If low (<20) extrarenal
113
Q

What are the causes of euvolaemic hyponatraemia?

A

SIADH
Hypothyroid
Addissons
SSRIs

114
Q

What are the causes of hypernatraemia?

A

Cushings
Conn’s
HONC/DKA
Diabetes insipidus

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