Final Flashcards
(201 cards)
Cirrhosis patho
- Cells become fibrotic adn dead -> enlarge
- Vessel becomes narrow
- Pressure increase, fluid abck up
- Distension, varice formation
- Third-spacing
Causes of cirrhosis
EtOH abuse
HCV
Fatty liver disease
Child Pugh Scoring
Grade A <7
Grade B 7-9
Grade C 10-15
Clinical manifestations of cirrhosis
Jaundice
LFTs (only acutely)
Low albumin
High PT and INR (d/t low clotting factors)
Decrase in platelets
Cirrhosis complications
Ascites
Portal HTN
Variceal bleeding
Spontaneous bacterial peritonitis
Hepatic encephalopathy
Hepatorenal syndrome
Ascites presentation
Full tense bulging abdomen
Ascites dx
Abdomen ultrasound then paracentesis
Ascites treatment
MRA (aldosteorne antag; spironolactone)
Add Loops to avoid hyperkalemia (40:100 ratio for optimal diuresis
Midodrine to raise bp if needed
LVP if above no longer works (remove 4-8L QOW; give with 8g IV albumin)
TIPS if above no longer works
Portal HTN dx
SAAG (serum albumin - paracentesis albumin) > 1.1
Portal HTN treatment
If varices present on endoscopy: non-selective beta blocker (start low and then titrate until HR ~60; HOLD if SBP <90, DBP <60 or HR <50
Agents: propranolol, nadolol carvedilol (strongest bp lowering effect)
Acute variceal bleeding treatment
Supportive care (isotonic fluids, O2 PRN, PRBC PRN for goal Hgb 8g/dL)
Octreotide
EVL - choke off bleeding
Ceftriaxone (or other 3rd gen cephalosporin) 7D F SBP PPX
Non-selective beta blocker once bleed stabilizes
Spontaneous bacterial perotonitis (SBP) pathogens
Enteric gram (-): E. coli, K. pneumoniae
Gram (+): S. pneumoniae
SBP dx
Paracentesis: calculate absolute PMN count and take culture
PMN count: WBC in ascitic fluid * %PMN
Have SBP if PMN >250
SBP treatment
3rd gen cephalosporiin (ceftriaxone, cefotaxime) 5D
can do cipro if anaylactic reaction to beta-lactams
Take a repeat paracentesis 48H after ABX start, PMN didn’t drop 25% -> escalate to carbapenems
IV albumin 1.5g once then 1g/kg on day 3
Which pts should receive SBP PPX indefinetly and what agents are used
PMHx of SBP
Low ascitic protein + other risk factors
Cipro or bactrim DS
Hepatic encephalopathy presentation
Altered mental status (d/t high ammonia levels, levels do NOT correspond with severity)
Slow to respond
Eventual coma
Hepatic encephalopathy treatment
Remove precipitating factors
Dairy and vegetable protein (even though they make ammonia, these specific proteins are less likely to cross BBB than animal)
Lactulose - traps ammonia in bowel to be eliminated in stool
Rifaximin - decreases the amount of ammonia-producing bacteria in colon
Hepatorenal syndrome dx
No improvement in SCr 2D after diuretic cessation and 2D of IV alumn
Cirrhosis with ascites with a SCr increase >0.3 from baseline or 50% increase from baseline in last 7D
Hepatorenal syndrome treatment
IV NE
IV albumin 1g/kg/day
Success if in 2 weeks SCr decreases to 1.5 or returns to <0.3 above baseline
D/C therapy if in 4 days SCr remains the same or rises above treatment values
Cirrhosis PKPD changes
Decreased blood flow -> higher systemic [ ] of high first pass drugs -> decrease dose
Loss of hepatocyte function -> affects phase I metabolism (CYP) -> try to use drugs with phase II metabolism
Decreased albumin production -> more unbound drug -> more therapeutic effect -> dose decrease
Increased SCr -> decreased renal function
Increased BBB permeability -> increased therapeutic response -> decrease dose
Fat soluble vitmains
A, D, E, K
Well retained in body and stored in fatty tissue (adipose, muscles, liver)
Takes a while to reach deficiency state but more likely to cause toxicity
Water soluble vitamins
B, C
Not retained well in body (except B12, stored in liver)
Readily excreted
Vitamin A function
Vision
Immunity
Cell differentiation
Vitamin A sources
Carrots
Leafy greens
Oranges
Dairy; animal products