NEET MDS Lessons
General Pathology
HYPERTENSIVE VASCULAR DISEASE
Malignant hypertension
A small percentage of HTN patients (5%) present with a rapidly rising blood pressure that, if untreated, leads to death within 1 to 2 years.
systolic pressures -> 200 mm Hg or diastolic pressures -> 120 mm Hg
Associated with renal failure and retinal hemorrhages
Most commonly is superimposed on preexisting benign hypertension
Hypertension (HTN) has the following complications
- stroke (CVD)
- multi-infarct dementia
- atherosclerotic coronary heart disease
- cardiac hypertrophy and heart failure (hypertensive heart disease)
- aortic dissection
- renal failure
Essential HTN Accounts for 90% to 95% of all cases
SecondaryHTN
Renal - > Acute glomerulonephritis Chronic renal disease
Endocrine - > Cushing syndrome, Hypothyroidism (myxedema) Hyperthyroidism (thyrotoxicosis) Pregnancy-induced (pre-eclampsia)
Cardiovascular - > Coarctation of aorta
Neurologic
Psychogenic, Increased intracranial pressure
PATHOGENESIS
most cases (95%) are idiopathic (essential hypertension)
Most of the remaining cases (secondary hypertension) are due to primary renal disease, renal artery narrowing
Gene defects in enzymes involved in aldosterone metabolism
Mutations in proteins that affect sodium resorption as in Liddle syndrome
Genetic factors - > familial clustering of hypertension
Environmental factors such as stress, obesity, smoking, physical inactivity, and high levels of salt consumption, modify the impact of genetic determinants
Morphology
HTN is associated with arteriolosclerosis (small arterial disease)
Two forms of small blood vessel disease are hypertension-related:
1- hyaline arteriolosclerosis
2- hyperplastic arteriolosclerosis
Hyaline arteriolosclerosis
Associated with benign hypertension.
-marked by homogeneous, pink hyaline thickening of the arteriolar walls, and luminal narrowing.
Hyperplastic arteriolosclerosis
It is more typical of severe hypertension.
- "onionskin," concentric, laminated thickening of arteriolar walls and luminal narrowing.
- The laminations consist of smooth muscle cells and thickened, reduplicated basement membrane.
DISORDERS OF BLOOD VESSEL HYPERREACTIVITY
Several disorders are characterized by inappropriate or exaggerated vasoconstriction of blood vessels:
1- Raynaud Phenomenon
2- Myocardial Vessel Vasospasm
Raynaud Phenomenon
- results from exaggerated vasoconstriction of arteries and arterioles in the extremities (the fingers and toes, but also sometimes the nose, earlobes, or lips).
-restricted blood flow induces paroxysmal pallor or cyanosis
- involved digits characteristically show "red-white-andblue" color changes from most proximal to most distal
Myocardial Vessel Vasospasm
Causes: 1- vasoactive mediators - > prolonged vascular contraction;
- endogenous (e.g., epinephrine released by pheochromocytomas) or exogenous (cocaine or phenylephrine).
2- Elevated thyroid hormone -> increase sensitivity of vessels to catecholamines
3- autoantibodies and T cells in scleroderma vascular instability and vasospasm.
4- extreme psychological stress (release of catecholamines)
Cardiac raynaud
When vasospasm of cardiac arterial or arteriolar bed is of sufficient duration (20 to 30 min ) myocardial infarction occurs
acute microscopic area of necrosis characterized by mycotic hypercontraction (contraction band necrosis)
subacute and chronic cases - > microscopic foci of granulation tissue or scar
Ichthyosis vulgaris is a genetic disease characterized by increased cohesiveness of the cells in the stratum corneum, resulting up in a piling up stratum corneum (scales like a fish).
Immunoglobulins. (Ig)
These are made up of polypeptide chains. Each molecule is constituted by two heavy and two light chains, linked by disulfide (S-S) bonds. The h~ chains are of 5 types, with corresponding, types or immunoglobulin. IgG (gamma), IgM (mu µ ), IgA(alpha α), IgD(delta ), IgE(epsilon)
Each of these can have light chains of either kappa (k) or lambda type.Each chain has a constant portion (constant for the subtype) land a variable portion (antigen specific).
Enzyme digestion can split the Ig molecule into.2 Fab (antibody binding) fragments and one Fc (crystallisable, complement binding ) fragment.
Characteristics of Immunoglobulin subclasses
I. Ig G:
(i) Predominant portion (80%) of Ig.
(ii) Molecular weight 150, 000
(iii) Sedimentation coefficient of 7S.
(iv) Crosses placental barrier and to extra cellular fluid.
- (v) Mostly neutralising effect. May be complement fixing.
(vi) Half life of 23 days.
2.IgM :
(i) Pentamer of Ig.
(ii) Molecular weight 900, 000
(iii) 19S.
(iv) More effective complement fixation and cells lysis
(v) Earliest to be produced in infections.
(vi) Does not cross placental barrier.
(vii) Halflife of 5 days.
3. Ig A :
- Secretory antibody. Found in intestinal, respiratory secretions tears, saliva and urine also.
- Secreted usually as a dinner with secretory piece.
- Mol. weight variable (160,000+)
- 7 S to 14 S.
- Half life of 6 days.
4.Ig D :
- Found in traces.
- 7 S.
- Does not cross placenta.
5. Ig E
- Normally not traceable
- 7-8 S (MoL weight 200,000)
- Cytophilic antibody, responsible for some hypersensitivity states,
A dermatofibroma is a benign tumor of the dermis, MC located on the lower extremity, where it has a nodular, pigmented appearance.
- composed of benign histiocytes.
Pneumoconioses—are environmentally related lung diseases that result from chronic inhalation of various substances.
1. Silicosis (stone mason’s disease)
a. Inhalant: silica dust.
b. Associated with extensive fibrosis of the lungs.
c. Patients have a higher susceptibility to tuberculosis infections.
2. Asbestosis
a. Inhalant: asbestos fibers.
b. Associated with the presence of pleural plaques.
c. Consequences include:
(1) Mesothelioma (malignant mesothelial tumor).
(2) Bronchogenic carcinoma.
3. Anthracosis
a. Inhalant: carbon dust.
b. Usually not as harmful as silicosis or asbestosis.
c. Associated with the presence of macrophages containing carbon.
Q Fever
An acute disease caused by Coxiella burnetii (Rickettsia burnetii) and
characterized by sudden onset of fever, headache, malaise, and interstitial
pneumonitis.
Symptoms and Signs
The incubation period varies from 9 to 28 days and averages 18 to 21 days. Onset
is abrupt, with fever, severe headache, chills, severe malaise, myalgia, and,
often, chest pains. Fever may rise to 40° C (104° F) and persist for 1 to > 3
wk. Unlike other rickettsial diseases, Q fever is not associated with a
cutaneous exanthem. A nonproductive cough and x-ray evidence of pneumonitis
often develop during the 2nd wk of illness.
In severe cases, lobar consolidation usually occurs, and the gross appearance of
the lungs may resemble that of bacterial pneumonia
About 1/3 of patients with protracted Q fever develop hepatitis, characterized
by fever, malaise, hepatomegaly with right upper abdominal pain, and possibly
jaundice. Liver biopsy specimens show diffuse granulomatous changes, and C.
burnetii may be identified by immunofluorescence.
Pleural effusion is a medical condition where fluid accumulates in the pleural cavity which surrounds the lungs, making it hard to breathe.
Four main types of fluids can accumulate in the pleural space:
Serous fluid (hydrothorax)
Blood (hemothorax)
Lipid (chylothorax)
Pus (pyothorax or empyema)
Causes:
Pleural effusion can result from reasons such as:
- Cancer, including lung cancer or breast cancer
- Infection such as pneumonia or tuberculosis
- Autoimmune disease such as lupus erythematosus
- Heart failure
- Bleeding, often due to chest trauma (hemothorax)
- Low oncotic pressure of the blood plasma
- lymphatic obstruction
- Accidental infusion of fluids
Congestive heart failure, bacterial pneumonia and lung cancer constitute the vast majority of causes in the developed countries, although tuberculosis is a common cause in the developing world.
Diagnosis:
- Gram stain and culture - identifies bacterial infections
- Cell count and differential - differentiates exudative from transudative effusions
- Cytology - identifies cancer cells, may also identify some infective organisms
- Chemical composition including protein, lactate dehydrogenase, amylase, pH and glucose - differentiates exudative from transudative effusions
- Other tests as suggested by the clinical situation - lipids, fungal culture, viral culture, specific immunoglobulins