UNIVERSITY OF BAGHDAD
COLLEGE OF PHARMACY
PATHOPHYSIOLOGY COURSE
THIRD STAGE 2020-2021
7th LECTURE
PATHOPHYSIOLOGY OF CARDIOVASCULAR
SYSTEM DISORDERS
[Link]. Dr. AJWADASSOMAIDAEE
Vascular disorders are responsible for more morbidity and
mortality than any other category of human diseases.
Although the most clinically significant lesions typically
involve arteries, venous diseases also occur.
Vascular pathology results in disease via two principal
mechanisms:
(1) Narrowing (stenosis) or complete obstruction of vessel
lumens, either progressively (e.g., by atherosclerosis) or
precipitously (e.g., by thrombosis or embolism).
(2) weakening of vessel walls, leading to dilation or rupture.
2
Containing
Heart, artery, Vein
General circulation
Pulmonary circulation
Functions
Deliver oxygen and nutrients
Carry away metabolic wastes
A Healthy circulatory system
♠ Normal blood volum
♠ Homeostasis
Normal homeostasis
vessel wall integrity Edema
intravascular pressure Hyperemia & congestion
osmolarity Thrombosis & Embolism
normal hemostasis Infarction
Hemorrhage
Shock
Three Major Causes of morbidity and mortality
♦ Myocardial infarction
♦ Pulmonary embolism
♦ Cerebral vascular accident
Summary
1. Edema
2. Hyperemia and Congestion
3. Hemorrhage
4. Thrombosis
5. Embolism
6. Ischemia / Infarction
7- Shock
8- Coronary heart disease & Myocardial infarction
9- Rheumatic heart disease
10- Heart failure
11- Acute pulmonary edema
12- Essential hypertension
13- Secondary hypertension
14- Malignant hypertension
15- Hypotension
16- Aneurysm versus varicose veins
EDEMA
Increased fluid in the
interstitial tissue spaces
General & local
Pathogenesis
– Vascular hydrostatic
pressure
– Plasma colloid osmotic
pressure
– Lymphatic drainage
Edema
Edema is an accumulation of fluid in the interstitium in
abnormal amount. Changes in the amount of fluid in the
interstitium can have several general causes: increased
hydrostatic pressure in the capillary, decreased plasma
proteins (albumin), osmotically active substances in the
interstitium, increased capillary permeability, or failure of
lymphatic drainage.
EDEMA Increased hydrostatic pressure ( cardiac
edema, etc.)
Reduced plasma osmotic pressure
(nephrotic, hepatic, malnutrient edema, etc. )
Lymphatic obstruction (filariasis infection —
elephantiasis，breast surgery, etc )
Sodium and water retention (ARF, etc)
elephantiasis Minimal Change Disease Pitting edema
EDEMA
• Morphology
LM:
Clearing and separation of the
extracellular matrix elements
Cell swelling
Subcutaneous edema
Pulmonary edema
Edema of the brain
EDEMA
Hydrothorax
hydropericardium
hydroperitoneum (ascites)
anasarca
Clinical correlation
from annoying to fatal
indicate subtle disease
benefit or harmful
1. Edema
1. hydrostatic pressure
– impaired venous return
congestive heart failure
constrictive pericarditis
liver cirrhosis – ascites
– venous obstruction or compression
thrombosis
external pressure
1. Edema
2. plasma colloid osmotic pressure
loss or reduced albumin synthesis
– nephrotic syndrome
– protein-losing gastroenteropathy
– liver cirrhosis
– malnutrition
1. Edema
3. lymphatic obstruction
lymphedema
– inflammatory elephantiasis
Filariasis - Wuchereria bancrofti
Wuchereria bancrofti is a human parasitic roundworm that is the
major cause of lymphatic filariasis. It is one of the three parasitic
worms, together with Brugia malayi and B. timori, that infect the
lymphatic system to cause lymphatic filariasis
Lymphatic filariasis, also known as elephantiasis, is a human
disease caused by parasitic worms known as filarial worms.[]
Some people, however, develop a syndrome called elephantiasis,
which is marked by severe swelling in the arms, legs, or genitals.
Erysipelas – Streptococcus pyogenes
– neoplastic – breast carcinoma
– post-surgical (LN resection) + postirradiation
1. Edema
subcutaneous tissue (pitting edema) + cavities
generalized x locally prominent
right-sided heart failure – lower limbs
left-sided heart failure - pulmonary edema
nephrotic syndrome – periorbital edema (eyelids)
brain edema – localized x generalized
– gyri flattening + sulci narrowing herniation
HYPEREMIA & CONGESTION
A local increased volume of blood in a particular
tissue
Arterial hyperemia (hyperemia)
An augmented blood flow inducing arteriolar and capillary dilation
Venous hyperemia (congestion)
Accumulation of Blood in Small Veins and capillaries result from
drainage difficulty of veins
HYPEREMIA & CONGESTION
Hyperemia:
Active process;
Red, raised tempreture,
increased volume ;
Enhanced function;
Congestion:
passive process;
general of local;
Reddish blue color
(cyanosis), low
temperature, increased
volume, edema;
Decreased function
HYPEREMIA
Types
Physiological: Shy, exercise, taking Meal
Pathological: Inflammatory, post-decompressed
Significance
－Benefits
Plenty supply of O2, functional enhancement, nutrition substance
－ Hazards
Headache , hemorrhage, stroke
CONGESTION
Causes:
Systemic: general or pulmonary
Cardiac dysfunction (right or left)
Local: local venous compression or obstruction
External Compression --- Tumor, Bandage
Occlusion of lumen --- Thrombosis, Embolism
Thickening of venous wall
Paralysis of neurogenic modulation --- Burn, frostbite
CONGESTION
Lung:
Acute pulmonary congestion
Gross: Plump swollen lung with
shining pleura, edematous fluid
flowing out while cutting the lung
LM:
Alveolar capillaries highly dilated (rosary-
like appearance) and engorged with
blood
Alveolar cavity filled with eosinophilic
edema fluid
Manifestation
Pink colored foamy sputum
CONGESTION
Lung:
Chronic pulmonary congestion
Gross: Hard, with brown spots scattered
—— Brown induration
LM:
Septa thickened and fibrosis
Alveolar spaces containing ‘heart failure
cells’— hemosiderin-laden macrophages
Manifestation
Rusty sputum, dyspnea, etc.
CONGESTION
Liver:
Acute hepatic congestion
LM:
— Dilation of central vein and sinusoids with
blood
— Atrophy, degeneration and necrosis of central
hepatocytes
CONGESTION
Liver:
Chronic hepatic congestion
Nutmeg liver
Gross: red-brown zones accentuated
against the yellow surrounding
zones
LM: centrilobular necrosis and congestion,
and perilobular fatty change; fibrosis
Long-standing, severe hepatic congestion:
hepatic fibrosis (cardiac cirrhosis)
Hyperemia and Congestion
= blood volume in particular tissue
a. hyperemia – active (arteriolar dilation)
– red color
– striated muscle exercise
b. congestion – passive (impaired venous return)
– systemic x local
– blue-red color (cyanosis), edema
– event. hypoxemic necrosis, e.g. bowel
– accumulation of deoxygenated Hb
– chronic chronic hypoxia regressive changes + small
hemorrhages siderophages=Heart failure cells are siderophages
(hemosiderin-containing macrophages) generated in the alveoli of patients with
left heart failure or chronic pulmonary edema, when the high pulmonary blood
pressure causes red cells to pass through the vascular wall
Hemorrhage
Causes
• Rupture of blood vessels
Trauma, Peptic ulcer, aneurism ?, atherosclerosis
• Diapedesis
Enlarged interendothelial gap (basement membrane
injury). The intergrity of the vessels remains intact
* Injury to vascular wall: sever infection, anoxia, toxins
Change in number and quality of platelets
uremia, leukemia, idiopathic
Disturbance of coagulation mechanism
congenital disease, DIC , deficiency of Vit. K
hemorrhage
Petechiae The clinical significance
Purpuras
depends on the volume,
Ecchymoses
the rate of loss and the
Hematoma
Hemothorax
site.
Hemopericardium Hemorrhagic shock
Hemoperitoneum Stroke
hemoarthrosis
3. Hemorrhage
= extravasation of blood from blood vessels
external (+ in hollow organs)
internal: within tissue – hematoma
hemorrhagic diatheses – insignificant injury
– vasculopathies
– thrombocytopenia
– coagulopathy
Disseminated Intravascular
Coagulation (DIC)
basis: widespread activation of thrombin
fibrin thrombi in microcirculation
1. stage
– multiple fibrin thrombi in microcirculation
consumption of PLT + coagulation proteins
2. stage
– fibrinolytic system activation serious
bleeding (Consumption of coagulation
substance and activation of fibrinolytic system)