NEET MDS Synopsis
Candidiasis
General Pathology
Systemic Candidiasis (Candidosis; Moniliasis)
Invasive infections caused by Candida sp, most often C. albicans, manifested by fungemia, endocarditis, meningitis, and/or focal lesions in liver, spleen, kidneys, bone, skin, and subcutaneous or other tissues.
Infections due to Candida sp account for about 80% of all major systemic fungal infections.
Symptoms and Signs
Esophagitis is most often manifested by dysphagia. Symptoms of respiratory tract infections are nonspecific, such as cough. Vaginal infections cause itching, burning, and discharge. Candidemia usually causes fever, but other symptoms are typically nonspecific. Sometimes, a syndrome develops resembling bacterial sepsis, with a fulminating course that may include shock, oliguria, renal shutdown, and disseminated intravascular coagulation.
Hematogenous endophthalmitis starts as white retinal plaques that can cause blindness as destructive inflammation progresses, extending to opacify the vitreous and causing potentially irreversible scarring. Most often, there are no symptoms in early stages of Candida endophthalmitis. If treatment is not begun before symptoms appear, significant or even total loss of vision is likely to occur in the affected eye. In neutropenic patients, eye involvement is more often manifested by retinal hemorrhages; papulonodular, erythematous, and vasculitic skin lesions may also develop.
Streptococcal pharyngitis
General Pathology
Streptococcal pharyngitis:
A disease of young people, enlarged lymphoid nodules and keratin plugs in the tonsillar pits is seen Complications include retro-pharyngeal abscess (quinsy)
Cellulitis of the deep tissues of the neck is Ludwig's angina
Scarlet fever ("scarlatina") is a strep throat caused by a streptococcus with the gene to make one of the erythrogenic toxins, Patients have a rash with PMNs
Streptococcal skin infections (Impetigo)
Erysipelas is a severe skin infection caused by group A strep; geographic of red, thickened, indurated areas of the skin are characteristic. Unlike staph infections, there is usually little or no tissue necrosis
Post-streptococcal hypersensitivity diseases include rheumatic fever, post-streptococcal glomerulonephritis, and some cases of erythema nodosum
Pyelonephritis
General Pathology
Pyelonephritis
- A bacterial infection that affects the renal tubules, interstitium, and renal pelvis.
- One of the most common renal diseases.
- Usually caused by gram-negative, rod-shaped bacteria that are part of the normal flora of the enteric tract. Most commonly caused by Escherichia coli, followed by Proteus, Klebsiella, and Enterobacter.
- The infecting bacteria are usually from the patient’s own enteric flora an example of an endogenous infection.
- Usually associated with a urinary tract infection (acute pyelonephritis) or involved with another precipitating condition, such as obstruction (chronic pyelonephritis).
Amelogenesis Imperfecta
PedodonticsClassification of Amelogenesis Imperfecta
Amelogenesis imperfecta (AI) is a group of genetic conditions that affect the
development of enamel, leading to various enamel defects. The classification of
amelogenesis imperfecta is based on the phenotype of the enamel and the mode of
inheritance. Below is a detailed classification of amelogenesis imperfecta.
Type I: Hypoplastic
Hypoplastic amelogenesis imperfecta is characterized by a deficiency in the
amount of enamel produced. The enamel may appear thin, pitted, or smooth,
depending on the specific subtype.
1A: Hypoplastic Pitted
Inheritance: Autosomal dominant
Description: Enamel is pitted and has a rough
surface texture.
1B: Hypoplastic, Local
Inheritance: Autosomal dominant
Description: Localized areas of hypoplasia
affecting specific teeth.
1C: Hypoplastic, Local
Inheritance: Autosomal recessive
Description: Similar to 1B but inherited in an
autosomal recessive manner.
1D: Hypoplastic, Smooth
Inheritance: Autosomal dominant
Description: Enamel appears smooth with a lack of
pits.
1E: Hypoplastic, Smooth
Inheritance: Linked dominant
Description: Similar to 1D but linked to a dominant
gene.
1F: Hypoplastic, Rough
Inheritance: Autosomal dominant
Description: Enamel has a rough texture with
hypoplastic features.
1G: Enamel Agenesis
Inheritance: Autosomal recessive
Description: Complete absence of enamel on affected
teeth.
Type II: Hypomaturation
Hypomaturation amelogenesis imperfecta is characterized by enamel that is
softer and more prone to wear than normal enamel, often with a mottled
appearance.
2A: Hypomaturation, Pigmented
Inheritance: Autosomal recessive
Description: Enamel has a pigmented appearance,
often with brown or yellow discoloration.
2B: Hypomaturation
Inheritance: X-linked recessive
Description: Similar to 2A but inherited through
the X chromosome.
2D: Snow-Capped Teeth
Inheritance: Autosomal dominant
Description: Characterized by a white, snow-capped
appearance on the incisal edges of teeth.
Type III: Hypocalcified
Hypocalcified amelogenesis imperfecta is characterized by enamel that is
poorly mineralized, leading to soft, chalky teeth that are prone to rapid wear
and caries.
3A:
Inheritance: Autosomal dominant
Description: Enamel is poorly calcified, leading to
significant structural weakness.
3B:
Inheritance: Autosomal recessive
Description: Similar to 3A but inherited in an
autosomal recessive manner.
Type IV: Hypomaturation, Hypoplastic with Taurodontism
This type combines features of both hypomaturation and hypoplasia, along with
taurodontism, which is characterized by elongated pulp chambers and short roots.
4A: Hypomaturation-Hypoplastic with Taurodontism
Inheritance: Autosomal dominant
Description: Enamel is both hypoplastic and
hypomature, with associated taurodontism.
4B: Hypoplastic-Hypomaturation with Taurodontism
Inheritance: Autosomal dominant
Description: Similar to 4A but with a focus on
hypoplastic features.
Umbilical cord prolapse
Obstetrics and Gynaecology
Umbilical cord prolapse
acute, life-threatening emergency for the fetus, in which a part of the umbilical cord lies between the antecedent part of the fetus (mostly head) and the pelvic wall, causing rupture of membranes
Epidemiology: rare (0.5% births)
Etiology: often seen in presentation anomalies (e.g., breech presentation, transverse fetal position), multiple pregnancy, long umbilical cord, or abnormal fetal movement (polyhydramnios, premature birth)
Clinical features: -
- an abrupt change from a previously normal CTG to one with fetal bradycardia or recurrent,
- severe decelerations,
- occuring after the rupture of membranes
Diagnostics: vaginal palpation → thick, pulsating cord is palpable
Treatment: Trendelenburg position; fetus is pushed back into the uterus; immediate tocolysis using β2-mimetics (e.g., fenoterol) → emergency cesarean section
CHARACTERISTICS AND CHEMISTRY OF HORMONES
Physiology
Each hormone in the body is unique. Each one is different in it's chemical composition, structure, and action. With respect to their chemical structure, hormones may be classified into three groups: amines, proteins, and steroids.
Amines- these simple hormones are structural variation of the amino acid tyrosine. This group includes thyroxine from the thyroid gland and epinephrine and norepinephrine from the adrenal medulla.
Proteins- these hormones are chains of amino acids. Insulin from the pancreas, growth hormone from the anterior pituitary gland, and calcitonin from the thyroid gland are all proteins. Short chains of amino acids are called peptides. Antidiuretic hormone and oxytocin, synthesized by the hypothalamus, are peptide hormones.
Steroids- cholesterol is the precursor for the steroid hormones, which include cortisol and aldosterone from the adrenal cortex, estrogen and progesterone from the ovaries, and testosterone from the testes.
Growth Spurts
PedodonticsGrowth Spurts in Children
Growth in children does not occur at a constant rate; instead, it is
characterized by periods of rapid increase known as growth spurts.
These spurts are significant phases in physical development and can vary in
timing and duration between individuals, particularly between boys and girls.
Growth Spurts: Sudden increases in growth that occur at
specific times during development. These spurts are crucial for overall
physical development and can impact various aspects of health and
well-being.
Timing of Growth Spurts
The timing of growth spurts can be categorized into several key periods:
Just Before Birth
Description: A significant growth phase occurs in
the fetus just prior to birth, where rapid growth prepares the infant
for life outside the womb.
One Year After Birth
Description: Infants experience a notable growth
spurt during their first year of life, characterized by rapid increases
in height and weight as they adapt to their new environment and begin to
develop motor skills.
Mixed Dentition Growth Spurt
Timing:
Boys: 8 to 11 years
Girls: 7 to 9 years
Description: This growth spurt coincides with the
transition from primary (baby) teeth to permanent teeth. It is a
critical period for dental development and can influence facial growth
and the alignment of teeth.
Adolescent Growth Spurt
Timing:
Boys: 14 to 16 years
Girls: 11 to 13 years
Description: This is one of the most significant
growth spurts, marking the onset of puberty. During this period, both
boys and girls experience rapid increases in height, weight, and muscle
mass, along with changes in body composition and secondary sexual
characteristics.
The small intestine
PhysiologyThe small intestine
Digestion within the small intestine produces a mixture of disaccharides, peptides, fatty acids, and monoglycerides. The final digestion and absorption of these substances occurs in the villi, which line the inner surface of the small intestine.
This scanning electron micrograph (courtesy of Keith R. Porter) shows the villi carpeting the inner surface of the small intestine.
The crypts at the base of the villi contain stem cells that continuously divide by mitosis producing
more stem cells
cells that migrate up the surface of the villus while differentiating into
columnar epithelial cells (the majority). They are responsible for digestion and absorption.
goblet cells, which secrete mucus;
endocrine cells, which secrete a variety of hormones;
Paneth cells, which secrete antimicrobial peptides that sterilize the contents of the intestine.
All of these cells replace older cells that continuously die by apoptosis.
The villi increase the surface area of the small intestine to many times what it would be if it were simply a tube with smooth walls. In addition, the apical (exposed) surface of the epithelial cells of each villus is covered with microvilli (also known as a "brush border"). Thanks largely to these, the total surface area of the intestine is almost 200 square meters, about the size of the singles area of a tennis court and some 100 times the surface area of the exterior of the body.
Incorporated in the plasma membrane of the microvilli are a number of enzymes that complete digestion:
aminopeptidases attack the amino terminal (N-terminal) of peptides producing amino acids.
disaccharidasesThese enzymes convert disaccharides into their monosaccharide subunits.
maltase hydrolyzes maltose into glucose.
sucrase hydrolyzes sucrose (common table sugar) into glucose and fructose.
lactase hydrolyzes lactose (milk sugar) into glucose and galactose.
Fructose simply diffuses into the villi, but both glucose and galactose are absorbed by active transport.
fatty acids and monoglycerides. These become resynthesized into fats as they enter the cells of the villus. The resulting small droplets of fat are then discharged by exocytosis into the lymph vessels, called lacteals, draining the villi.