CM- Portal Hypertension Flashcards Preview

GI, Liver, GallBladder, Pancreas > CM- Portal Hypertension > Flashcards

Flashcards in CM- Portal Hypertension Deck (53):
1

Patients with obstructive or biliary cirrhosis often present initially with ______ and __________. Patients with chronic parenchymal liver diseases on the other hand commonly present with _________.

Obstructive/biliary: pruritis and jaudice

Parenchymal: complications of portal hypertension like variceal hemorrhage and/or ascites

2

What is hepatic blood supply?
What does portal blood provide to the liver?

The major source is the portal vein which derives venous blood from splanchnic bed (capillaries in the intestinal tract) to splenic vein, superior and inferior mesenteric v.

The minor source is hepatic artery.

The portal blood brings nutrients from the intestines and hormones from the pancreas into the liver.

3

What pressure differential determine what is considered portal hypertension?

Normal portal v. pressure is 5-10mmHg.

1. Portal or splenic vein pressure greater than 15mmHg
--OR--
2. portal pressure that is 5mmHg above IVC pressure is considered portal hypertension

4

How does normal portal venous pressure compare to systemic venous pressure?

There are no valves between the heart and the splanchnic bed capillaries so they should be equal

5

How do changes in flow and resistance change pressure?

Pressure is proportional to flow and resistance.
If flow increases, pressure will increase
If resistance increases, pressure will increase both which can cause portal hypertension

6

What are the 2 instances where increased flow leads to portal hypertension?

1. tropical splenomegaly (recurrent malaria)
2. splenic AV fistulas

7

What are the major components of resistance to portal blood flow? Why?

Precapillary and presinusoidal because there is virtually no resistance to flow through the hepatic sinusoids in the normal liver.

8

Why is it crucial that there be no resistance to flow through the hepatic sinusoids?

The sinusoid epithelium has pores that allows free passage of proteins across into the space of Disse and lymphatic circulation.
If there was sinusoidal outflow resistance, there would be excess movement of protein and fluid into the space of disse

9

How does the location of the deposition of fibrous tissue affect resistance to portal flow?

If disease is near the terminal hepatic venule, there will be intra- and post sinusoidal increased resistance to flow--> portal hypertension

If the disease is periportal there will be a predominant component of pre-sinusoidal obstruction to portal flow

10

What are 2 causes of post-sinusoidal portal hypertension?

1. Thrombosis in the hepatic vein (Budd-Chiari)
2. increased RA pressure (CHF, constrictive pericarditis)

11

How does schistosomiasis cause portal hypertension?

Schistosomiasis causes granuloma formation which causes portal fibrosis and blocking intrahepatic portal branches. This causes pre-sinusoidal portal hypertension

12

What are the 3 main types of portal hypertension?
What are the 3 subtypes of intrahepatic?

Pre-hepatic
- splenic vein thrombosis
- portal vein thrombosis

Intrahepatic
- pre-sinusoidal (schistosomiasis)
- sinusoidal (alcoholic cirrhosis)
- post-sinusoidal (veno-occlusive disease)

Post-hepatic
- heart failure
- cor pulmonale
-constrictive pericarditis

13

What type of portal hypertension is associated with formation of varices?

Intra-hepatic and pre-hepatic because this increases the portal pressure but not the systemic pressure.
Over time, portal-systemic collateral will form

14

Why don't patients with increased RA pressure develop varices?

They have increased systemic AND portal circulation. There is no gradient, so they will not develop collaterals

15

Where do portal-systemic collaterals form?
What are 4 examples of collaterals?
Which is most likely to hemorrhage?

At the transition zone of squamous and glandular epithelium:
1. gastroesophageal junction (esoph. varices)*****
2. anus (hemorrhoids)
3. falciform ligament (recanalization of umbilical vein and development of periumbilical veins) = caput medusa
4. where spleen, pancreas, and intestines give rise to retroperitoneal portal-systemic vascular channels

16

What is the effect of pre and intrahepatic portal hypertension on the spleen?

Splenomegaly will occur and is associated with hypersplenism:
-thrombocytopenia (common)
- leukopenia(uncommon)
-anemia (least)

17

What are complications of acute upper
gastrointestinal hemorrhage from the varices?

Where is the most likely site of rupture?

hematemesis
melena (black tarry feces)
orthostasis

The most likely site of rupture is the distal 1/3 of esophagus

18

What are the 3 main factors that determine whether a varices will rupture causing a GI bleed?

1. portal-systemic gradient above 12mmHg
2. variceal size
3. thickness of overlying mucousa

19

Aside from varices, what other 2 vascular manifestations are seen with chronic liver disease?

1. palmar erythema (liver palms)
2. spider nevi

(both can also be observed in pregnancy)

20

How is the source of a GI bleed usually identified?
What condition must the patient be in to do this?
What is treatment?

direct endoscopic inspection :
1. esophago-gastrodudodenosopy (EGD)
2. colonoscopy

patient must be resuscitated and stabilized before these procedures are done

Treatment is band ligation of the varices done at the time of the endoscopy

21

What are the 3 pharmaceutical choices for management of varices?
What is the mode of action of each?
What are the side effects?

ALL 3 just decrease portal blood flow. They do NOTHING to the resistance.

1. B- blocker (oral)
- splanchnic vasoconstrictor
- inhibits splanchnic vasodilation

2. vasopressin (IV)
- splanchnic vasoconstriction
- ischemia (because of the lack of specificity to splanchnic area..also constricts systemic/coronary)

3. Somatostatin (IV)
- splanchnic vasoconstriction

22

What are the 2 treatments that decrease portal resistance, lowering the risk of variceal rupture and GI bleed?

what is the major side effect of both?

1. surgical - form a portal-systemic shunt from the splenic vein to the left renal vein (instead of the portal vein)

2. Radiologic shunts- (TIPS) trans-jugular-intrahepatic, portal systemic shunt. Fluoroscopic guidance from internal jugular through IVC to hepatic vein. Dye is injected into the portal system to see where a stent can be placed.

Both increase the risk of hepatic encephalopathy because blood is no longer passing through the liver to be filtered

23

What determines survival after variceal hemorrhage?

Hepatic function-
The best outcome is in people with pre-hepatic portal hypertension

24

Why is ascites rare in pre-hepatic and pre-sinusoidal hypertension?

Ascites occurs when increased sinusoidal pressure signals extra-hepatic NO release and triggers Na retention

25

Which situation will have BOTH varices and ascites?

Sinusoidal portal hypertension (alcoholic cirrhosis, viral cirrhosis)

26

Under normal circumstances ________ protein fluid leaves the splanchnic capillaries and enter the interstitial spaces of the stomach and intestines. It is removed by _________ and returns to the blood via _____ and _______.

low protein fluid leaves the capillaries

It is removed from the interstitium by lymphatic circulation and returns to the blood via cisterna chyli and thoracic duct

27

In normal circumstances ___________protein fluid leaves the _____________ and enters hepatic interstitial space and is returned to the blood via lymphatic circulation.

high protein leaves the hepatic sinusoids

This is because the epithelium is discontinuous

28

How does sinusoidal portal hypertension lead to the development of ascites?

Sinusoidal portal hypertension increases extra-hepatic NO which causes splanchnic vasodilation.
This increases portal blood flow.
The low EABV from the vasodilation triggers renal compensation to retain Na and free H20. This expands plasma volume.

Hydrostatic pressure is increased in splanchnic capillaries and hepatic sinusoids. In addition hypoalbuminemia occurs decreasing oncotic pressure (due to H20 and Na retention). This makes more fluid flows into the interstitial space overwhelming the lymphatic systems ability to remove it

29

What is peritonitis?
What are the two major causes?

ascites that occurs as part of an intra-abdominal infection or when ascites from portal hypertension become infected.

1. Secondary peritonitis- infection due to spread from a perforation or abscess
2. Spontaneous bacterial peritonitis (SBP) from an unknown source

30

Spontaneous Bacterial Peritonitis (SBP) appears to be confined to people with _______ ascitic protein levels and is likely related to ______________.

low ascitic protein (usuall below 1g/dl, almost always below 2.5) and is likely due to inadequate opsonization to control bacterial seeding

31

What are the major clinical symptoms of ascites?

1. abdominal swelling
2. early satiety
3. enlarged inguinal/periumbilical hernias
4. ab discomfort due to streching of ab wall

If infected: fever and pain

32

What is the most specific physical exam finding of ascites?

shifting dullness on abdominal percussion.

The patient lays down and the examiner percusses the abdomen to discover the pocket of air. The patient rolls toward the other side. If they have ascites the pocket of air will move to the other side (to be highest)

33

What are the 4 most useful tests when assessing fluid from an abdominal paracentesis?

1. ascitic fluid albumin level
2. total protein content
3. WBC count
4. differential WBC count

34

Patients with post-sinusoidal obstruction to portal flow (CHF, Budd-Chiari) tend to have ________ total protein levels than those with sinusoidal (cirrhotic).

Higher

Post-sinusoidal >2.5g/dL
Cirrhotic <2.5 g/dL

35

What are the 3 major non-portal hypertensive causes of ascites? Do they have high protein content or low?

1. peritoneal TB - high protein
2. carcinomatosis- high protein
3. nephrotic syndrome - low protein

36

Why does cirrhosis have low protein content in ascites?

the majority of the fluid comes from splanchnic bed (transudative) with a partial contribution from hepatic sinusoid

37

Why does cardiac ascites have high protein content in the ascites?

There is a large contribution of hepatic lymph and interstitial fluid which is high protein due to the fenestrations

38

What is the best strategy for classification of ascitic fluid into etiologic categories?
What has a high serum-ascites value?
What has a low serum-ascites value?

Serum-ascites albumin gradient

>1.1 = portal hypertension
<1.1 = NOT portal hypertension

39

You do a pericentesis and get high serum-ascites albumin gradient. There is a low total fluid protein. What is the likely cause?

Cirrhosis

40

You do pericentesis and get high SAAG and high total fluid protein. What is the likely cause?

RHF, CHF, constrictive pericarditis, Budd-Chiari

41

You do pericentesis and get low SAAG and low total protein. What is the likely cause?

Nephrotic syndrome/ protein losing states

42

You do pericentesis and get low SAAG and high total protein. What is the likely cause ?

carcinomatosis, TB, peritoneal infection, inflammation

43

When analyzing cells from pericentesis, you notice <500 WBC mostly macrophages. What do you suspect?

uncomplicated cirrhosis

44

How does immune composition differ from TB, bacterial infection and malignancy in fluid from pericentesis?

TB- mostly T lymphocytes and rBc's

Bacterial- PMNs greater than 250

Malignancy- variable numbers of WBC and RBC

45

What is management of ascites due to portal hypertension?

1. dietary Na restriction
2. diuretic therapy

If insufficient diuresis occurs:
1. Therapeutic paracentesis is a temporary measure
2. Liver transplantation
3. TIPS

46

When does portal-systemic shunting occur intra-hepatically?

when fibrous tissue has replaced the basement membrane of sinusoids and things can't filter through epithelial fenestrations.
Thus, blood goes directly from portal to systemic circulation w/o passing through the liver

47

What is the worst sequelae of portal-systemic shunts?

Hepatic encephalopathy because there is decreased hepatic metabolism and clearance of ammonia/nitrogenous compounds

48

What is the clinical presentation of hepatic encephalopathy?

disturbances of consciousness
impaired intellectual focus
asterexis
constructional apraxia

49

What lab value tells you that encephalopathy is hepatic and not another type of metabolic encephalopathy?

Ammonia level

50

When a patient presents with encephalopathy, what tests are run?

blood, urine, and ascitic fluid analysis/cultures
electrolytes
CBC
Urine screen for drugs

51

What does the EEG look like in someone with encephalopathy?
What does the CT show?

EEG- slow, high amplitude waves (delta waves)

CT- cerebral edema

52

What factors are known to precipitate or exacerbate encephalopathy?

1. infections
2. GI bleeds
3. dietary protein
4, hypokalemic alkalosis
5. benzodiazapine (w/o ammonia elevation)

53

What are the 2 major treatments for managing encephalopathy? Which is better?

1. lactulose (non-absorbable sugar) that induces osmotic diarrhea to decrease systemic ammonia

2. non-absorbable antibiotics to kill bacteria that generate ammonia by metabolizing urea

3. protein restriction is not clinically helpful chronically