1

Pathophysiology of Hypovolemic Shock Secondary to Massive Upper

Gastrointestinal Bleeding Secondary to Ruptured Esophageal Varices Secondary
to Portal Hypertension Secondary to Liver Cirrhosis Secondary to Chronic
Hepatitis C Infection
Predisposing Factors: Precipitating Factors:
-Age: 54y/o -Compromised Immune System
-Gender: Female -Poor Diet
-Family History -Socioeconomic Status
-Alcoholic Drinker for 35 years -Occupation
-Smoker for 17 years -Contact with Infected blood

Excessive Alcohol Ingestion Introduction of Hepatitis C

virus

Increased liver synthesis of

triglycerides and fatty acids, Attacks Liver
reduction in oxidation of fatty
acids, and decreased release
of lipoprotein

Fat accumulation in the

parenchymal cells of the liver
and distention of cytoplasm
with fats

Liver Steatosis/Fatty Liver

Hepatocyte damage

Inflammation of the liver

(Hepatitis)

Alteration in Blood and Stimulates liver to produce Induction of Immune response

Lymph flow
Liver parenchyma destruction
Fibrosis/Scarring
collagen
Antigen-antibody complexes
Collagen builds up quickly
Activation of complement
system

LIVER CIRRHOSIS A
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Pathophysiology of Hypovolemic Shock Secondary to Massive Upper
Gastrointestinal Bleeding Secondary to Ruptured Esophageal Varices Secondary
to Portal Hypertension Secondary to Liver Cirrhosis Secondary to Chronic
Hepatitis C Infection
A

Immune complex formation in

circulation

Immune complex deposition in

vascular

Vasculitis ( Inflammation of
Blood vessels)

Impairs blood supply

Ischemia in the liver

Virus is not killed

Viral antigen persists in the

liver

Viral Infection

CHRONIC HEPATITIS C
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Pathophysiology of Hypovolemic Shock Secondary to Massive Upper
Gastrointestinal Bleeding Secondary to Ruptured Esophageal Varices Secondary
to Portal Hypertension Secondary to Liver Cirrhosis Secondary to Chronic
Hepatitis C Infection

LIVER CIRRHOSIS

Vascular Compression Increase Arterial Loading

Increase resistance of blood Increase flow through hepatic

flow to the liver artery

Decrease blood flow to the Increase blood volume in

hepatic sinusoid and vein

Portal Congestion

PORTAL HYPERTENSION

Faulty protein synthesis

Increase pressure in capillary Hepatic Shunting
bed
Hypoalbuminemia
Diversion of blood to
Increase capillary collateral channel
Decrease colloidal
osmotic pressure
Fluid shift to extravascular Blood bypasses to the liver
compartment

Increase portal flow

Ascites

C
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Pathophysiology of Hypovolemic Shock Secondary to Massive Upper
Gastrointestinal Bleeding Secondary to Ruptured Esophageal Varices Secondary
to Portal Hypertension Secondary to Liver Cirrhosis Secondary to Chronic
Hepatitis C Infection
C

Esophageal Varices

Protrusion in esophageal
lumen

Erosion

Rupture

Bleeding Hematemesis and Melena

MASSIVE UPPER
GASTROINTESTINAL
BLEEDING

Blood loss

Intravascular volume

Decrease cardiac output

Antidiuretic hormone, Shift of interstitial Catecholamine

aldosterone secretion fluid

Increased volume Increased heart rate, Increased systemic

force of contraction vascular resistance

Increased cardiac output

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Pathophysiology of Hypovolemic Shock Secondary to Massive Upper
Gastrointestinal Bleeding Secondary to Ruptured Esophageal Varices Secondary
to Portal Hypertension Secondary to Liver Cirrhosis Secondary to Chronic
Hepatitis C Infection
Increased cardiac output

Continued volume loss Decreased systemic Decreased Pulmonary

pressure pressure

Decreased cardiac output

Decreased tissue
perfusion

Impaired cellular
metabolism

HYPOVOLEMIC
SHOCK
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Pathophysiology of Hypovolemic Shock Secondary to Massive Upper
Gastrointestinal Bleeding Secondary to Ruptured Esophageal Varices Secondary
to Portal Hypertension Secondary to Liver Cirrhosis Secondary to Chronic
Hepatitis C Infection
B

Inhalation of droplet infected with

Mycobacterium Tuberculosis Hypersensitivity to the organism

Trapped in the upper airways Inside the giant cells, caseous

necrosis occurs (granular cheesy
appearance)
Activated primary defenses
(mucus-secreting goblet cell and
cilia) Proliferation of T-lymphocytes in
the surrounding of the central core
of the caseous necrosis causing
If untreated, bacteria reaches and some lesions
deposits itself in lung periphery
(Lower part of the upper lobe or
Upper part of the lower lobe: Fibrosis and Calcification happens
alveoli)

As the lesion ages, it then results to

Bacteria is quickly surrounded by
granuloma formation (tubercle)
polymorphonuclear leukocytes and
engulfed by alveolar macrophages

Collagenous scar tissue

Mycobacterium organisms are encapsulates tubercle to separate
carried off by the lymphatics to the organism from the body
hilar lymph nodes (Ghon Complex)
Progresses to grow and multiply
Macrophages (epithelial cells)
engulfs the bacteria
Cell Mediated immunity

Macrophages surround them and

wall them off in tiny, hard capsules PULMONARY TUBERCULOSIS

Hypersensitivity to the organism

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Pathophysiology of Hypovolemic Shock Secondary to Massive Upper
Gastrointestinal Bleeding Secondary to Ruptured Esophageal Varices Secondary
to Portal Hypertension Secondary to Liver Cirrhosis Secondary to Chronic
Hepatitis C Infection

PULMONARY TUBERCULOSIS

For poorly immunocompromised patients, the

necrotic liquefies and fibrous walls losses it
structural integrity

Semiliquid necrotic material is drained into the

bronchous or in the nearby blood vessels, leaving an
air-filled cavity at the original site

If drained in the bronchous as purulent discharge, it If drained in the blood vessel, it could enter the blood
could infect other people through droplet stream or in the lymphatic system; where new
transmission caseous granulomas may form

EXTRAPULMONARY
TUBERCULOSIS

LEGEND:
PRECIPITATING FACTORS PREDISPOSING FACTORS

DISEASE PROCESS SIGNS AND SYMPTOMS

DISEASE CONTINUATION

COMPLICATIONS MAY LEAD TO