Abdomen Flashcards
Causes of liver cirrhosis**
- Chronic viral hepatitis (Eg: hepatitis B, C)
- Alcoholic liver disease
- Metabolic liver disease (Eg: hemochromatosis, Wilson’s disease, non-alcoholic fatty liver disease)
- Autoimmune liver disease (Eg: autoimmune hepatitis, primary biliary cholangitis)
CAGE screening tools*
- C: felt should Cut down?
- A: Annoyed by criticism?
- G: felt Guilty?
- E: first thing in morning (Eye-opener)?
0-1: low risk of problem drinking
2-3: high suspicion for alcoholism
4: diagnostic for alcoholism
Investigation for liver cirrhosis*
> Laboratory
- FBC: decrease WCC, platelet, anemia
- LFT: decrease albumin
- Coagulation profile
- Renal function test
- Hepatitis serology
> Imaging
- Ultrasound: shrinking of liver, nodular surface
- Duplex Doppler ultrasonography: assess patency of hepatic, portal and mesenteric veins
- CT scan: detect hepatomegaly and HCC
> Paracentesis
- Culture and sensitivity, gram stain, SAAG
> Liver biopsy
Trigger for hepatic encephalopathy*
- Drugs - benzodiazepine, alcohols
- Increase ammonia production, absorption or entry into brain - excess dietary intake of protein, GI bleeding, infection, constipation
- Dehydration - vomiting, diarrhea, diuretics
- Portosystemic shunting
Signs of liver cirrhosis**
- Leukonychia
- Clubbing
- Palmar erythema
- Dupuytren contracture
- Spider naevi
- Gynecomastia
- Ascites
- Splenomegaly
SAAG formula
(Serum albumin) - (Albumin level in ascites fluid)
Child Pugh Scoring
Cirrhosis mortality: Class A-C
- Albumin
- Bilirubin
- Coagulopathy - PT, INR
- Distension (Ascites)
- Encephalopathy
Grading of hepatic encephalopathy
I - confused or altered mood
II - drowsiness/ inappropriate behavior
III - stuporous but arousable
IV - comatose, unresponsive to painful stimuli
Management of hepatic encephalopathy*
- Eliminate precipitating factors: correct hypovolemia, treat GI bleed and infection, avoid sedatives
- Lactulose/ Rifaximin (target 2-3 soft stools per day)
- Nutritional support (prolonged protein restriction not recommended, eat frequent small meals)
Pathophysiology of hepatic encephalopathy**
- Nitrogenous waste builds up and passes to the brain, where astrocytes clear it by conversion of glutamate to glutamine
- Excess glutamine cause osmotic imbalance and shift of fluid into these cells - hence cerebral edema
Signs to look for in nephrotic*
- Hydration status - at risk of hypovolemia
- Peripheral edema
- Bedside capillary blood glucose
- Urine dipstick: proteinuria, hematuria
- Systemic:
Abdomen: ascites, hepatosplenomegaly
CVS: sign of heart failure
Investigation for nephrotic*****
> Establish the diagnosis - 24-hour urine protein collection or more practically spot urine protein:creatinine ratio (urine PCR) □ Proteinuria >= 3.5 g per 24 hours □ Urine PCR >= 300 mg/mmol - Serum albumin level - Serum lipid profile - Urine FEME
> Complications
- Renal profile
- Hematocrit
> Underlying etiology
- Blood glucose
- Hepatitis B and C serology
- Autoimmune screening
- Renal ultrasound
- Renal biopsy
Supportive management for nephrotic syndrome****
- Volume status accessed regularly (Eg: daily weight, BP, input and output chart)
- Treat edema (IV loop diuretics; Restrict daily sodium intake to <2.0g)
- Treat proteinuria and hypertension (ACE inhibitor; Target BP: SBP <120mmHg)
- Treatment of hyperlipidemia (Lifestyle modification)
- Immunization (Eg: pneumococcal, influenza, meningococcal, herpes zoster)
Definition of nephrotic syndrome*****
- Proteinuria >3g/24 hours
- Hypoalbuminemia <30g/L
- Edema
Pre-treatment screening for nephrotic syndrome****
- Most treatment is immunosuppressive therapy, common infection should be screened to prevent flare
- Eg: hepatitis B/ C, HIV, syphilis, tuberculosis
Follow up for nephrotic syndrome****
- Clinically: BP, edema, signs of steroid toxicity, side effects of immunosuppressive
- Urine dipstick, renal function, urine PCI
Definition of oliguria
- <400ml/24 hours OR
- <0.5ml/kg/hour
Causes of nephrotic vs nephritic syndrome***
> Nephrotic
- Minimal change disease
- Focal segmental glomerulosclerosis
- Membranous nephropathy
- Diabetic nephropathy
- Lupus nephritis
> Nephritic
- IgA nephropathy
- Post-streptococcal GN
- Anti-GBM disease
- HSP
Urea:Creatinine Ratio*
40-100:1 - normal or post renal cause of AKI
> 100:1 - pre-renal cause (urea absorption increased compared to creatinine)
<40:1 - intrinsic renal damage (urea unable to be absorbed -> become like creatinine -> ratio gets closer to 1)
Stages of CKD based on eGFR*
- Stage 1: >=90
- Stage 2: 89-60
- Stage 3a: 59-45
- Stage 3b: 44-30
- Stage 4: 29-15
- Stage 5: <15
Complications of CKD**
○ Anemia ○ Renal osteodystrophy: bone pain ○ Ischemic heart disease ○ Thromboembolic events ○ Frequent infection
Pathophysiology of anemia in CKD
- Normochromic, normocytic anemia
- Due to reduce production of erythropoietin by kidney
- Reduce stimulation of bone marrow -> reduce RBC production
Pathophysiology of mineral and bone disorder in CKD
- Decrease conversion of calcidiol to calcitriol by the kidney
- Decrease calcium absorption from small intestine
- Decrease calcium in blood -> decrease inhibition of PTH release
- Increase PTH in blood
Management of mineral and bone disorder in CKD
- Phosphate >1.5 mmol/L: dietary restriction +- phosphate binder
- Vit D deficient: Vit D supplements
- Increase PTH: activated Vit D analogue (eg: 1a-calcidol, calcitriol, paricalcitol)
Target HbA1c in CKD patient
HbA1c: <=7%
Investigation for SLE
> Establish diagnosis
- Autoantibodies: ANA, anti-ds DNA, antiphospholipid ab
- Complement level: decrease C3, C4
> Other test
- FBC: anemia
- ESR
- Renal profile: elevated creatinine
- Urinalysis: cellular cast
Management of SLE*
> DMARDs
- Hydroxychloroquine: for all SLE patient
- Corticosteroid: acute flare
- Immunosuppressive: poor symptom control despite hydroxychloroquine and steroid
- Rituximab: severe renal and extrarenal disease refractory to immunosuppressive
> Adjunctive
- Rashes: topical steroids, sunscreen
- Arthralgia: NSAIDs
Diagnostic criteria for SLE
○ Skin
- Malar rash (butterfly rash)
- Discoid rash (chronic, can scar)
- Photosensitivity (other rashes from sun exposure)
○ Mucosa
- Ulcers (mouth)
○ Serosa
- Serositis (pleuritis, pericarditis)
○ Joints
- Arthritis (2 or more)
○ Kidney
- Renal disorder (abnormal urine protein, diffuse proliferative glomerulonephritis)
○ Brain
- Neurological disorders (seizure, psychosis)
○ Blood
- Anemia, thrombocytopenia, leukopenia
○ Antibodies
- Antinuclear antibody (ANA)
○ Other autoantibody
- Anti-smith (target ribonucleoproteins)
- Anti-dsDNA
- Antiphospholipid
Causes of chronic kidney disease***
○ Diabetes - 24% ○ Glomerulonephritis - 13% ○ Increase BP/ renovascular disease - 11% ○ Pre-renal - Renal hypoperfusion (eg: hypotension, renal artery stenosis) ○ Renal - Interstitial (eg: drug, tumor) ○ Post-renal - Luminal (eg: stone, clot) - Mural (malignancy, BPH, stricture) - Extrinsic compression
Complication of CKD***
- Anemia (Erythropoiesis stimulating agents: iron replacement)
- Sodium retention and volume overload (Sodium restriction/ Diuretics)
- Hyperkalemia (Dietary restriction)
- Metabolic acidosis (Sodium bicarbonate)
- Mineral and bone disorder: decrease calcitriol, calcium, increase PTH, phosphate ( dietary restriction + phosphate binder, Vit D supplement)
Investigation for CKD***
○ BUSE/Cr: increase urea and creatinine
○ Electrolyte: hyperkalemia, hyperphosphatemia, hypocalcemia
○ Urinalysis: UFEME
○ Renal ultrasound: shrinking of kidney size
> Investigate the cause
§ Doppler ultrasound, CT angiography: RAS
§ Renal biopsy: glomerulonephritis
> Evaluate complication
§ FBC: anemia
§ PTH (high), Calcitriol (low)
Risk factor for nephrotic syndrome
> Medical
- DM, Lupus, amyloidosis
> NSAIDs
> Infection
- HIV, Hep B/C, malaria
Indication for renal biopsy
- If underlying cause cannot be ascertained from initial assessment
- Only done by urologist
Complication of nephrotic syndrome
- Protein malnutrition
- Hypovolemia
- AKI
- Thromboembolism
- Infection
What is dry weight
- Lowest tolerated post-dialysis weight where there are minimal signs or symptoms of either hypo/ hypervolemia
- Required frequent re-estimation, influenced by fluctuation of lean body mass and total fat content
Hemodialysis vs CAPD
> Hemodialysis
- Dialysis machine
- 3-5 times/ week, usually in dialysis center
- Better clearance
- Cx: disequilibrium syndrome, air embolism, dilated superficial vein
> Peritoneal dialysis
- Use peritoneal lining as filter
- Daily, done from home
- Fewer hemodynamic complication
- Cx: abdominal hernia, peritonitis, peritoneal membrane scarring
How to follow up ACEI
- RF checked 3-5 days after (renal artery stenosis/ older patient with HPT)
- Termination of ACEI if serum creatinine increase >30% above baseline within first 6-8 weeks
What is Wilson’s disease
- Inherited disorder of copper excretion with excess deposition in liver and CNS
Signs of Wilson’s disease
- CNS: tremor, dysarthria, dysphagia, dementia
- Kayser-Fleischer rings (copper in iris)
Does Hep A cause jaundice? Investigation
- Jaundice in 40-70% of patient
- Ix: AST/ ALT, Serum IgM/G anti-HAV antibodies
Complication of liver cirrhosis*
> Hepatic failure
- Coagulopathy
- Encephalopathy
- Hypoalbuminemia
- Sepsis
> Portal hypertension
- Ascites
- Splenomegaly
- Caput medusa
> HCC
Classification and causes of jaundice
> Pre-hepatic (dark stool, normal urine, mainly hemolytic)
- Inherited: thalassemia, G6PD, spherocytosis, sickle cell anemia
- Acquired: malaria, SLE, HUS
> Hepatic (normal stool, tea urine)
- viral hepatitis
- autoimmune hepatitis (eg: SLE)
- liver cirrhosis/ chronic liver disease (eg: alcoholic liver disease, Wilson’s disease)
> Post-hepatic (pale stool, tea urine)
- Intraluminal: gallstones, parasites
- Mural: biliary stricture, distal cholangioma
- Extraluminal: Ca head of pancreas
Liver enzyme corresponding to which part of liver
- Hepatocellular pattern: AST, ALT
- Cholestatic pattern: ALP, GGT, bilirubin
- Direct bilirubin = conjugated
CKD fluid restriction calculation
- Determine by urine output per day
- Fluid allowance = urine output + 500ml (daily loss)
Physical signs for CKD
○ Urine dipstick: proteinuria, glycosuria ○ Capillary blood glucose ○ General examination - Hands: half-and-half nail, AV fistula - Eyes: periorbital edema - Neck: raised JVP - Back, lower limb edema ○ Systemic - Respiratory: bibasal crepitation - Abdomen: ascites - Diabetic: fundoscopic, neurological, peripheral artery
Pathophysiology of hematemesis in liver cirrhosis
- Cirrhosis cause increase resistance of blood flow through fibrotic liver
- increase BP in hepatic circulation cause blood to backs up into the collateral venous system
- Liver unable to synthesis clotting factors or anti-coagulant proteins -> prone to bleed
Indication for urgent hemodialysis
“AEIOU”
- Acidosis
- Electrolyte imbalance
- Intoxication
- Fluid overload
- Uremic encephalopathy
Genetic basis for polycystic kidney disease
> Autosomal dominant
- Type 1 (85%): PKD1 gene on chromosome 16
- Type 2: PKD2 gene on chromosome 4
> Autosomal recessive
- Chromosome 6
Presentation for cyst infection, hemorrhage
- Loin and abdominal pain
- Hematuria is more often c/b rupture of cyst into collecting system than hemorrhage as most cyst do not communicate with collecting system
Complication of polycystic kidney disease
- Hypertension
- Frequent UTI, cyst infection
- Renal calculi
- Anemia
- Berry aneurysm
- Progression to ESRF
Indication for nephrectomy in PKD
- Enormous kidney (resulting in discomfort and reduce QoL)
- Recurrent infection
- Suspected malignancy
- Uncontrolled renal hemorrhage
Pathogenesis for CKD-MBD
- Secondary hyperPTH occurs in response to:
® Phosphate retention
® Decreased free ionized calcium concentration
® Decrease calcitriol concentration - This cause abnormalities in bone turnover, mineralization or strength
Management of CKD-MBD
> Reduce phosphate level
- Phosphate restriction
- Phosphate binders (with meal)
- Phosphate removal through dialysis
> Calcitriol or synthetic vitamin D analogue
> Parathyroidectomy (if refractory to medical)
How frequent perform dialysis
○ CAPD
- 4 exchanges/day
- 20-30 minutes/session
○ Automated PD
- 3 cycles/night
○ Hemodialysis
- 4 hours
- 3 times/week
Complication of hemodialysis
> Early
- Disequilibrium syndrome
- Air embolism
> Late
- Dilated superficial veins due to central vein stenosis/ thrombosis
Contraindication of hemodialysis
- Absolute
• Inability to secure vascular access
- Relative • Difficult vascular access • Needle phobia • Cardiac failure • Coagulopathy
Mechanism of renal failure in ACE-I usage
- In bilateral renal artery stenosis
- Afferent pressure is reduced by narrowed vessels
- ACE-I preferentially dilate efferent vessels
- GFR falls, renal ischemic nephropathy develops and renal failure ensures
Causes of abdominal distension
- Fat
- Fluid
- Fetus
- Flatus
- Feces
