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Internal Medicine > Abdomen > Flashcards

Abdomen Flashcards

1
Q

Causes of liver cirrhosis**

A
  • 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)
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2
Q

CAGE screening tools*

A
  • 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

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3
Q

Investigation for liver cirrhosis*

A

> 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

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4
Q

Trigger for hepatic encephalopathy*

A
  • 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
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5
Q

Signs of liver cirrhosis**

A
  • Leukonychia
  • Clubbing
  • Palmar erythema
  • Dupuytren contracture
  • Spider naevi
  • Gynecomastia
  • Ascites
  • Splenomegaly
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6
Q

SAAG formula

A

(Serum albumin) - (Albumin level in ascites fluid)

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7
Q

Child Pugh Scoring

A

Cirrhosis mortality: Class A-C

  • Albumin
  • Bilirubin
  • Coagulopathy - PT, INR
  • Distension (Ascites)
  • Encephalopathy
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8
Q

Grading of hepatic encephalopathy

A

I - confused or altered mood
II - drowsiness/ inappropriate behavior
III - stuporous but arousable
IV - comatose, unresponsive to painful stimuli

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9
Q

Management of hepatic encephalopathy*

A
  • 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)
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10
Q

Pathophysiology of hepatic encephalopathy**

A
  • 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
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11
Q

Signs to look for in nephrotic*

A
  • 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
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12
Q

Investigation for nephrotic*****

A 
> 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
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13
Q

Supportive management for nephrotic syndrome****

A
  • 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)
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14
Q

Definition of nephrotic syndrome*****

A
  • Proteinuria >3g/24 hours
  • Hypoalbuminemia <30g/L
  • Edema
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15
Q

Pre-treatment screening for nephrotic syndrome****

A
  • Most treatment is immunosuppressive therapy, common infection should be screened to prevent flare
  • Eg: hepatitis B/ C, HIV, syphilis, tuberculosis
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16
Q

Follow up for nephrotic syndrome****

A
  • Clinically: BP, edema, signs of steroid toxicity, side effects of immunosuppressive
  • Urine dipstick, renal function, urine PCI
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17
Q

Definition of oliguria

A
  • <400ml/24 hours OR

- <0.5ml/kg/hour

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18
Q

Causes of nephrotic vs nephritic syndrome***

A

> Nephrotic

  • Minimal change disease
  • Focal segmental glomerulosclerosis
  • Membranous nephropathy
  • Diabetic nephropathy
  • Lupus nephritis

> Nephritic

  • IgA nephropathy
  • Post-streptococcal GN
  • Anti-GBM disease
  • HSP
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19
Q

Urea:Creatinine Ratio*

A

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)

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20
Q

Stages of CKD based on eGFR*

A
  • Stage 1: >=90
  • Stage 2: 89-60
  • Stage 3a: 59-45
  • Stage 3b: 44-30
  • Stage 4: 29-15
  • Stage 5: <15
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21
Q

Complications of CKD**

A 
○ Anemia
○ Renal osteodystrophy: bone pain
○ Ischemic heart disease
○ Thromboembolic events
○ Frequent infection
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22
Q

Pathophysiology of anemia in CKD

A
  • Normochromic, normocytic anemia
  • Due to reduce production of erythropoietin by kidney
  • Reduce stimulation of bone marrow -> reduce RBC production
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23
Q

Pathophysiology of mineral and bone disorder in CKD

A
  • 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
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24
Q

Management of mineral and bone disorder in CKD

A
  • 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)
25
Q

Target HbA1c in CKD patient

A

HbA1c: <=7%

26
Q

Investigation for SLE

A

> 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
27
Q

Management of SLE*

A

> 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
28
Q

Diagnostic criteria for SLE

A

○ 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
29
Q

Causes of chronic kidney disease***

A 
○ 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
30
Q

Complication of CKD***

A
  • 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)
31
Q

Investigation for CKD***

A

○ 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)

32
Q

Risk factor for nephrotic syndrome

A

> Medical
- DM, Lupus, amyloidosis

> NSAIDs

> Infection
- HIV, Hep B/C, malaria

33
Q

Indication for renal biopsy

A
  • If underlying cause cannot be ascertained from initial assessment
  • Only done by urologist
34
Q

Complication of nephrotic syndrome

A
  • Protein malnutrition
  • Hypovolemia
  • AKI
  • Thromboembolism
  • Infection
35
Q

What is dry weight

A
  • 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
36
Q

Hemodialysis vs CAPD

A

> 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
37
Q

How to follow up ACEI

A
  • 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
38
Q

What is Wilson’s disease

A
  • Inherited disorder of copper excretion with excess deposition in liver and CNS
39
Q

Signs of Wilson’s disease

A
  • CNS: tremor, dysarthria, dysphagia, dementia

- Kayser-Fleischer rings (copper in iris)

40
Q

Does Hep A cause jaundice? Investigation

A
  • Jaundice in 40-70% of patient

- Ix: AST/ ALT, Serum IgM/G anti-HAV antibodies

41
Q

Complication of liver cirrhosis*

A

> Hepatic failure

  • Coagulopathy
  • Encephalopathy
  • Hypoalbuminemia
  • Sepsis

> Portal hypertension

  • Ascites
  • Splenomegaly
  • Caput medusa

> HCC

42
Q

Classification and causes of jaundice

A

> 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
43
Q

Liver enzyme corresponding to which part of liver

A
  • Hepatocellular pattern: AST, ALT
  • Cholestatic pattern: ALP, GGT, bilirubin
  • Direct bilirubin = conjugated
44
Q

CKD fluid restriction calculation

A
  • Determine by urine output per day

- Fluid allowance = urine output + 500ml (daily loss)

45
Q

Physical signs for CKD

A 
○ 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
46
Q

Pathophysiology of hematemesis in liver cirrhosis

A
  • 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
47
Q

Indication for urgent hemodialysis

A

“AEIOU”

  • Acidosis
  • Electrolyte imbalance
  • Intoxication
  • Fluid overload
  • Uremic encephalopathy
48
Q

Genetic basis for polycystic kidney disease

A

> Autosomal dominant

  • Type 1 (85%): PKD1 gene on chromosome 16
  • Type 2: PKD2 gene on chromosome 4

> Autosomal recessive
- Chromosome 6

49
Q

Presentation for cyst infection, hemorrhage

A
  • 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
50
Q

Complication of polycystic kidney disease

A
  • Hypertension
  • Frequent UTI, cyst infection
  • Renal calculi
  • Anemia
  • Berry aneurysm
  • Progression to ESRF
51
Q

Indication for nephrectomy in PKD

A
  • Enormous kidney (resulting in discomfort and reduce QoL)
  • Recurrent infection
  • Suspected malignancy
  • Uncontrolled renal hemorrhage
52
Q

Pathogenesis for CKD-MBD

A
  • 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
53
Q

Management of CKD-MBD

A

> Reduce phosphate level

  • Phosphate restriction
  • Phosphate binders (with meal)
  • Phosphate removal through dialysis

> Calcitriol or synthetic vitamin D analogue

> Parathyroidectomy (if refractory to medical)

54
Q

How frequent perform dialysis

A

○ CAPD

  • 4 exchanges/day
  • 20-30 minutes/session

○ Automated PD
- 3 cycles/night

○ Hemodialysis

  • 4 hours
  • 3 times/week
55
Q

Complication of hemodialysis

A

> Early

  • Disequilibrium syndrome
  • Air embolism

> Late
- Dilated superficial veins due to central vein stenosis/ thrombosis

56
Q

Contraindication of hemodialysis

A
  • Absolute
    • Inability to secure vascular access
- Relative
• Difficult vascular access
• Needle phobia
• Cardiac failure
• Coagulopathy
57
Q

Mechanism of renal failure in ACE-I usage

A
  • 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
58
Q

Causes of abdominal distension

A
  • Fat
  • Fluid
  • Fetus
  • Flatus
  • Feces

Internal Medicine (12 decks)

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