Brainscape's Knowledge GenomeTM

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


See full index

MBBS IV - Junior Clerkship WCS > JC68 (Medicine) - Cirrhosis Complications > Flashcards

JC68 (Medicine) - Cirrhosis Complications Flashcards

1
Q

Causes of liver cirrhosis

A 
Common: 
Chronic viral hepatitis: Chronic hepatitis B (>60%)
Alcoholic liver disease
Non-alcoholic fatty liver disease
Cryptogenic (15%)

Other:
Autoimmune causes: PSC, autoimmune hepatitis
Metabolic causes: Wilson’s disease, Haemochromatosis
Biliary obstruction: Primary biliary cholangitis, Secondary biliary cirrhosis
Vascular causes: Veno-occlusive disease, Cardiac cirrhosis

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

List 6 major complications of cirrhosis

A

Ascites and Spontaneous Bacterial Peritonitis

Hepatorenal syndrome

Variceal bleeding

Encephalopathy

HCC

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

Pathophysiology of liver cirrhosis

A

Liver injury results in cytokine production by Kupffer cells and hepatocytes → activates stellate cells in space of Disse

Stellate cells transform into myofibroblast-like cell upon activation, producing
→ Collagen → fibrosis
→ Pro-inflammatory cytokines → hepatocyte damage
→ MMPs → break down normal ECM and replace with scar tissue

Autocrine loops: activated stellate cells produce TGF-β, PDGF and ROS that perpetuates its own activation

Result: progressive hepatic fibrosis with widespread hepatocyte loss and persistent chronic inflammation

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

S/S of hepatic insufficiency due to liver cirrhosis

A

Jaundice

Ankle edema, leukonychia - Hypoalbuminaemia

Easy bruising, purpura - Coagulopathy, Thrombocytopenia

Confusion, Flapping tremor - Hepatic encephalopathy

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

S/S of portal hypertension due to liver cirrhosis

A

Splenomegaly, Pancytopenia - Easy bruising, anaemic S/S, frequent infection

Caput medusae, Variceal bleeding - UGIB due to portosystemic shunts

Ascites, SBP, hepatic hydrothorax - Splanchnic vasodilation, arterial underfilling and Na retention

Oligoura, Hepatorenal syndrome - vasocontriction from RAAS activation due to arterial underfilling

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

Endocrine changes associated with liver cirrhosis

A

Male hypogonadism: due to primary gonad injury or HPG axis suppression
- Testicular atrophy, impotence, infertility, low libido

Feminization, Gynaecomastia: due to increase androgen production and convertion to estradiol
- Gynaecomastia, Inversion of male pubic hair pattern, loss of axillary and pubic hair

Female hypogonadism
- Breast atrophy, Anovulation, Amenorrhea, Low libido

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

Vascular lesions caused by liver cirrhosis
Pathogenesis
Ddx for each lesion

A

Spider naevus
Palmar erythema

 Due to ↑oestradiol: testosterone ratio
 ≥3 spider naevi significant, seen mainly in SVC drainage area (i.e. above nipple line)
 D/dx for spiders: pregnancy, RA, scleroderma
 D/dx for palmar erythema: pregnancy, RA, hyperthyroidism, haem malignancies

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

S/S cholestasis due to liver cirrhosis

A

Xanthelasma, Xanthomas
Due to hypercholesterolaemia from impaired biliary cholesterol excretion

Pruritus, Scratch marks
Due to impaired bile acid excretion leading to skin accumulation and pruritus

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

Differentiate chronic liver failure and liver decompensation

A

Liver decompensation occurs when metabolic capacity of the liver is exceeded

characterized by development of encephalopathy and ascites

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

Pathogenesis of ascites due to liver cirrhosis

A

Cirrhosis leads to portal hypertension

> > Increase portosystemic shunt and vasodilator release&raquo_space; Splanchnic vasodilation (Low pressure due to dilatation, not truly hypovolemia)

> > Decrease total systemic vascular resistance&raquo_space; systemic arterial underfilling (body reacts to apparent hypovolemia, retains water and salt in response)

Results:
Increase RAAS/ SNS for renal tubular reabsorption of sodium - sodium retention, ascites, edema
Increase Vasopressin to reabsorb water in DCT - dilutional hypoNatremia
Lower systemic vasodilator/ Increase local vasoconstriction - Renal vasoconstriction and hypoperfusion, hepatorenal syndrome

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

Ascites Ddx

A

Common:
- Malignancy: Primary peritoneal mesothelioma, Peritoneal metastasis, eg. Ca stomach
- Liver cirrhosis and Portal hypertension
- Cardiac failure
- Iatrogenic due to CAPD

Others:
- Hypoalbuminemia: liver decompensation, Nephrotic syndrome, Protein-losing enteropathy, Severe malnutrition
- Peritonitis: pancreatitis, Tuberculous peritonitis
- Hemoperitoneum

Rare:
- Myxedema
- Urological injury
- Abdominal pregnancy

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

S/S ascites

A

Asymptomatic: if mild (<1L)
Progressive abdominal distension ± abdominal discomfort
Pressure symptoms:
→ Shortness of breath due to pressure on diaphragm
→ Early satiety due to pressure on stomach

P/E findings:
□ Shifting dullness if >1L
□ Fluid thrill if ascites is marked
□ Features of ↑intra-abdominal pressure: bulging flanks, everted umbilicus, herniae, abdominal striae, divarication of recti, scrotal oedema

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

Ascites

Diagnostic methods

A

Imaging:

  • USG (1st line): free intraperitoneal fluid (hypoechoic) ± other features of portal HTN
  • CT/MRI (2nd line)

Diagnostic Paracentesis
- percutaneous, USG-guided, typically at LLQ

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

Diagnostic paracentesis

  • Indication
  • Technique
  • All useful exams and differentials
A

□ Indication: ALL new-onset ascites
□ Technique: percutaneous, USG-guided, typically at LLQ

Appearance:
→ Clear or straw-coloured: uncomplicated cirrhotic ascites
→ Turbid or cloudy: infection
→ Milky (chylous): hyperlipidaemia, TB peritonitis, malignancy (due to lymphatic obstruction)
→ Pink or bloody: traumatic tap, bleeding tendency or malignant ascites

Serum-ascites albumin gradient (SAAG) = serum [Alb] – ascites [Alb]
→ >11g/L → portal hypertension, i.e. cirrhosis, HF, PVT
→ <11g/L → exudative, i.e. malignant, infection, nephrotic syndrome

Cell count and differential:
→ WBC ≥500/mm3 and PMN >250/mm3 diagnostic of SBP

Microbiology:
→ Gram stain and culture
→ AFB smear, culture, ADA

(Cytology for malignant cell, Protein/glucose levels are NOT USEFUL)

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

Ascites

Management options for mild and severe ascites

A

General:

  • Bedrest - ↓RAAS activity and ↑renal blood flow
  • Dietary sodium restriction - 2g/day
  • Fluid restriction - 1-1.5L/day for dilutional hypoNa
  • Management of underlying liver disease, esp alcohol abstinence
  • Avoid drugs affecting renal blood flow to prevent hepatorenal syndrome

Severe:

  • Therapeutic paracentesis
  • Diuretic therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Ascites Diuretic therapy

  • Target weight loss
  • Types, typical regimen
A

Target: 1kg/day weight loss

Regimen: PO spironolactone ± furosemide

Types:
K+-sparing diuretics:
→ Spironolactone (Aldactone A)
→ Amiloride (ENaC blocker)

Loop diuretics: alone or add-on K+ sparing diuretics
→ Furosemide (Lasix)
→ Bumetanide (Burinex)

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

Side effects of diuretic therapy for ascites

Indications to stop diuretic therapy

A

Spironolactone: hyperkalaemia and tender gynaecomastia in male

Amiloride (ENaC blocker): hyperK, NO gynaecomastia

Furosemide (Lasix): IV injection precipitate acute renal failure

STOP all diuretics if Na <120, progressive renal failure, ↑HE, incapacitating muscle cramps
→ Monitor K: stop Lasix if <3mmol/L, stop spironolactone if >6mmol/L

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

Therapeutic paracentesis

  • Indications
  • Target fluid extraction
  • Concurrent therapies
A

indicated for tense or diuretic-resistant ascites, with peripheral edema present

Target: large volume (4-6L) taps

Concurrent Albumin infusion: 6-8g per L fluid removed for large volume taps (≥5L)

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

Therapeutic paracentesis

  • Complications and precautions
A

Bleeding from puncture site: prevented by FFP and/or platelet concentrate

Sepsis: exclude SBP before paracentesis

Caecal perforation with Rt-sided punctures → should puncture at LLQ (Lt McBurnley’s point)

Renal impairment (may in turn precipitate hepatic encephalopathy) → caution in those with ↓BP + ↑serum Cr, monitor vitals during paracentesis

20
Q

Second-line treatment options for refractory ascites

A

Oral midodrine: vasopressor increase renal Na excretion

TIPS to treat portal hypertension

Liver transplant for decompensated cirrhosis

Peritoneo-venous shunt for palliation

21
Q

Spontaneous bacterial peritonitis

  • Definition
  • Complications
A

Ascitic fluid infection without an evident intra-abdominal surgically treatable source

Complications:
bacteremia, shock and multiorgan failure

22
Q

Differentiate different forms of infected ascites

A
  1. Mono-microbial bacterascites
    - Culture positive for one organism
    - Normal PMN count
  2. Culture-negative Neutrocytic Ascites
    - Culture negative
    - High PMN count without alternative causes
    - Early SBP
  3. SBP
    - Culture positive
    - High PMN count
23
Q

Pathogenesis of SBP

  • Precipitating factors
  • Pathophysiology
  • Bacteriology
A

Precipitating factors of bacteremia:

  • Deficiency serum complements
  • Poor reticulo-endothelial system function
  • GI hemorrhage
  • Invasive procedures

Consequence depends on ascitic fluid opsonic activity
→ Poor → SBP
→ Moderate → CNNA (considered an early form of SBP)
→ Good → resolution of bacterascites with macrophage clearance

□ E. coli (43%), K. pneumoniae (11%), Streptococcus spp (28%), Enterobacteriaceae (4%)

24
Q

Diagnostic criteria of SBP

A

Diagnostic paracentesis:

→ Protein: often low → reflects ↓opsonin activity and liability to infection
→ Cell count: note that for every 250 RBC/mm3 one PMN should be subtracted
- >500 WBC/mm3 → suspicious
- >250 PMN/mm3 → diagnostic if S/S of SBP present
- >500 PMN/mm3 → diagnostic if S/S of SBP absent
→ Culture: usually Gram-negative or streptococci but may be negative (does not preclude SBP diagnosis as in CNNA)

25
Q

SBP

Clinical features

A

13% asymptomatic

Diffuse abdominal discomfort: pain (59%), tenderness (49%)

Diarrhoea (32%) due to concomitant intestinal bacterial overgrowth

Systemic upset: fever (69%), altered mental status (54%), hypotension (21%)

Ileus (30%)

26
Q

Secondary bacterial peritonitis vs SBP

How to differentiate

A

Secondary bacterial peritonitis:

ascitic fluid analysis showing (Runyon’s criteria)

  • Total protein >10g/L
  • Glucose <50mg/dL
  • LDH > serum ULN
27
Q

SBP

Empirical antibiotic treatment

  • Drug choice
  • Indications
  • Timing and duration
A

Empirical antibiotic therapy:
→ Indications: symptomatic or ascitic fluid PMN >250/mm3
→ Choice: IV 3G cephalosporin (ceftriaxone or cefotaxime)
→ Effect: usually see exponential fall in PMN count after initiation
→ Duration: usually recommend 5-10 days of Abx, can stop if PMN ≤250 + clinical improvement

28
Q

SBP

Treatment plan
- All treatment options

A

Discontinue β-blockers: a/w poorer outcome in SBP
Empirical antibiotic therapy - Ceftriaxone IV
Repeat paracentesis 48h later if complicated

(Albumin infusion if Hepatorenal syndrome)

29
Q

SBP Prophylaxis regimen

Indication
Function
Benefits

A

NORFLOXACIN PROPHYLAXIS

Indication:
Cirrhosis with GI bleeding
Previous SBP, or ascitic fluid protein <1.5g/d with impaired RFT or liver failure

Function: long-term selective intestinal decontamination
Highly active vs G- bacilli but low activity vs anaerobes (hence preserves flora)

Benefits:
Incompletely absorbed by gut → ↓S/E
Rarely causes resistance

30
Q

Hepatorenal syndrome

  • Definition
  • Prevalence
  • Pathogenesis
A

Hepatorenal syndrome (HRS): renal failure in patients with severe liver disease in absence of any pathological cause for development of renal failure

Prevalence: ~10% of patients with advanced cirrhosis complicated by ascites

Cause: ↓renal perfusion due to RAAS/SNS activation secondary to splanchnic vasodilatation and systemic underfilling

31
Q

Ddx renal failure with liver diseases

A

□ Hypovolaemia due to overdiuresis (commonest cause), GI bleeding
→ ALWAYS recheck meds and adjust accordingly, do NOT assume HRS

□ Sepsis due to pre-renal failure
□ Nephrotoxic drugs
□ Parenchymal renal disease
□ Hepatorenal syndrome: if unexplained by any of the above cause

32
Q

Hepato-renal syndrome

  • Precipitants
  • Diagnostic criteria by biochemical tests
A

□ Clinically evident liver disease: can be both acute or chronic
□ Precipitant by an acute insult, eg. SBP, GI bleeding

Diagnostic criteria:
1. Renal impairment: progressive ↑serum Cr, serum sodium <130mEq/L

  1. Oliguria: usually <500mL/d
  2. Intact tubular function as reflected by
    - Urine Na <10mEq/L, i.e. no natriuresis
    - Urine osmo > plasma osmo, i.e. no failure in concentrating urine
  3. No proteinuria (<500mg/d) or haematuria
33
Q

Hepato-renal syndrome

Clinical classifications

A

Type 1 HRS: ≥2× serum Cr to >221mmol/L under 2 weeks
→ A/w very poor prognosis (median survival <1mo w/o treatment)
→ Should r/o other important causes of acute renal failure

Type 2 HRS: renal impairment that is less severe than in T1HRS
→ Usually a/w diuretic-resistant ascites

34
Q

Hepato-renal syndrome

How to clinically diagnose?

A

diagnosis of exclusion! – rule out
□ Pre-renal failure: over-diuresis, sepsis-related AKI
□ Renal failure: use of nephrotoxin, gloermulonephritis/renal vasculitis
□ Post-renal failure: renal stones

35
Q

Hepato-renal syndrome

Treatment options + refractory treatment options

A

Treatment of underlying liver disease

Optimize BP to lessen arterial underfilling
→ Glypressin/terlipressin ± albumin as 1st line
→ Octreotide + midodrine ± albumin as alternative
→ Norepinephrine ± albumin: mainly in critically ill patients

Optimize renal haemodynamics:
→ Therapeutic paracentesis for tense ascites, drop BP

Therapy for refractory cases:
→ TIPS
→ Dialysis

36
Q

Therapy to improve arterial underfilling in hepato-renal syndrome
MoA

A

Glypressin/terlipressin ± albumin as 1st line

  • ADH analogues: ↑BP and renal perfusion pressure (main mechanism), ↑central blood volume and ↓SNS activation
  • Albumin: to improve intravascular volume

Octreotide + midodrine ± albumin as alternative

  • Octreotide: ↓endogenous vasodilator release → ↓splanchnic vasodilation
  • Midodrine: systemic vasoconstrictor → ↑BP
37
Q

Causes of bleeding in cirrhotic patients

A

Varices (50-90%): oesophageal or gastric most common, HVPG >12mmHg

Portal hypertensive gastropathy (PHG)

Peptic ulcer disease

Generalized bleeding tendency

Others, eg. Mallory-Weiss tears (in alcoholic cirrhosis)

38
Q

Management plan for variceal bleeding

A

Shock, haemodynamic stabilization

  • Monitor vitals, maintain SBP 90-100mmHg
  • Volume resuscitation
  • Packed cells, FFP/ platelets

Correct coagulopathy:
- Vitamin K1 replacement if cholestatic

Emergency OGD: find bleed and intervention

Manage complications e.g. HE

39
Q

Variceal bleeding

Treatment options for haemostasis
- endoscopic options, medical, surgical …etc

A

Endoscopic treatment:

  • Band ligation + Injection Sclerotherapy
  • Variceal obliteration by tissue adhesive, injection of cyanoacrylate

Drug:
- Vasoconstrictors: decrease portal venous pressure
→ Terlipressin (1st line)
→ Octreotide: used if IHD

Sengstaken-Blakemore tub/ Balloon Tamponade

Emergency surgery if failed endoscopic therapy
→ Transjugular intrahepatic portosystemic shunt (TIPS)
→ Shunt surgery: portocaval shunts, splenorenal shunt
→ Non-shunt surgery: oesophageal transection, Sugiura procedure

40
Q

Band ligation + Injection sclerotherapy for variceal bleed

Function
Complications
Disadvantage
Effectiveness

A

Function: Immediately stop bleeding + sclerotherapy to vasoconstrict bleeding vessels

Complications:

  • Transient esophageal pain
  • Esophageal ulcers
  • Stricture
  • Infections: mediastinitis, aspiration pneumonia
  • Dislodge/ sloughing bands by later endoscopy

Disadvantage:
Cannot reach gastric varices

Effectiveness
- 90% acute bleed, high recurrence, 60% overall

41
Q

Vasoactive drugs for variceal bleed

  • Examples
  • MoA of each
A

IV terlipressin: preferred agent (1st line)
MoA: synthetic ADH-analogue → slow, sustained release of ADH → constriction of mesenteric arterioles → ↓blood flow to gut → ↓portal venous inflow

IV octreotide: 2nd line agent, preferred in IHD/PVD
→ Pharmacology: synthetic octapeptide sharing 4AAs with somatostatin → longer half-life with ↑potency
→ MoA: action not well-defined, a/w ↓splanchnic blood flow

42
Q

Prevention of Varices rebleeding

A

Propranolol or other B blockers

Repeated band ligation

TIPS - Transjugular Intrahepatic Portosystemic Shunt

Liver Transplant

43
Q

TIPS

Procedure
Effectiveness

A

Transjugular intrahepatic portosystemic shunt (TIPS)

Colapinto catheter inserted transjugularly into middle hepatic vein and wedged there
advanced through liver parenchyma to Rt branch of portal vein
stent deployed to open up channel (painful)

Efficacy: achieve haemostasis in 90-100% pt

44
Q

TIPS

Indication
Contraindication

A 
Indications:
→ Variceal bleeding:
- As definitive Tx in resistant and recurrent bleeding or acute uncontrolled bleeding
- As secondary prophylaxis
→ Refractory ascites
→ Refractory hepatic hydrothorax
→ Budd-Chiari syndrome
→ Pre-transplant portal decompression

C/I:
→ Severe liver failure if not pre-transplant (risk of hepatic encephalopathy)
→ Hepatocellular carcinoma (needle tract seeding)
→ Liver abscess or cholangitis
→ DIC or severe coagulopathy
→ Cavernous transformation of portal vein (CTPA):
→ IJV, SVC, IVC thrombosis

45
Q

TIPS

Acute complications

A

Bleeding:
- Severe/ fatal intra-abdominal bleed from liver capsule perforation or portal bifurcation
- Hemobilia, liver haematoma

Vascular:
- Thromboembolism with clot in stent
- Volume overload with HF due to rapid channeling of portal blood
- DIC

Contrast nephropathy

Sepsis

46
Q

TIPS

Chronic complications

A

Hepatic encephalopathy

Recurrent bleeding: due to non-portal hypertensive bleed or from inadequate portal decompression

Stent stenosis or occlusion

MBBS IV - Junior Clerkship WCS (131 decks)

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