NEET MDS Synopsis
The Salivary Glands
AnatomyThe Salivary Glands
There are three large, paired salivary glands: the parotid, submandibular, and sublingual glands.
In addition to the main salivary glands, there are numerous small accessory salivary glands scattered over the palate, lips, cheeks, tonsils, and tongue.
TUBERCULOSIS
General Pathology
TUBERCULOSIS
A chronic, recurrent infection, most commonly in the lungs
Etiology, Epidemiology, and Incidence
TB refers only to disease caused by Mycobacterium tuberculosis, M. bovis, or M. africanum. Other mycobacteria cause diseases similar to TB
Pathogenesis
The stages of TB are primary or initial infection, latent or dormant infection, and recrudescent or adult-type TB.
Primary TB may become active at any age, producing clinical TB in any organ, most often the apical area of the lung but also the kidney, long bones, vertebrae, lymph nodes, and other sites. Often, activation occurs within 1 to 2 yr of initial infection, but may be delayed years or decades and activate after onset of diabetes mellitus, during periods of stress, after treatment with corticosteroids or other immunosuppressants, in adolescence, or in later life (> 70 yr of age), but especially after HIV infection. The initial infection leaves nodular scars in the apices of one or both lungs, called Simon foci, which are the most common seeds for later active TB. The frequency of activation seems unaffected by calcified scars of primary infection (Ghon foci) or by residual calcified hilar lymph nodes. Subtotal gastrectomy and silicosis also predispose to development of active TB.
Pulmonary Tuberculosis
recrudescent disease occurs in nodular scars in the apex of one or both lungs (Simon foci) and may spread through the bronchi to other portions
Recrudescence may occur while a primary focus of TB is still healing but is more often delayed until some other disease facilitates reactivation of the infection.
In an immunocompetent person whose tuberculin test is positive (>= 10 mm), exposure to TB rarely results in a new infection, because T-lymphocyte immunity controls small, exogenous inocula promptly and completely.
Symptoms and Signs:
Cough is the most common symptom,
At first, it is minimally productive of yellow or green mucus, usually on rising in the morning, but becomes more productive as the disease progresses
Dyspnea may result from rupture of the lung or from a pleural effusion caused by a vigorous inflammatory reaction
Hilar lymphadenopathy is the most common finding in children. due to lymphatic drainage from a small lesion, usually located in the best ventilated portions of the lung (lower and middle lobes), where most of the inhaled organisms are carried.
swelling of the nodes is common
Untreated infection may progress to miliary TB or tuberculous meningitis and, if long neglected, rarely may lead to pulmonary cavitation.
TB in the elderly presents special problems. Long-dormant infection may reactivate, most commonly in the lung but sometimes in the brain or a kidney, long bone, vertebra, lymph node, or anywhere that bacilli were seeded during the primary infection earlier in life
TB may develop when infection in an old calcific lymph node reactivates and leaks caseous material into a lobar or segmental bronchus, causing a pneumonia that persists despite broad-spectrum antibiotic therapy.
With HIV infection, progression to clinical TB is much more common and rapid.
HIV also reduces both inflammatory reaction and cavitation of pulmonary lesions. As a result, a patient's chest x-ray may be normal, even though AFB are present in sufficient numbers to show on a sputum smear. Recrudescent TB is almost always indicated when such an infection develops while the CD4+ T-lymphocyte count is >= 200/µL. By contrast, the diagnosis is usually infection by M. avium-intracellulare if the CD4+ count is < 50. The latter is noninfectious for others.
Pleural TB develops when a small subpleural pulmonary lesion ruptures, extruding caseous material into the pleural space. The most common type, serous exudate, results from rupture of a pimple-sized lesion of primary TB and contains very few organisms.
Tuberculous empyema with or without bronchopleural fistula is caused by a more massive contamination of the pleural space resulting from rupture of a large tuberculous lesion. Such a rupture allows air to escape and collapse the lung. Either type requires prompt drainage of pus and initiation of multiple drug therapy
Extrapulmonary Tuberculosis
Remote tuberculous lesions can be considered as metastases from the primary site in the lung, comparable to metastases from a primary neoplasm. TB of the tonsils, lymph nodes, abdominal organs, bones, and joints were once commonly caused by ingestion of milk infected with M. bovis.
GENITOURINARY TUBERCULOSIS
The kidney is one of the most common sites for extrapulmonary (metastatic) TB. Often after decades of dormancy, a small cortical focus may enlarge and destroy a large part of the renal parenchyma.
Salpingo-oophoritis can be a complication of primary TB after onset of menarche, when the fallopian tubes become vascular.
TUBERCULOUS MENINGITIS
Spread of TB to the subarachnoid space may occur as part of generalized dissemination through the bloodstream or from a superficial tubercle in the brain
Symptoms are fever (temperature rising to 38.3° C [101° F]), unremitting headache, nausea, and drowsiness, which may progress to stupor and coma. Stiff neck (Brudzinski's sign) and straight leg raising are inconstant but are helpful signs, if present. Stages of tuberculous meningitis are (1) clear sensorium with abnormal CSF, (2) drowsiness or stupor with focal neurologic signs, and (3) coma. Likelihood that CNS defects will become permanent increases with the stage. Symptoms may progress suddenly if the lesion causes thrombosis of a major cerebral vessel.
Diagnosis is made by examining CSF. The most helpful CSF findings include a glucose level < 1/2 that in the serum and an elevated protein level along with a pleocytosis, largely of lymphocytes. Examination of CSF by PCR is most helpful, rapid, and highly specific.
MILIARY TUBERCULOSIS
When a tuberculous lesion leaks into a blood vessel, massive dissemination of organisms may occur, causing millions of 1- to 3-mm metastatic lesions. Such spread, named miliary because the lesions resemble millet seeds, is most common in children < 4 yr and in the elderly.
TUBERCULOUS LYMPHADENITIS
In primary infection with M. tuberculosis, the infection spreads from the infected site in the lung to the hilar nodes. If the inoculum is not too large, other nodes generally are not involved. However, if the infection is not controlled, other nodes in the superior mediastinum may become involved. If organisms reach the thoracic duct, general dissemination may occur. From the supraclavicular area, nodes in the anterior cervical chain may be inoculated, thus sowing the seeds for tuberculous lymphadenitis at a later time. Most infected nodes heal, but the organisms may lie dormant and viable for years or decades and can again multiply and produce active disease.
Characteristics of Facilitated Diffusion & Active Transport
PhysiologyCharacteristics of Facilitated Diffusion & Active Transport - both require the use of carriers that are specific to particular substances (that is, each type of carrier can 'carry' one type of substance) and both can exhibit saturation (movement across a membrane is limited by number of carriers & the speed with which they move materials
The Adrenal Glands
Physiology
The Adrenal Glands
The adrenal glands are two small structures situated one at top each kidney. Both in anatomy and in function, they consist of two distinct regions:
an outer layer, the adrenal cortex, which surrounds
the adrenal medulla.
The Adrenal Cortex
cells of the adrenal cortex secrete a variety of steroid hormones.
glucocorticoids (e.g., cortisol)
mineralocorticoids (e.g., aldosterone)
androgens (e.g., testosterone)
Production of all three classes is triggered by the secretion of ACTH from the anterior lobe of the pituitary.
Glucocorticoids
They Effect by raising the level of blood sugar (glucose). One way they do this is by stimulating gluconeogenesis in the liver: the conversion of fat and protein into intermediate metabolites that are ultimately converted into glucose.
The most abundant glucocorticoid is cortisol (also called hydrocortisone).
Cortisol and the other glucocorticoids also have a potent anti-inflammatory effect on the body. They depress the immune response, especially cell-mediated immune responses.
Mineralocorticoids
The most important of them is the steroid aldosterone. Aldosterone acts on the kidney promoting the reabsorption of sodium ions (Na+) into the blood. Water follows the salt and this helps maintain normal blood pressure.
Aldosterone also
acts on sweat glands to reduce the loss of sodium in perspiration;
acts on taste cells to increase the sensitivity of the taste buds to sources of sodium.
The secretion of aldosterone is stimulated by:
a drop in the level of sodium ions in the blood;
a rise in the level of potassium ions in the blood;
angiotensin II
ACTH (as is that of cortisol)
Androgens
The adrenal cortex secretes precursors to androgens such as testosterone.
Excessive production of adrenal androgens can cause premature puberty in young boys.
In females, the adrenal cortex is a major source of androgens. Their hypersecretion may produce a masculine pattern of body hair and cessation of menstruation.
Addison's Disease: Hyposecretion of the adrenal cortices
Addison's disease has many causes, such as
destruction of the adrenal glands by infection;
their destruction by an autoimmune attack;
an inherited mutation in the ACTH receptor on adrenal cells.
Cushing's Syndrome: Excessive levels of glucocorticoids
In Cushing's syndrome, the level of adrenal hormones, especially of the glucocorticoids, is too high.It can be caused by:
excessive production of ACTH by the anterior lobe of the pituitary;
excessive production of adrenal hormones themselves (e.g., because of a tumor), or (quite commonly)
as a result of glucocorticoid therapy for some other disorder such as
rheumatoid arthritis or
preventing the rejection of an organ transplant.
The Adrenal Medulla
The adrenal medulla consists of masses of neurons that are part of the sympathetic branch of the autonomic nervous system. Instead of releasing their neurotransmitters at a synapse, these neurons release them into the blood. Thus, although part of the nervous system, the adrenal medulla functions as an endocrine gland.The adrenal medulla releases:
adrenaline (also called epinephrine) and
noradrenaline (also called norepinephrine)
Both are derived from the amino acid tyrosine.
Release of adrenaline and noradrenaline is triggered by nervous stimulation in response to physical or mental stress. The hormones bind to adrenergic receptors transmembrane proteins in the plasma membrane of many cell types.
Some of the effects are:
increase in the rate and strength of the heartbeat resulting in increased blood pressure;
blood shunted from the skin and viscera to the skeletal muscles, coronary arteries, liver, and brain;
rise in blood sugar;
increased metabolic rate;
bronchi dilate;
pupils dilate;
hair stands on end (gooseflesh in humans);
clotting time of the blood is reduced;
increased ACTH secretion from the anterior lobe of the pituitary.
All of these effects prepare the body to take immediate and vigorous action.
Selective serotonin reuptake inhibitors
Pharmacology
Selective serotonin reuptake inhibitors (SSRIs)
e.g. fluoxetine, paroxetine, citalopram, and sertraline
- Most commonly used antidepressant category
- Less likely to cause anticholinergic side effects
- Relatively safest antidepressant group in overdose
- Selectively inhibits reuptake of serotonin(5-HT)
Mode of Action;
- Well absorbed when given orally
- Plasma half-lives of 18-24 h allowing once daily dosagedaily dosage
- Metabolised through CYP450 system and most SSRIs inhibit some CYP isoforms
- Therapeutic effect is delayed for 2-4 weeks
ADVERSE DRUG REACTIONS
- Insomnia, increased anxiety, irritability
- Decreased libido
- Erectile dysfunction, anorgasmia, and ejaculatory delay
- Bleeding disorders
- Withdrawal syndrome
A dermatofibroma
General Pathology
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.
Alveolar bone (process)
Dental Anatomy
Alveolar bone (process)
1. The bone in the jaws that contains the teeth alveoli (sockets).
2. Three types of bone :
a. Cribriform plate (alveolar bone proper)
(1) Directly lines and forms the tooth socket. It is compact bone that contains many holes, allowing for the passage of blood vessels. It has no periosteum.
(2) Serves as the attachment site for PDL (Sharpey’s) fibers.
(3) The tooth socket is constantly being remodeled in response to occlusal forces. The bone laid down on the cribriform plate, which also provides attachment for PDL fibers, is known as bundle bone.
(4) It is radiographically known as the lamina dura.
b. Cortical (compact) bone
(1) Lines the buccal and lingual surfaces of the mandible and maxilla.
(2) Is typical compact bone with a periosteum and contains Haversian systems.
(3) Is generally thinner in the maxilla and thicker in the mandible, especially around the buccal area of the mandibular premolar and molar.
c. Trabecular (cancellous, spongy) bone
(1) Is typical cancellous bone containing Haversian systems.
(2) Is absent in the maxillary anterior teeth region.
3. Alveolar crest (septa)
a. The height of the alveolar crest is usually 1.5 to 2 mm below the CEJ junction.
b. The width is determined by the shape of adjacent teeth.
(1) Narrow crests—found between teeth with relatively flat surfaces.
(2) Widened crests—found between teeth with convex surfaces or teeth spaced apart.
Krebs Cycle
Biochemistry
Glycolysis enzymes are located in the cytosol of cells. Pyruvate enters the mitochondrion to be metabolized further
Mitochondrial compartments: The mitochondrial matrix contains Pyruvate Dehydrogenase and enzymes of Krebs Cycle, plus other pathways such as fatty acid oxidation.
Pyruvate Dehydrogenase catalyzes oxidative decarboxylation of pyruvate, to form acetyl-CoA
FAD (Flavin Adenine Dinucleotide) is a derivative of the B-vitamin riboflavin (dimethylisoalloxazine-ribitol). The flavin ring system undergoes oxidation/reduction as shown below. Whereas NAD+ is a coenzyme that reversibly binds to enzymes, FAD is a prosthetic group, that is permanently part of the complex.
FAD accepts and donates 2 electrons with 2 protons (2 H):
Thiamine pyrophosphate (TPP) is a derivative of thiamine (vitamin B1). Nutritional deficiency of thiamine leads to the disease beriberi. Beriberi affects especially the brain, because TPP is required for carbohydrate metabolism, and the brain depends on glucose metabolism for energy
Acetyl CoA, a product of the Pyruvate Dehydrogenase reaction, is a central compound in metabolism. The "high energy" thioester linkage makes it an excellent donor of the acetate moiety
For example, acetyl CoA functions as:
input to the Krebs Cycle, where the acetate moiety is further degraded to CO2.
donor of acetate for synthesis of fatty acids, ketone bodies, and cholesterol.
ATPs formed in TCA cycle from one molecule of Pyruvate
1. 3ATP 7. 3ATP 5. 3 ATP
8. 1 ATP 9. 2 ATP 11.3 ATP Total =15 ATP.
ATPS formed from one molecule of Acetyl CoA =12ATP
ATPs formed from one molecule of glucose after complete oxidation
One molecule of glucose -->2 molecules of pyruvate
['By glycolysis] ->8 ATP
2 molecules of pyruvate [By TCA cycle] -> 30 ATP
Total = 38 ATP