Therapeutics Final Spring 2Nd Year Ucsd Sspps

Front 1

Components of lipoproteins?

Back 1

Outer layer is phospholipid and apolipoproteins and XOL. the inside is XOL esters and TGs

Front 2

Percentage of blood XOL that is VLDL?

Back 2

15-20%

Front 3

How to estimate amount of VLDL?

Back 3

TG/5

Front 4

What does LPL do to VLDL?

Back 4

Removes TGs from VLDL and puts it into adipose for storage, so VLDL becomes VLDL remnants (XOL more concentrated), and becomes IDL and then LDL

Front 5

Where does LDL come from?

Back 5

VLDL becomes depleted of TGs, and more concentrated with XOL

Front 6

What is difference in apoproteins between VLDL, VLDL remnants, IDL, LDL?

Back 6

VLDL has B-100, E, and C;
VLDL remnants and IDL just have B-100 and E;
LDL just has B-100

Front 7

What is the reverse XOL transport?

Back 7

HDL picks up XOL esters from peripheral cells using LCAT (activated by cofactor A1 on HDL), and then either goes back to the liver or turns into VLDL via CETP (XOL ester transfer protein)

Front 8

What percentage of serum XOL is LDL?

Back 8

60-70%, and greater contribution to atherosclerosis.

Front 9

How much of LDL does liver remove?

Back 9

½. The other half is taken up by peripheral cells and macrophages

Front 10

What percentage of serum XOL is HDL?

Back 10

20-25%

Front 11

What happens in CETP deficiency?

Back 11

Can’t make VLDL and IDL from HDL, so HDL goes very high, and have very low incidence of CHD

Front 12

Characterisitics of chylomicrons?

Back 12

High in TGs, transport gut fats to liver

Front 13

What do apolipoproteins C-II and C-III do?

Back 13

C-II is a cofactor for LPL. C-III is a marker for high risk of atherosclerosis

Front 14

High apo B is a marker for what?

Back 14

High CHD risk (because B is on LDL and VLDL)

Front 15

What does lipoprotein A-I do?

Back 15

Activates LCAT → esterify free XOL

Front 16

Characteristics of polygenic hyperXOLemia?

Back 16

Most common lipid disorder, due to genetic and environmental factors. Has moderate LDL (130-250), and 20% have hx of premature CAD. Managed well with diet and drugs

Front 17

Characteristics of atherogenic dyslipidemia?

Back 17

Responsible for 25% of patients with a lipid disorder, TGs 150-500, low HDL (<40). Commonly have obesity, metabolic syndrome, DM. Low LPL makes TG-rich VLDL, which is exchanged for XOL

Front 18

Outward signs of FH?

Back 18

Arcus senilis, tendon xanthomas

Front 19

What is hypoalphalipoproteinemia?

Back 19

HDL<40, but no elevated TG. Rare, but higher CHD. Primary goal is decreasing LDL. Low A-1 means can’t do reverse XOL transport as well.

Front 20

What is the problem caused by inflammation in atherosclerotic patient?

Back 20

Inflammation, among other things, can weaken atherosclerotic plaques

Front 21

Basic steps in plaque formation?

Back 21

LDL accumulates in intimal space. Oxidized LDL, macrophage ingestion, foam cells, fatty streak, collagen synthesis, lesions stronger

Front 22

What change in blood XOL corresponds with what % increase risk of CHD?

Back 22

1% more XOL means 1-2% higher risk of CHD

Front 23

Incidence of CHD in women compared to men?

Back 23

Lower in women up to menopause, then equal or increased

Front 24

What did ASTEROID study show?

Back 24

March 2006, JAMA, showed statins can shrink and stabilize plaques

Front 25

How do statins shrink plaques?

Back 25

Decrease lipid component and increase fibrous component, so less chance of rupture

Front 26

Effect of lower LDL on vascular function?

Back 26

Reverse endothelial damage, so more NOS function, and better vasodilation

Front 27

What does CRP indicate?

Back 27

c-reactive protein is a measure of inflammation in atherosclerosis

Front 28

How often should check lipid profile in adults >20yo?

Back 28

Every 5 years according to the NCEP ATP III

Front 29

Classifications of LDL levels?

Back 29

Optimal is <100, near optimal is ≤129, borderline is ≤159, high is ≤189, very high is ≥190

Front 30

What are the classsifications of total XOL?

Back 30

Desirable is <200, borderline is <240, high is ≥240

Front 31

Classifications for HDL levels?

Back 31

Low is <40. High is ≥60

Front 32

List the 5 major risk factors defined by ATP III guidelines?

Back 32

(1) Smoking
(2) HTN, which means on anti-HTN meds or BP >140/90)
(3) low HDL (<40)
(4) Family hx of CHD (if male, 1st degree relative <55, female <65)
(5) Age (men ≥45, women ≥55)

Front 33

What is significance of metabolic syndrome in lipid disorders?

Back 33

It is equivalent to CHD as a risk factor

Front 34

What is significance of DM in lipid disorders?

Back 34

It is equivalent to CHD as a risk factor

Front 35

LDL goal for ATP risk factors?

Back 35

If CHD or equivalent (DM or metabolic syndrome), then goal is <100, but 70 is better. If 2+ risk factors, goal is <130. If zero or 1 risk factors, then goal is <160.

Front 36

What is significance of HDL as risk factor in lipid disorders?

Back 36

If high HDL (>60), it is a negative risk factor

Front 37

What ATP III categories correspond to what % chance of Coronary event in the next 10 years?

Back 37

CHD or equivalent is a 20% risk.

2+ risk factors is ≤20% risk of heart event

0-1 risk factor is <10% risk of event in the next 10 years

Front 38

What scoring system is most accurate for calculating risk of cardiac event?

Back 38

Framingham risk scores. The system calculates a 10yr % risk based on points for age, gender, total XOL, HDL, smoking status, and systolic BP.

Front 39

What are categories of TG levels?

Back 39

Normal is <150. Borderline is <200. High is <500. Very high is ≥500

Front 40

TGs as a risk factor?

Back 40

High TGs is a risk factor for CHD

Front 41

Diagnosis of metabolic syndrome?

Back 41

3 or more of:
waist circumference >40in (men), >35in (women).
TGs ≥150,
HDL <40 (men), <50 (women),
BP ≥130/85
fasting glucose ≥110

Front 42

Causes of secondary dyslipidemia?

Back 42

DM, hypothyroid, obstructive liver disease, chronic renal failure, drugs (progestins, anabolic steroids, corticosteroids, cyclosporins, sirolimus, beta-blockers, protease inhibitors, thiazides, isotretinoin, mirtazapine).

Front 43

Effect of EtOH on lipids?

Back 43

Increase TGs and HDL

Front 44

appropriate medical hx and procedures to assess lipid patient?

Back 44

Look for atherosclerosis (if in one artery, probably in many or all), hx of MI, angina, stroke. Do treadmill for ischemia on ECG, exercise thallium, electron beam CT to look for Ca buildup, carotid bruit or stenosis>50%, AAA (abdominal aortic aneurysm), DM

Front 45

Gemfibrozil interaction with statins?

Back 45

Increase statins 2-4 times (except for Flu)

Front 46

When to consider lifestyle changes versus drug treatment for high lipids?

Back 46

For each risk category, initiate drug therapy if 30 LDL points above goal (e.g. CHD or equivalent goal is <100, but if ≥130, use drug therapy. If 100-129, try TLC first)

Front 47

4 main TLCs for lowering lipids?

Back 47

Low sat fat in diet, increase physical activity, weight reduction, smoking cessation

Front 48

What fats should replace saturated fats in the TLC diet?

Back 48

Monounsaturated (canola, olive oil, avocados), and Omega-3

Front 49

What is unique about the mediterranean diet?

Back 49

Daily physical activity

Front 50

Key food choices in the TLC diet?

Back 50

Lean meat, grill or broil, smaller portion. Skim or 1% milk, butter-substitutes, low-fat soft cheese instead of hard cheese, frozen yogurt instead of ice cream, avoid sauce, cream, and fatty foods

Front 51

What effect does viscous fiber, soluble fiber, and plant sterols have on XOL?

Back 51

Can lower LDL 5-15% by decreasing absorption of XOL in the gut

Front 52

Examples of foods and products that have plant sterols for reducing LDL?

Back 52

Benecol spreads (1.7g), Avocado, soybeans, chickpeas, almonds, corn oil, olive oil (from 132 to 30mg)

Front 53

How do stanols and sterols decrease XOL absorption?

Back 53

By competing with XOL for incorporation into mixed micelles, but are absorbed much less. So, with less being absorbed, LDL receptors are upregulated. Benecol (sterols) lowers XOL 10-15% even in patients already taking statins

Front 54

Steps in TLC treatment for lipid patient?

Back 54

Begin lifestyle changes (reduce sat fat, increase physical activity), after 6 weeks assess XOL intensify therapy (reinforce low fat diet, add sterols/stanols, increase fiber intake), then after six weeks if goal not achieved, consider drug treatment (treat for metabolic syndrome, increase weight management and physical activity), and then reassess every 4-6 months

Front 55

Goal for rate of weight loss in TLC?

Back 55

10% over 6 months

Front 56

Goal for BMI?

Back 56

18.5-24.9

Front 57

Desired waist circumference in TLC?

Back 57

<40 males, <35 females

Front 58

What are the Statins in order of potency for decreasing LDL?

Back 58

generic: Rosu, Ator, Sim, Lo, Pra, Flu
brand: crestor, lipitor, zocor, mevacor, pravachol, lescol

Front 59

Which dosing level gives biggest bang for the buck in statins?

Back 59

Lowest dose

Front 60

Which statins do not necessarily need to be taken at night?

Back 60

Rosu and Ator (they are the most potent and also have the longest half-lives)

Front 61

Adverse effects of statins?

Back 61

HA, GI (pain, constipation, dyspepsia), Myalgia, increase LFTs, and rarely rhabdomyelysis, myoglobinuria, acute tubular necrosis (more with higher doses)

Front 62

Which statins interact CYPs?

Back 62

3 interact with 3A4: Ator, Lo, Sim.

2 interact with 2C9: Flu (and Rosu slightly)

Pra is the only one of the six we learned that doesn't inhibit CYPs

Front 63

Examples of drugs that inhibit 3A4 (so can be a problem with Ator, Lo, Sim)?

Back 63

Clarithromycin, erythromycin, diltiazem, verapamil, felodipine, ketoconazole, miconazole, ritonavir, Nefazodone, Alprazolam, Midazolam, Triazolam, Cyclosporine, Estradiol, Loratidine, Terfenadine

Front 64

Examples of drugs that inhibit 2C9 (so can be a problem with Flu and Rosu)?

Back 64

Alprenolol, Diclofenac, Hexabarbital, Tolbutamide, Warfarin. Especially look out for warfarin and Flu

Front 65

Which statins cannot be used with warfarin?

Back 65

Flu and Rosu (2C9 interaction)

Front 66

Statins in the elderly?

Back 66

Should have smaller dose due to smaller frame, less renal function, and multiple medications

Front 67

Which statin is okay to take with Warfarin?

Back 67

Pravastatin (not metabolized). Flu and Rosu can be a problem with warfarin due to CYP2C9 inhibition

Front 68

Effect of bile acid resins on lipid profile?

Back 68

Decrease LDL 15-27%, and increase VLDL, TGs from liver by 3-10%

Front 69

Bile acid resins on the market?

Back 69

Cholestyramine (Questran)
Colestipol (oderless, tasteless powder or tablets)
Colesevelam ("Welchol" tablets, best tolerated)

Front 70

Bile acid resins adverse effects? How to minimize them?

Back 70

Decreased fat soluble vitamins absorption, GI (bloating, constipation, flatulence, epigastric fullness, nausea).

Reduce effects by Increasing fluid and fiber intake, mix in juice, minimize air entrapment (use straw), educate patient. Tablet better than powder

Front 71

Drug drug interactions with Bile acid resins?

Back 71

Older BARs interfere with absorption of dig, warfarin, b-blockers, HCTZ, thyroxine, iron, nicotinic acid, loperamide, and other ionic drugs. However, Colesevelam (Welchol) appears to be okay

Front 72

How does Ezetimibe work? Effectiveness?

Back 72

Block XOL absorption in the gut. Even though it increases XOL synthesis 90%, circulating LDL decreases about 20%. Comes in only one strength, once daily 10mg tab which can lower LDL 18-22%, with no effect on HDL or TGs. Is combined with simvastatin in Vytorin as 10/10, 10/20, 10/40, 10/80

Front 73

Adverse effects of Ezetimibe?

Back 73

Diarrhea, cough, fatigue, arthralgias

Front 74

What is Niacin, and what is the effect on the lipid profile?

Back 74

Vitamin B3, lowers LDL 15-30%, increases HDL 20-35%, decreases TGs 30-60%, and decreases Lp(a) 30%

Front 75

What is the only drug that can lower Lp(a)?

Back 75

Niacin

Front 76

Adverse effects of Niacin?

Back 76

Flushing is the major one, bit occurs more with immediate release (OTC). Sustained release (OTC) has less flushing, but has increased risk of liver tox. Extended release (Rx) has nice balance with less flushing and less liver tox

Front 77

Difference in Niacin products in lowering lipids?

Back 77

ER (Rx) and IR (OTC) lower XOL same. But, IR lowers TGs and increases HDL more than ER.

Front 78

Two pathways for metabolism of niacin that explains adverse effects?

Back 78

Pathway I is high affinity but low capacity, and leads to Nicotinamide which causes liver tox.
Pathway II is high capacity, leads to nicotinuric acid which causes flushing.
Slowing the release (Rx ER formulation) helps to balance the two pathways, so less of each effect. The liver tox is reversible

Front 79

Pt education for Niacin?

Back 79

To prevent flushinf, take with food, aspirin 30 minutes before morning dose. For Niaspan, give dose before bed.

Front 80

Side effects of Niacin besides flushing and liver tox?

Back 80

GI upset (nausea, activate peptic ulcer, dyspepsia), transient increase in glucose levels (bad for DM), darkening of skin

Front 81

Effect of fibric acid derivatives on lipid profile?

Back 81

Decrease LDL 10-25%, increase HDL 10-30%, decrease TGs 30-60%

Front 82

Examples of fibrates?

Back 82

Gemfibrozil (Lopid), Fenofibrate (Tricor), Clofibrate (Atromid S)

Front 83

How do Fibrates work?

Back 83

Activated PPAR-alpha (peroxisome proliferator activated receptors, and nuclear hormone receptor) to increase A-I, A-II (apoproteins for HDL), which increases HDL. It also decreases C-III, which decreases VLDL. It also increases LPL to increase lipolysis. So, catabolize TG-particles and decrease VLDL secretion

Front 84

ADRs of fibrates?

Back 84

Well-tolerated, but can cause mild GI symptoms, muscle pain, weakness (do not use with statins), cholelithiasis (due to increased bile output). Fenofibrate can cause rash (2-4%)

Front 85

Safety of fibrates?

Back 85

Clofibrate and Gemfibrozil decrease MIs, but same or increase in overall mortality. There is not data for fenofibrate

Front 86

Possible combination therapies for lowering LDL?

Back 86

Stain + ezetimibe (vytorin);
statin + BAR;
statin + Niacin + BAR (decrease LDL 45-61%).

Front 87

What is Vytorin?

Back 87

Simvastatin + Ezetimibe

Front 88

What is Advicor?

Back 88

ER Niacin (Niaspan) + lovastatin

Front 89

What is Caduet?

Back 89

Atorvastatin + amlodipine (Ca channel blocker)

Front 90

What is Pravigard PAC?

Back 90

Pravastatin + ASA

Front 91

Effect of omega-3s on lipids?

Back 91

Lowers TGs 30-60%

Front 92

Estrogen for lipid disorders?

Back 92

Can lower LDL and increase HDL, but no change in CHD death, but actually increases CHD events and death at first, then possibly some improvement after 4-5yrs

Front 93

Considerations for treating lipids in elderly?

Back 93

They benefit more than young persons do from decreased LDL. But, elderly are more prone to ADRs due to differences in body composition, renal function, other physiological changes. Start low doses, titrate up

Front 94

Considerations for treating lipids in women?

Back 94

HDL a better indicator of CHD risk. During pregnancy, XOL and TGs increase, but there is no need for Rx. If high risk, condider BARs. Statins are contraindicated in pregnancy (and liver disease)

Front 95

Considerations for treating lipids in children?

Back 95

Drug therapy not until 10yo

Front 96

Which niacin product should never be used for lowering TGs? Why?

Back 96

Sustained release (OTC) due to liver tox at doses necessary for TG lowering

Front 97

Max dose for niacin?

Back 97

2g for ER, 3g for IR

Front 98

Titration schedule for Niacin?

Back 98

For IR, start at 125mgBID, and every week increase to 250, 500, 500, 1000, 1500 (max 3g). For ER, every 4 weeks increase from 500 to 1000 to 1500 if tolerated. Take QHS with food (max 2 g daily)

Front 99

Endocrine function of kidney?

Back 99

Renin, PGs, kinins, eythropoietin

Front 100

Metabolic activities of kidney?

Back 100

Insulin and glucagon metabolism, Acvitates vit D3

Front 101

Excretory function of kidney?

Back 101

Glomerular filtration, tubular secretion and reabsorption

Front 102

Homeostatic function of kidney?

Back 102

Removes waste, maintains fluid and lyte and acid/base balance, regulates BP

Front 103

Major events in PT of nephron?

Back 103

70% reabsorption of filtered load (AA, glucose, HCO3, water)

Front 104

Major events in LOH of nephron?

Back 104

Reabsorption of K, Mg, Ca, and mainenance of osmotic gradient

Front 105

Major events in DT of nephron?

Back 105

Reabsorption of water, HCO3, secretion of K and H

Front 106

Appearance of abnormal urine?

Back 106

Cloudy, foamy, turbid, or any change in color

Front 107

What can cause acidic urine?

Back 107

Ammonium, ascorbic acid, acetic acid bladder irrigation, cranberry juice, DKA

reference range for urine pH is 5-8

Front 108

What can cause alkaline urine?

Back 108

Acetazolamide, bicarb, thiazide, citrate and acetate salts, UTI

reference range for urine pH is 5-8

Front 109

What does leukocytes in the urine mean?

Back 109

UTI or urethritis

Front 110

What does RBCs in urine mean?

Back 110

Infection, coagulopathies, glomerulonephritis, necrosis, tumors, renal stones

Front 111

What do hyaline casts in urine indicate?

Back 111

Dehydration, strenuous exercise, fever, proteinuria, CHF

Front 112

What does cellular casts in urine indicate?

Back 112

Intrinsic kidney disease (can be from WBC, RBCs, tubular cells

Front 113

What do waxy/granular casts in urine mean?

Back 113

Not pathogenic

Front 114

Relationship between urea clearance and BUN?

Back 114

If urea clearance decreases, BUN will increase, and vice versa. However, BUN can rise and fall with dietary changes and high catabolic rate, without affecting urea clearance

Front 115

BUN/Scre ratio?

Back 115

Normally 10:1 – 15:1, but can initially rise to >20:1 in acute renal failure

Front 116

List of medications that are associated with elevated Scre? KNOW THIS LIST!

Back 116

ACEIs, Acyclovir, AMGs, amphotericin B, Cephalosporins, Cisplatin, cyclosporins, dextran, foscarnet, mannitol, NSAIDS, pentamidine, rifampin, tacrolimus, tetracycline, vanco

Front 117

Why is CrCl not a good measure of GFR in renal impairment?

Back 117

With decreased filtration, the secretory component of CrCl is a bigger fraction of the total (which is normally about 10%, but may increase to 100% due to nephron hypertrophy in renal insufficiency), so it greatly overestimates renal function

Front 118

Factors that can affect variability in CrCl (but not necessarily GFR)?

Back 118

Age, weight, gender, exercise, diet (protein), diurnal variation, elderly, malnourished, children

Front 119

What things can affect Scre, but not CrCl?

Back 119

Vigorous prolonged exercise, muscle wasting, muscle growth.

Front 120

What weight should be used in Cockcroft-Gault calcualtion?

Back 120

Ideal body weight

The equation is (140-age)(kg wt)/(72*plasma creatinine)

If female pt, multiply result by 0.85

Front 121

3 classifications of azotemia?

Back 121

Pre-renal, renal, or post-renal

Front 122

Difference between azotemia and uremia?

Back 122

Azotemia is high nitrogenous stuff in blood. Uremia is a syndrome with sxs of N/V, mental status change

Front 123

What is pre-renal azotemia?

Back 123

Rapidly revesible form caused by decreased perfusion. Responsible for 50% of ARF cases. Nephrons functionally intact. It occurs from anything that has low blood flow or volume. But, it can also be from hypercalcemia, which can constrict afferent arteriole. It can also happen from vascular thrombus or medications like ACEIs, cyclosporine, NSAIDS, osmotic diuretics, catecholamines

Front 124

What is intra-renal (or renal) azotemia?

Back 124

Actual damage to nephrons. In ICU, usually from acute tubular necrosis, which occurs from prolonged hypoperfusion to kidney (so it can result from untreated pre-renal azotemia). Also, nephrotoxic substances can cause it.

Front 125

What are some endogenous toxins that can cause intra-renal azotemia?

Back 125

Myoglobin, hemoglobin, uric acid, Ca-Phos compounds.

Front 126

What are some exogenous toxins (drugs) that can cause intra-renal azotemia?

Back 126

AMGs, penecillins, cephalosporins, acyclovir, ampho B, cisplatin, methotrexate, cipro, IV dyes

Front 127

Miscellaneous causes of intra-renal azotemia?

Back 127

Inflammation from acute glomerulonephritis, pyelonephritis, infection, tumors, myeloma

Front 128

What is post-renal azotemia?

Back 128

Reversible form resulting from any obstruction to urine flow. It is uncommon (<10% of renal failure cases). It can be caused by BPH, malignancy, urethral stricture, ureteral obstruction, trauma, spinal cord dysfunction

Front 129

What are the phases of acute renal failure?

Back 129

(1) insult to oliguria or nonoliguria, (2) diuretic phase, (3) recovery phase

Front 130

What is the insult to oliguria phase of acute renal failure?

Back 130

Oliguria, lasts 8-14 days, seen often with ischemic acute tubular necrosis, and has higher mortality/morbidity than nonoliguric insult

Front 131

What is the insult to nonoliguric phase of renal failure?

Back 131

Normal urine flow (>400ml.day), with elevated BUN/Cr. Lasts 5-8 days with high urine output, but high serum Na and K. seen most often with nephrotoxic acute tubular necrosis (as opposed to ischemic ATN). It has a better prognosis that oliguric insult

Front 132

What is the diuretic phase of acute renal failure?

Back 132

Urine output of >400ml.day, lasts 2-8 days, lab values stop rising and stabilize. If pt gets RRT, may not see diuresis phase

Front 133

What is the recovery phase of acute renal failure?

Back 133

Lasts 3-12 months, labs first stabilize then return to normal, 15% of pts have residual renal insufficiency and 5% will require RRT

Front 134

Clinical signs of acute renal failure?

Back 134

Fluid retention, Gi bleeding, confusion, seizures, coma

Front 135

How to treat acute renal failure?

Back 135

Remove nephrotoxic agent, start diuretics, hydrate (increase perfusion and decrease tubular workload)

Front 136

How to manage and monitor acute renal failure?

Back 136

Dialysis, renal imaging, renal biopsy

Front 137

how to manage post renal transplant with ATN?

Back 137

d/c tacrolimus and start thymoglobulin, renally adjust all meds, give NS boluses, lasix, renal ultrasound, biopsy

Front 138

When do dialysis in acute renal failure?

Back 138

AEIOU:
Acidosis
Electrolytes (hyperkalemia)
Intoxication/overdose
Overload (fluid)
Uremia or azotemia (BUN>100 or Cr>2 or rise more than 1 in 24 hrs.

Front 139

What is chronic renal failure?

Back 139

Progressive deterioration of kidney function leading to uremia, occurs slowly, and is IRREVERSIBLE.

Front 140

Most common causes of chronic renal failure?

Back 140

un- or under-treated HTN, and/or DM, especially type I.

Front 141

What are characteristics of stage I chronic renal failure?

Back 141

Renal function decreased 40-60%, asymptomatic, with exocrine and regulatory function intact. Creatinine elevates to twice normal.

Front 142

What amount of kidney function must be lost before s/s manifest?

Back 142

60%. Although serum Cr starts to rise before this

Front 143

Characterisitics of stage II chronic renal failure?

Back 143

Renal function is 20-40% of normal, incerased BUN/Cr, with polyuria, nocturia, anemia. Creatinine rises to 4x normal, and hormone secretion starts to decline

Front 144

Characteristics of stage III chronic renal failure?

Back 144

aka ESRD. Renal function is <15%, excretory, regulatory, and hormonal functions are severely impaired, creatinine is >10, can’t keep homeostasis, uremia develops affecting all body symptoms

Front 145

Clinical CNS manifestations of chronic renal failure?

Back 145

Fatigue, malaise, HA, drowsiness, dementia, insomnia, stupor, coma

Front 146

Clinical CV manifestations of chronic renal failure?

Back 146

Edema, lyte imbalance, HTN, hypotension, pericarditis, atheromatosis, cardiomyopathy

Front 147

Clinical GI manifestations of chronic renal failure?

Back 147

N/V, gastritis, anorexia, GI ulcers, Gi bleeding, stomatitis, pancreatitis

Front 148

Miscellaneous clinical manifestations of chronic renal failure?

Back 148

Anemia, oliguria/anuria, muscle twitches, cramps, bone disease, thirst, yellow skin, pruritis, poor wound healing, sleep disorders, decreased libido, impotence

Front 149

Major risk factors for developing CRF?

Back 149

DM, BP, dyslipidemia, smoking, anemia, Ca and Phos

Front 150

How manage HTN and CRF in diabetes?

Back 150

Reduce BP to <130/80, use multiple HTN drugs, minimize proteinuria, LDL<70, HgbA1C<7%, modest dietary protein restriction (0.8-1g/kg/day), low salt (<2g/day), stop smoking

Front 151

How manage hyperkalemia (a major risk factor for developing CRF)?

Back 151

-Calcium gluconate IV (protect heart from high K),
-Glucose and insulin (activates Na/K ATPase),
-NaHCO3 (shift K into cells),
-Na polystyrene sulfonate (SPS), to exchange Na for K, po or pr.
-Dialysis

Front 152

How to manage Ca and Phos imbalace (a major risk factor for developing CRF)?

Back 152

Caused by decreased Vit D activation in kidney, and high phos due to low GFR and high PTH resistance in bone. Give aluminum antacids, Ca salts, Sevelamer, Calcitriol (1,25-dihyroxy-vitD3) 0.25mf/day, ergocalciferol (activated ergosterol, vit D2) at 500mcg/day

Front 153

How to treat anemia (a major risk factor for developing CRF)?

Back 153

Epo 50-100U/kg TIW IV or SQ. goal is Hct of 30-35%. Can also do blood transfusion, iron, and folate

Front 154

Common sxs of acute viral hepatitis?

Back 154

Myalgia, N/V, fatigue and malaise, change in smell and taste, right upper abdominal pain, coryza (cold), photophobia, HA, diarrhea (may have pale stool and dark urine)

Front 155

AST or ALT more specific for liver?

Back 155

ALT

Front 156

Chronic hepatitis is asssociated with what major risks within 5 years of infection?

Back 156

There is a 5 yr risk of hepatic decompensation (ascities, jaundice, variceal bleeding)

Front 157

Incubation of hep A?

Back 157

14-45 days, average 30 days.

hep B is 45-180 days
hep C is 2-26 weeks (as short as hep A and as long as hep B)

Front 158

Complications of hepatitis A?

Back 158

Fulminant hepatitis, cholestatic hepatitis, relapse, anicteric jaundice in kids, and icteric jaundice in adults. Almost all have chronic sequelae

Front 159

Risk factors for hep A outbreak?

Back 159

-usually occurs in context of community outbreaks associated with poor sanitation
-infection common from person to person in same household (which is facilitated by asymptomatic infection in kids)
-in 40-50% of cases, not risk factor is identifiable

Front 160

HAV clinical presentation?

Back 160

-preicteric: flu-like sxs
-abrupt onset of anorexia, N/V, right upper quadrant pain, and flu-like sxs
-Icteric hepatitis accompanied by dark urine, acholic (light colored) stools, worse systemic sxs, and pruritus.

PE: icteric sclera, skin, and secretions, mild wt loss, hepatomegaly

Lab:
-positive IgM anti-HAV, mildly high bili, gamma-globulins, ALT, AST (twice normal).
-If cholestatic disease, alk phos, GGT, and total bili rise

Front 161

When in sequence of hep A infection are each of the following most prominent? IgM, ALT, viremia, HAV in stool, IgG, symptoms?

Back 161

Viremia and HAV in stool in weeks 1-5.
ALT and IgM high in weeks 4-6.
IgG rises throughout the illness and beyond (at least 13 weeks).
Sxs are in weeks 2-8.

Front 162

Treatment for hep A?

Back 162

Supportive (usually self-limiting, diet, rest, fluid, avoid alcohol, hepatotoxic drugs). Post-vaccination and IG 0.02ml/kg IM once within 14 days, 85% effective

Front 163

How to prevent hep A?

Back 163

-Avoid tap water when traveling internationally,
-practice good hygeine,
-hep A vaccine,
-immune globulin (pre- and post-exposure. For short travel, 0.02ml/kg IM once. For long travel or continued exposure without vaccination (such as in household members), 0.06ml/kg IM Q 5 months

Front 164

Indications for hepA IG?

Back 164

Foreign travel to highly endemic areas, or post-exposure

Front 165

Indications for hep A vaccine?

Back 165

Anyone >2 yo in highly endemic areas, travelers to endemic areas, MSM, illegal drug users, occupational exposure, blood product recipients, chronic liver disease

Front 166

Important lab tests to diagnose hep B infection?

Back 166

Bilirubin, AST, ALT, alk phos, PT, albumin, serum globulin, CBC, coagulation

Front 167

Cancer and hep B?

Back 167

Liver cancer common in areas of the world where hep B is common

Front 168

How common is symptomatic manifestation of acute hep B infection? Fulminant?

Back 168

30% syptomatic. 70% are asymptomatic, with fulminant consisting of 0.1-0.5%.

Front 169

Percentage of hep B infections that becomes chronic?

Back 169

5-10% (defined as lasting more than 6 mos)

15-40% of those cause liver failure

Front 170

Of hep-B-caused chronic infectious cases, how many lead to liver failure?

Back 170

15-40%

but only 5-10% of hep B infections turn chronic (last more than 6 mos)

Front 171

Relative ease of transmission of HBV, HCV, and HIV in IV drug use, sexual contact, perinatal, and occupational exposure?

Back 171

HBV is most easily transmitted in each case except IV drug use, in which HCV is slightly more easily transmitted.

Front 172

What is the most common way to get infected with HBV, HCV, or HIV in the U.S.?

Back 172

Through contact with body fluids and blood

Front 173

Steps taken to prevent hep B?

Back 173

Vaccination, management of HBaAg+ patients (test all family members, vaccinate, test sex partner after hep B sequence for antibodies, educate family members)

Front 174

Difference in serology between acute Hep B with recovery and progression from acute to chronic hep B?

Back 174

In both cases, antiHBc IgM goes up then down over about 8 months, and total HBc goes up and stays up. However, in recovery, HBe and Hbs go away within 3 & 6 months (respectively), followed by appearance of anti-HBe and anti-HBs. But in chronic, HBe stays around a long time, until anti-HBe shows up maybe years later.

Front 175

Which HBV genotype is most common is N. America? SouthEast Asia?

Back 175

GT-A in america (A for America)
GT-B and C most common is SouthEast Asia

Front 176

Which HBV genotype is most associated with positive outcome? With necroinflammation and hepatoma?

Back 176

GT-A has best outcome. GT-C has highest necroinflammation and hepatoma (HCC) in older patients

Front 177

Which HBV genotype responds best to interferon?

Back 177

GT-B better than GT-C

Front 178

What stage of hepB infection is likely if HBsAg is positive?

Back 178

Acute or chronic or carrier hep B. (but not in past exposure or immunized)

Front 179

What stage of hepB infection is likely if positive anti-HBsAg?

Back 179

Past exposure (not acute, since not enough time to make it)

Front 180

What stage of hepB infection is likely if positive for HBeAg?

Back 180

Acute or chronic hep B (same reasoning as HBs). Not from immunization or past exposure

Front 181

What stage of hepB infection is likely if positive for anti-HBcAg?

Back 181

Acute or chronic or carrier or past exposures, but not immunization (vaccine doesn’t give HBc)

Front 182

What stage of hepB infection is likely if positive for IgM anti-HBcAg?

Back 182

Acute infection. It rises and falls within 6 months or so after infection. But total anti-HBc will be present in either acute infection or past exposures, but not from vaccination

Front 183

What stage of hepB infection is likely if positive for HBV DNA?

Back 183

Acute and possibly chronic and carrier. But not from past exposure or vaccination

Front 184

What stage of hepB infection is likely if ALT is elevated?

Back 184

Acute and chronic infection, but not past exposure or vaccination

Front 185

What lab tests increase/decrease in liver disease?

Back 185

Increased ALT, AST, bili, PT. decreased albumin. Liver histology and ultrasound can also be used to identify disease stage and grade, and tumors/cirrhosis

Front 186

Goals of chronic Hep B treatment?

Back 186

Sustained suppression of HBV replication and remission of liver disease. Want normal ALT, negative HBV DNA, loss of HBeAG +/- anti Hbe, improvement in liver histology, loss of HBsAG+/- HBsAG

Front 187

Dosing for chronic hepB IG?

Back 187

For post exposure prophylaxis. 0.06ml/kg IM, or 0.5ml for <12mo of age

Front 188

Definition of HBV response to therapy?

Back 188

Reduction in inflammation and fibrosis on biopsy, normal ALT, suppressed HBV DNA, disappearance of HBe and appearance of anti-HBe. Especially important to monitor ALT and HBV DNA

Front 189

IFN treatment for Hep B?

Back 189

subQ for 16 weeks. Then watch for seroconversion to HBe- or anti-HBe.
Has significant side effects and high cost, but no risk of resisitance. 90% normalization of LFTs, 25-40% loss of HBe and HBV DNA at 6 months. Maintains response for 2-11 years. Better response in women, adults, HIV negative, symptomatic acute infection, high ALT. can cause decompensation in cirrhotic pts

Front 190

Lamivudine for hep B treatment?

Back 190

Oral for 12 months. needs renal dose adjustment in renal insufficiency. Has high risk of resistance to YMDD mutant. Lamivudine is also used in HIV, but at a much higher dose. A prodrug, a nucleoside analogue (like entecavir), must be triphophorylated to be active. Directly inhibits viral replication.

Front 191

Adefovir treatment for heb B?

Back 191

Oral daily for 12 months. needs renal dose adjustment in renal pts. Has low incidence (2-3% at 2 years) of resistance. A nucleotide analogue also a prodrug. Active against wild type and YMDD mutant.

Front 192

Entecavir for hep B treatment?

Back 192

Oral for 12 months, needs renal adjustment (QOD for 20-48ml/min or q72h for 10-19ml/min, or even q weekly if on dialysis). Best histological improvement, but also most expensive. Nucleoside analogue (like lamivudine), triphosphorylated to be active. Not active against HIV, directly inhibits viral replication.

Front 193

Lamivudine resistance?

Back 193

YMDD mutant is less virulent than wild-type, and occure 14-32% after 1 year, or up to 50% after 3 years. Test for elevated LFTs and HBV DNA. If needed, start adefovir and then d/c lamivudine when HBV DNA goes down

Front 194

Adverse effects of entecavir?

Back 194

HA, insomnia, N/V, NASH, lactic acidosis and severe hepatomegaly with steatosis

Entecavir provides best histological improvement, but also most expensive. Nucleoside analogue (like lamivudine), triphosphorylated to be active. Not active against HIV, directly inhibits viral replication.

Front 195

How is response to hep C treament defined?

Back 195

Liver enzymes (ALT), histology (biopsy), virology (HCV load), and SVR (sustained virologic response) 24 weeks after treatment cessation. EVR (early virologic response) is considered a negative HCV RNA or 2-log drop at week 12-24. If this doesn’t happen, then continued treatment has 97% failure rate, so reponse at 12 weeks predicts longterm response

Front 196

Which hep C genotype is most common is U.S.?

Back 196

Type 1 by far (75%), which is also the most difficult to treat.

Front 197

difference between protectiveness of antibodies in HCV and HBV?

Back 197

Anti-HCV is not protective in hep C like anti-HBV is in hep B

Front 198

Interferon treatment for hep C?

Back 198

Mechanism unclear (maybe immunomodulatory) give 50% initial dose, or gradual titration. d/c if intolerable side effects. Give TIW or pegylated once weekly

Front 199

How is treatment for hep C based on hep C genotype?

Back 199

If genotype 1, treat with IFN and ribavirin for one year. If genotype 2, treat with IFN and ribavirin for 6 months

Front 200

For treating genotype 1 hep C, what does the algorithm say should be done at any time starting at week 12, all the way up to 24 months post treatment, if HCV RNA is detected?

Back 200

At week 12, if RNA hasn’t dropped at least 2 log units, or if at any other time after that, RNA is detectable, the algorithm says to stop therapy, follow clinically, enroll in clinical trial, consider alternative therapies, or consider maintenance pegylated IFN monotherapy if advanced fibrosis

Front 201

For treating genotype 1 hep C, when does the algorithm say HCV RNA should be tested, and what is dose of ribavirin?

Back 201

Dose of ribavirin is 1000mg or 1200mg daily if <75kg or >75kg. Check HCV RNA at 12 weeks on therapy, 24 weeks, 48 weeks (end of therapy), and 24 weeks post-therapy. Only continue therapy if RNA is undetectable (or has dropped more than 2 log units after first 12 weeks).

Front 202

Algorithm for IFN and ribavirin treatment for genotype 2 or 3 hep C infection?

Back 202

Pegylated or standard IFN and ribavirin 800mg for 24 weeks. Check RNA at end of therapy and 24 weeks post-treatment. In either case, if RNA is detectable, follow clinically, enroll in clinical trial, consider alternative treatments, or consider maintenance IFN monotherapy if advanced fibrosis

Front 203

Indications for hep C treatment?

Back 203

≥18yo, high ALT, significant hepatitis with fibrosis, compensated liver disease (no ascites or encephalopathy), prior treatment for HCV, hx of depression, but controlled.

Front 204

Contraindications for hep C treatment?

Back 204

Major, uncontrolled depression (IFN-induced), renal, heart, or lung transplant recipient, automimmune hepatitis, untreated hyperthyroidism (IFN can mess up thyroid function), pregnancy, or no contraception use, severe co-morbidity, <3yo, hypersensitivity to HCV drugs..

Front 205

Key side effects of interferon?

Back 205

Flu-like and depression, MANY others

Front 206

Adverse effects of lamivudine treatment?

Back 206

Rash, insomnia, HA, N/V, pancreatitis, peripheral neuropathy, rare non-alcoholic steatic hepatitis (NASH) with nucleoside analogues

Front 207

Adverse effects of adefovir?

Back 207

N/D, flatulence, abd pain, HA, neuropathy, asthenia, nephrotoxic (fanconi type picture increase Cr, PO4). Beware of hepatic flares, renal tox, HIV resisitance, lactic acidosis

Front 208

How know when not to treat Hep B?

Back 208

Don’t treat acute. Wait and see. In chronic and carrier, HBs is positive for more than 6 months. But, if HBe is negative and HBV DNA is negative, then pt is carrier, and there is not need for therapy.

Front 209

How to establish whether hep B pt has gone from acute to chronic (and not carrier) status? And what to evaluate next?

Back 209

Chronic and carriers are HBs positive. But, if also HBe positive and HBV DNA positive, then it is a chronic case, and must see if ALT is >200 and if DNA is <200. If yes, treat with IFN x16 weeks. If not, then treat with lamivudine or entecavir. And in both cases, monitor seroconversion from HBe to anti-HBe. If stay or become DNA positive, consider adefovir, tenofovir, or investigational drugs.

Front 210

If chronic hep B pt has received IFN or lamivudine therapy, and assessment of seroconversion from HBe to anti-HBe has been made, what steps are next in the treatment algorithm?

Back 210

If conversion hasn’t happened, continue therapy maybe indefinitely or consider lamivudine or entecavir. If seroconversion has occurred, stop therapy and continue to monitor.

Front 211

% of exposed hep C pts that resolve after acute phase?

Back 211

25%.

75% turn into chronic infection (0f which 80% become stable, and 20% get cirrhosis)

Front 212

% of chronic hep C cases that become stable (as opposed to cirrhotic)?

Back 212

80% (of the 75% of cases of HCV that become chronic. The other 25% resolve after acute infection).

Front 213

% of hep-C cirrhotic pts that disease progresses slowly?

Back 213

75%.

So, it starts with infection. 75% of those turn chronic. 20% of those develop cirrhosis. And in 75% of those, the disease develops slowly while the other 25% go quickly into liver failure and death (usually facilitated by alcohol and/or HIV)

Front 214

% of hep C cirrhotic pts that go into liver failure, HCC, transplant, or death?

Back 214

25% (usually exacerbated by HIV and/or EtOH)

The other 75% have cirrhosis develop slowly

Front 215

What group(s) have highest hep C infection rate in U.S?

Back 215

Hemophilia, IVD users, and hemodialysis pts. (all from blood products)

Front 216

Difference in serology between recovery from acute hep C and chronic hep C infection?

Back 216

In both, anti-HCV rises then plateaus. And in both, sxs occur in months 1-5, or longer. But, in chronic, HCV RNA persists instead of dropping off like in recovery. And ALT is sporadically high in chronic, but goes to normal in recovery

Front 217

Key monitoring parameters for hep C treatment?

Back 217

Baseline ALT, CBC monthly, TSH, pregnancy monthly, genotype, HCV RNA every 3 months, liver biopsy, HIV. Then monthly ALT, CBC. Q 3 months TSH, HCV RNA at week 12, 24, and 48. Monitor depression

Front 218

4 negative predictors of response to hep C treatment?

Back 218

Cirrhosis, male, HCV RNA>10^6 copies/ml, genotype 1

Front 219

3 therapeutic options to treat treatment relapse of hep C?

Back 219

Higher dose IFN monotherapy, combo for 24 weeks, longer treatment duration (48 weeks), or pegylated IFN monotherapy

Front 220

Contraindications for pegIFN treatment?

Back 220

Creatinine clearance <50ml/min, severe depression, psychiatric instability, active substance abuse, uncontrolled autoimmune disorder (thyroid, DM, RA, etc)

Front 221

Contraindications for ribavirin?

Back 221

Unstable cardiac disease, severe COPD, asthma, renal dysfunction, hemoglobinopathies, pregnancy (or risk of)

Front 222

Side effects of ribavirin?

Back 222

Hemolytic anemia, teratogenicity, cough and dyspnea, rash, pruritus, insomnia, anorexia

Front 223

Anemia and SVR?

Back 223

SVR is sustained virologic response. It is decreased in anemia because hemolysis from ribavirin is worse and bone marrow is suppressed from IFN, so side effects are worse, and compliance goes down the tube. So, in anemia, ribavirin dose needs to be decreased or d/c’d

Front 224

Nucleic acid is RNA. Hep A and/or B and/or C?

Back 224

A and C, not B. HBV is a DNA virus.

Front 225

Major source of the virus is blood/body fluids. Hep A and/or B and/or C?

Back 225

Hep B and C, but not A. Major source of A is feces

Front 226

Becomes a chronic condition about 70% of the time. Hep A and/or B and/or C?

Back 226

Hep C. Hep B becomes chronic 5-10% of the time, and Hep A does not turn into a chronic infection

Front 227

Can cause acute hepatitis Hep A and/or B and/or C?

Back 227

Hep A and B, but very rarely from Hep C

Front 228

Which acute infection is treated? Hep A and/or B and/or C?

Back 228

HAV can only be acute, never chronic, and the only treatment is supportive. HBV infection isn’t treated unless/until it turns chronic. HCV infection is very rarely acute.

Front 229

Treated with IFN for 16 weeks. Hep A and/or B and/or C?

Back 229

HBV infection if HBe+ is treated with 16 weeks of IFN subQ, or 12-18 months is HBe-. IFN alone or in combination with ribavirin is used to treat hepC infection too, but either for 6 months (if genotype 2 or 3), or 1 year (if genotype 1). HAV is not treated pharmacologically.

Front 230

Treated with ribavirin alone? Hep A and/or B and/or C?

Back 230

None of them. However, Ribavirin is used in combination with IFN to treat HepC infection (for 6 months if HCV is genotype 2 or 3), (or 1 year if HCV is genotype 1). Alternatively, IFN can be used alone in the same way.

Front 231

Vaccine available. Hep A and/or B and/or C?

Back 231

A and B, not C

Front 232

Can cause HCC (hepatocellular carcinoma). Hep A and/or B and/or C?

Back 232

All three

Front 233

Good hygeine is critical in preventing transmission. Hep A and/or B and/or C?

Back 233

Hep A mostly (avoid food and water in highly endemic areas). Hep B transmission is likely with needles, tattoos, piercings, and sex. Hep C is prevented from screening blood donors, and risk behavior modification.

Front 234

Transmitted perinatally (from mother to infant). Hep A and/or B and/or C?

Back 234

Hep B, and rarely hep C.

Front 235

Transmitted sexually. Hep A and/or B and/or C?

Back 235

A and B, and rarely C

Front 236

Incubation time is as little as 2 weeks. Hep A and/or B and/or C?

Back 236

A and C. Hep A incubation is 14-45 days. Hep B is 45-180 days. Hep C is 2-26 weeks.

Front 237

Is anicteric in 75% of patients. Hep A and/or B and/or C?

Back 237

Hep C. However, Hep A is anicteric in kids but not adults, and Hep B is anicteric in 70% of kids <5yo and 50-70% in individuals ≥5yo.

Front 238

When to use which dose of Ribavirin: 800mg, 1000mg, or 1200mg?

Back 238

800mg daily, in combination with IFN should be used for six months (24 weeks) of treatment for genotype 2 or 3 hep C infection. The higher doses are used to treat genotype 1 hep C infection for one year. 1000mg is for pt weighing <75kg, and 1200mg is for patient weighing ≥75kg.

Front 239

When are lamivudine or adefovir or entecavir used to treat hepatitis?

Back 239

If after six months, patient is HBs positive AS WELL AS HBe positive AND HBV DNA positive, then check ALT and DNA. If ALT is >200 and DNA is <200, treat with IFN x16 weeks. If not, then treat with lamivudine or adefovir or entecavir. All three are oral 12 months, and must be adjusted in cases of renal insufficiency

Front 240

Can cause fulminant (precipitous, aggressive, and rapid) hepatitis. Hep A and/or B and/or C?

Back 240

Relatively common is Hep A, but only 0.1-0.5% of Hep B infections. (no info for Hep C)

Front 241

Cholestasis and relapse hepatitis are common complications. Hep A and/or B and/or C?

Back 241

Hep A. However, Hep C commonly leads to cirrhosis and liver failure.

Front 242

Symptoms include flu-like sxs, dark urine, pale stools, pruritus, upper right quadrant pain. Hep A and/or B and/or C?

Back 242

Hep A. Hep B presents with fatigue, anxiety, malaise, ascities, jaundice, variceal bleeding, encephalopathy, vomiting, seizures, icterus

Front 243

What is included as supportive therapy in hepatitis A infection?

Back 243

Diet, rest, fluids, no EtOH or hepatotoxic drugs

Front 244

Indications for hepA vaccine?

Back 244

Adults and children ≥2yo in highly endemic areas, or if illicit drug use, MSM, chronic liver disease, liver transplant, or chronic exposure

Front 245

Indications for Hep B vaccine?

Back 245

(1) if exposed, (2) all infants, kids, adolescents, (3) sex partners, household contacts, MSM, IV drug use, travel to highly endemic areas, occupational exposure, inmates

Front 246

Goals of Hep B therapy?

Back 246

Sustained suppression of HBV replication, remission of liver disease, normal ALT, negative or low HBV DNA, loss of HBe and HBs, improvement in liver histology (biopsy)

Front 247

In which type of Hep B infection is HBsAg present for >6 mos? (A).Acute, resolved, (B).Chronic, (C).carrier

Back 247

B and C, but negative after six months in acute resolved case.

Front 248

In which type of hep B infection is ALT normal? (A).Acute, resolved, (B).Chronic, (C).carrier

Back 248

A and C, but not B. In chronic state, ALT is intermittently elevated beyond 2 times the upper limit of normal.

Front 249

In which type of hep B infection is serum HBV DNA present in >10^5 copies per ml? (A).Acute, resolved, (B).Chronic, (C).carrier

Back 249

B.chronic. In carrier status, it is present, but less than 10^5 copies per ml. In acute resolved, it is undetectable

Front 250

In which type of hep B infection is histology biopsy inflammation score <4? (A).Acute, resolved, (B).Chronic, (C).carrier

Back 250

C.carrier. In chronic cases, score is ≥4, and in acute resolved, there is no significant inflammation on liver biopsy

Front 251

In which type of hep B infection is anti-HBc present? (A).Acute, resolved, (B).Chronic, (C).carrier

Back 251

All three. This is the antibody to the core antigen. However, the antibody is not produced in vaccinated individuals who have never been exposed (because the vaccine doesn’t contain the core antigen?)

Front 252

How does cirrhosis occur?

Back 252

Cells are injured and destroyed, and in the process of regeneration, nodular fibrous tissue replaces normal lung parenchyma

Front 253

Two types of changes to liver cell function in cirrhosis?

Back 253

(intrinsic) = Metabolic dysfunction, and synthesis dysfunction (structural) = change in blood flow such as portal blood pressure change

Front 254

Describe the liver lobule?

Back 254

Has portal triad (actually four vessels) made of portal vein (from gut), hepatic artery (oxygenated blood from heart), bile duct (to collect bile) and lymphatic vessel (to collect lymphatic fluid)