NEET MDS Lessons
General Pathology
CONGESTION
Congestion or hyperaemia means an increase in the content of blood in an organ. It may be :
A. Active - due to increased arterial flow to the organ with dilatation of micro vessels as in
- Inflammation.
- Increased metabolic activity.
- Neurogenic blushing.
B. Passive - due to decreased venous drainage resulting in pooling of blood. There is always an associated element of oedema.
INFARCTION
Definition : a localized area of ischaemic necrosis in an organ infarcts may be:
Pale :as in
→ Arterial obstruction.
→ solid organs.
Red as in
→ Venous occlusion
→ Loose tissue.
Morphology
Gross: infarcts are usually wedge shaped the apex towards the occluded vessel They are
separated from the surrounding tissue by an hyperemic inflammatory zone
Microscopic:
- An area of coagulative necrosis with a rim of congested vessels and acute inflammatory infiltration of the tissue .
- The polymorphs ale later replaced by mononuclear cells and granulation tissue.
- With time, scar tissue replaces necrosed tissue.
Leukaemias
Uncontrolled proliferation of leukocyte precursors (may be with associated red cell and platelet series proliferation).
Factors which may playa causal role are.
- Viral
- Radiation.
- Genetic.
Classification
1. Acule leukaemia:
a. Lymphocytic (lymphoblastic).
b. Myelocytic and promyelocytic (myeloblastic).
c. Monocytic.
d. Myelomonocytic.
e. Undifferentiated (Stem cell).
2. Chronic leukaemia:
a. Lymphocytic
b. Myelocytic
3. Miscellaneous:
a. Erythroleukaemia (De Guglielmo's disease).
b. Eosinophilic leukaemia.
c. Megakaryocytic leukaemia.
EMBOLISM
An embolus is a detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin
99% due to dislodged thrombus
Types:
1. Thrombo-embolism
2. Fat embolism
3. Air embolism
4. Nitrogen embolism
Emboli result in partial or complete vascular occlusion.
The consequences of thromboembolism include ischemic necrosis (infarction) of downstream tissue
PULMONARY THROMBOEMBOLISM
- 95% originate from deep veins of L.L
Special variants: - Saddle embolus: at bifurcation of Pulmonary artery
Paradoxical embolus: Passage of an embolus from venous to systemic circulation through IAD, IVD
CLINICAL CONSEQUENCE OF PULMONARY THROMBOEMBOLISM :
Most pulmonary emboli (60% to 80%) are clinically silent because they are small
a. Organization: 60 – 80 %
b. Sudden death, Right ventricle failure, CV collapse when more than 60 % of pulmonary vessels are obstructed.
c. Pulmonary hemorrhage: obstruction of medium sized arteries.
d. Pulmonary Hypertension and right ventricular failure due to multiple emboli over a long time.
Systemic thromboembolism
Emboli traveling within the arterial circulation
80% due to intracardiac mural thrombi
2/3 Lt. ventricular failure
The major targets are:
1. Lower limbs 75%
2. Brain 10%
3. Intestines
4. Kidneys
5. Spleen
Fat embolism
Causes
1. Skeletal injury (fractures of long bones )
2. Adipose tissue Injury
Mechanical obstruction is exacerbated by free fatty acid release from the fat globules, causing local toxic injury to endothelium. - In skeletal injury, fat embolism occurs in 90% of cases, but only 10% or less have clinical findings
Fat embolism syndrome is characterized by
A. Pulmonary Insufficiency
B. Neurologic symptoms
C. Anemia
D. Thrombocytopenia
E. Death in 10% of the case
Symptoms appears 1-3 days after injury
Tachypnea, Dyspnea, Tachycardia and Neurological symptoms
Air Embolism
causes: 1. Obstetric procedures
2. Chest wall injury
3. Decompression sickness: in Scuba and deep-sea divers ((nitrogen ))
More then 100ml of air is required to produce clinical effect.
Clinical consequence
1. Painful joints: due to rapid formation of gas bubbles within Sk. Muscles and supporting tissues.
2. Focal ischemia in brain and heart
3. Lung edema, Hemorrhage, atelectasis, emphysema, which all lead to Respiratory distress. (chokes)
4. caisson disease: gas emboli in the bones leads to multiple foci of ischemic necrosis, usually the heads of the femurs, tibias, and humeri
Amniotic fluid embolism
- Mortality Rate = 20%-40%
- Very rare complication of labor
- due to infusion of amniotic fluid into maternal circulation via tears in placental membranes and rupture of uterine veins.
- sudden severe dyspnea, cyanosis, and hypotensive shock, followed by seizures, DIC and coma
- Findings: Squamous cells, languo hair, fat, mucin …..etc within the pulmonary microcirculation
HERPES SIMPLEX
An infection with herpes simplex virus characterized by one or many clusters of small vesicles filled with clear fluid on slightly raised inflammatory bases.
The two types of herpes simplex virus (HSV) are HSV-1 and HSV-2. HSV-1 commonly causes herpes labialis, herpetic stomatitis, and keratitis; HSV-2 usually causes genital herpes, is transmitted primarily by direct (usually sexual) contact with lesions, and results in skin lesions
Primary infection of HSV-1 typically causes a gingivostomatitis, which is most common in infants and young children. Symptoms include irritability, anorexia, fever, gingival inflammation, and painful ulcers of the mouth.
Primary infection of HSV-2 typically occurs on the vulva and vagina or penis in young adults
Herpetic whitlow, a swollen, painful, and erythematous lesion of the distal phalanx, results from inoculation of HSV through a cutaneous break or abrasion and is most common in health care workers.
Chickenpox (varicella)
- primarily a childhood disease (70%)
- incubation period 14-16 days; highly contagious; infectious 2 days before the vesicles until the last one dries.
- present with generalized, intensely pruritic skin lesions starting as macules vesicles pustules (MVP-most valuable player) usually traveling centrifugally to the face and out to the extremities; unlike smallpox vesicles, chickenpox vesicles appear in varying stages of development as successive crops of lesions appear; intranuclear inclusions similar to HSV.
- pneumonia develops in 1/3 of adults; MCC death in chickenpox.
- association with Reye's syndrome if child takes aspirin.
Clinical & biologic death
Clinical death
Clinical death is the reversible transmission between life and biologic death. Clinical death is defined as the period of respiratory, circulatory and brain arrest during which initiation of resuscitation can lead to recovery.
Signs indicating clinical death are
• The patient is without pulse or blood pressure and is completely unresponsive to the most painful stimulus.
• The pupils are widely dilated
• Some reflex reactions to external stimulation are preserved. For example, during intubations, respiration may be restored in response to stimulation of the receptors of the superior laryngeal nerve, the nucleus of which is located in the medulla oblongata near the respiratory center.
• Recovery can occur with resuscitation.
Biological Death
Biological death (sure sign of death), which sets in after clinical death, is an irreversible state
of cellular destruction. It manifests with irreversible cessation of circulatory and respiratory
functions, or irreversible cessation of all functions of the entire brain, including brain stem.