NEET MDS Synopsis
The Arteries of the Face
AnatomyThe Arteries of the Face
The superficial arteries are derived from the external carotid arteries.
The Facial Artery
This is the chief artery of the face.
It arises from the external carotid artery and winds its way to the inferior border of the mandible, just anterior to the masseter muscle.
It hooks around the inferior border of the mandible and grooves the bone. Here the artery is superficial, just beneath the platysma and its pulsation can be felt.
In its course over the face to the medial angle of the eye, the facial artery crosses the mandible, buccinator muscle, and maxilla.
It lies deep to the zygomaticus major.
The facial artery ends by sending branches to the lip and side of the nose.
The part of the artery that runs along the side of the nose to supply the eyelids is called the angular artery.
The Superficial Temporal Artery
This artery is the smaller of the two terminal branches of the external carotid artery (the other is the maxillary artery).
It begins deep to the parotid gland, posterior to the neck of the mandible, and ascends superficial to the posterior end of the zygomatic process of the temporal bone. It then enters the temporal fossa.
The superficial temporal artery ends in the scalp by dividing into the frontal and parietal branches.
Pulsation of this artery can be felt by compressing the root of the zygomatic process of the temporal bone.
The Transverse Facial Artery
This small artery arises from the superficial temporal artery before it emerges from the parotid gland.
It crosses the face superficial to the masseter muscle, about a fingerbreadth inferior to the zygomatic arch.
It divides into numerous branches that supply the parotid gland and duct, the masseter muscle, and the skin of the face.
It anastomoses with branches of the facial artery.
Autosomal Recessive Diseases List
Pathology
Abetalipoproteinemia: decrease ApoB-48, Apo B-100; pigmentary degeneration of retina, acanthocytes, steatorrhea, cerebellar ataxia.
Acute Fatty Liver of Pregnancy: microvesicular steatosis in the liver, mitochondrial dysfunction in the oxidation of fatty acids leading to an accumulation in hepatocytes
Alkaptonuria: homogentisate oxidase deficiency, increase homogenistic acid, ochronosis, dark blue urine.
AcylCoA Dehydrogenase deficiency (MCAD): fasting hypoglycemia, no ketone bodies, dicarboxilic acidemia.
Bernard Soulier Sd: gp1b deficiency, prolonged bleeding time
Bloom Sd: chromosome 15, Ashkenazi Jews, BLM gene.
Carpenter Sd: craniosynostosis, acrocephaly, craniofacial asymmetry, increased ICP, cutaneous syndactyly, polydactily, mild-profound MR.
Chediak Higashi Sd: Lyst gene mutation, microtubule polymerization defect, no phagolysosome formation, albinism.
Chondrodystrophy: normal-sized trunk and abnormally short limbs and extremities (dwarfism)
Congenital Adrenal Hyperplasia: 17alpha or 21beta or 11 beta hydroxylase deficiency; enlargemente od adrenal glands due to increase ACTH
Congenital Hepatic Fibrosis: hepatic (periporta) fibrosis, irregularly shaped proliferating bile duct, portal hypertension, renal cystic disease.
Cystic Fibrosis: CFTR gene, Phe508, defective Chloride channel, chromosome 7.
Dubin-Johnson Sd: direct hyperBbnemia, cMOAT deficiency, black liver
Endocardial Fibroelastosis: restrictive/infiltrative cardiomyopathy, thick fibroelastic tissue in endocardium of young children, <2yo
Familial Mediterranean Fever: chromosome 16, recurrent autoinflammatory disease, characterized by F°, PMN disfx, sudden attacks pain/inflammation (7 types of attacks (abdominal, joints, chest, scrotal, myalgias, erysipeloid, fever). Complication: AA-amyloidosis
Fanconi Anemia: genetic loss of DNA crosslink repair, often progresses to AML, short stature, ↑incidence of tumors/leukemia, aplastic anemia
Friedreich’s Ataxia: GAA triplet repeat, chromosome 9, neuronal degeneration, progressive gait & limb ataxia, arreflexia, hypertrophic cardiomyopathy, axonal sensory neuropathy, kyphoscoliosis, dysarthria, hand clumsiness, loss of sense of position, impaired vibratory sensation.
Gaucher’s disease: glucocerebrosidase deficiency, glucocerebroside accumulation, femur necrosis, crumpled paper inclusions in macrophages.
Ganzman’s thromboasthenia: gpIIbIIIa deficiency, deficient platelet aggregation.
Hartnup Disease: tryptophan deficiency, leads to niacin deficiency, pellagra-like dermatosis
Hemochromatosis: HFE gene, C282Y MC mutation, chromosome 6, unrestricted reabsorption of Fe+ in SI, iron deposits in organs, bronze diabetes, DM1, malabsorption, cardiomyopathy, joint degeneration, increased iron, ferritin, TIBC. Complications: liver cirrhosis, hepatocelullar carcinoma
Homocystinuria: due to B6 deficiency (defective Cystathionine synthase) or due to B9,B12 deficiency (defective Homocysteine Methyltrasnferase), dislocated lenses (in & down), DVT, stroke, atherosclerosis, MR.
Krabbe's Disease: Galactocerebrosidase deficiency, galactocerebroside accumulation, gobloid cells, optic atrophy, peripheral neuropathy.
Leukocyte Adhesion Defect (LAD): CD-18+ deficiency, omphalitis in newborns, chronic recurrent bacterial infxs, increase WBC count, no abscess or pus formation.
Metachromic Leukodystrophy: Aryl-sulfatase A deficiency, sulfatides accumulation, Demyelination (central & peripheral), Ataxia, Demantia (DAD)
Niemann-Pick Disease: sphingomyelinase deficiency, sphingomyelin accumulation, HSM, cherry-red macula, foam cells.
Phenylketonuria (PKU): phenylalanine hydroxylase deficiency, Phe accumulation, MR, microcephaly, diet low in Phe!!! also in pregnancy, avoid aspartame, musty odor.
Polycystic Kidney Disease (children): ARPKD, rogressive & fatal renal failure, multiple enlarged cysts perpendicualr to renal capsule, association with liver cysts. Bilateral palpable mass.
Rotor Sd: direct hyperBbnemia, cMOAT deficiency, no black liver
Shwaman Diamond Sd: exocrine pancreatic insufficiency (2°MCC in children after CF), bone marrow dysfunction, skeletal abnormalities, short stature.
Situs inversus: assoc w/ Kartagener sd
Sicke Cell Disease and Trait: Hb S, beta globin chain, chromosome 11, position 6, nucleotide codon change (glutamic acid --> valine), vaso-occlusive crisis (pain), autosplenectomy, acute chest pain sd, priapism, hand-foot sd, leg ulcers, aplastic crisis, drepanocytes & Howell-Jolly bodies, hemolytic anemia, jaundice, bone marrow hyperplasia
Tay-Sachs Disease: Hexoaminidase A deficiency, GM2 accumulation, cherry-red macula, onion skin lysosomes.
Thalasemia: alpha (chromosome 16, gene deletion), beta (chromosome 11, point mutation)
Werner Disease: adult progeria
Wilson’s Disease: Chromosome 13, WD gene, ATP7B gene (encondes for Copper transporting ATPase), copper accumulation in liver, brain (putamen), eyes (Descemet membrane - Kayser-Fleischer ring), decreased ceruloplasmin.
Xeroderma Pigmentosa: defective excision endonuclease, no repair of thymine dymers caused by UV radiation, excessive freckling, multiple skin cancers.
Walsham’s Forceps
General SurgeryWalsham’s Forceps
Walsham’s forceps are specialized surgical instruments used
primarily in the manipulation and reduction of fractured nasal fragments. They
are particularly useful in the management of nasal fractures, allowing for
precise adjustment and stabilization of the bone fragments during the reduction
process.
Design:
Curved Blades: Walsham’s forceps feature two curved
blades—one padded and one unpadded. The curvature of the blades allows
for better access and manipulation of the nasal structures.
Padded Blade: The padded blade is designed to
provide a gentle grip on the external surface of the nasal bone and
surrounding tissues, minimizing trauma during manipulation.
Unpadded Blade: The unpadded blade is inserted into
the nostril and is used to secure the internal aspect of the nasal bone
and associated fragments.
Usage:
Insertion: The unpadded blade is carefully passed
up the nostril to reach the fractured nasal bone and the associated
fragment of the frontal process of the maxilla.
Securing Fragments: Once in position, the nasal
bone and the associated fragment are secured between the padded blade
externally and the unpadded blade internally.
Manipulation: The surgeon can then manipulate the
fragments into their correct anatomical position, ensuring proper
alignment and stabilization.
Indications:
Walsham’s forceps are indicated for use in cases of nasal fractures,
particularly when there is displacement of the nasal bones or associated
structures. They are commonly used in both emergency and elective
settings for nasal fracture management.
Advantages:
Precision: The design of the forceps allows for
precise manipulation of the nasal fragments, which is crucial for
achieving optimal alignment and aesthetic outcomes.
Minimized Trauma: The padded blade helps to reduce
trauma to the surrounding soft tissues, which can be a concern during
the reduction of nasal fractures.
Postoperative Considerations:
After manipulation and reduction of the nasal fragments, appropriate
postoperative care is essential to monitor for complications such as
swelling, infection, or malunion. Follow-up appointments may be
necessary to assess healing and ensure that the nasal structure remains
stable.
Ketone Body
Biochemistry
During fasting or carbohydrate starvation, oxaloacetate is depleted in liver because it is used for gluconeogenesis. This impedes entry of acetyl-CoA into Krebs cycle. Acetyl-CoA then is converted in liver mitochondria to ketone bodies, acetoacetate and b-hydroxybutyrate.
Three enzymes are involved in synthesis of ketone bodies:
b-Ketothiolase. The final step of the b-oxidation pathway runs backwards, condensing 2 acetyl-CoA to produce acetoacetyl-CoA, with release of one CoA.
HMG-CoA Synthase catalyzes condensation of a third acetate moiety (from acetyl-CoA) with acetoacetyl-CoA to form hydroxymethylglutaryl-CoA (HMG-CoA).
HMG-CoA Lyase cleaves HMG-CoA to yield acetoacetate plus acetyl-CoA.
b-Hydroxybutyrate Dehydrogenase catalyzes inter-conversion of the ketone bodies acetoacetate and b-hydroxybutyrate.
Ketone bodies are transported in the blood to other tissue cells, where they are converted back to acetyl-CoA for catabolism in Krebs cycle
Tetracycline
Pharmacology
Tetracycline
Tetracycline is an antibiotic produced by the streptomyces bacterium
Mechanism and Resistance Tetracycline inhibits cell growth by inhibiting translation. It binds to the 30S ribosomal subunit and prevents the amino-acyl tRNA from binding to the A site of the ribosome. This prevents the addition of amino acids to the elongating peptide chain, preventing synthesis of proteins. The binding is reversible in nature.
Example: Chlortetracycline, oxytetracycline, demethylchlortetracycline, rolitetracycline, limecycline, clomocycline, methacycline, doxycycline, minocycline
Source: Streptomyces spp.; some are also semi-synthetic
Spectrum of activity: Broad-spectrum. Exhibits activity against a wide range of Gram-positive, Gram-negative bacteria, atypical organisms such as chlamydiae, mycoplasmas, rickettsiae and protozoan parasites.
Effect on bacteria: Bacteriostatic
Cells become resistant to tetracyline by at least two mechanisms: efflux and ribosomal protection.
Contraindications Tetracycline use should be avoided during pregnancy and in the very young (less than 6 years) because it will result in permanent staining of teeth causing an unsightly cosmetic result.
Tetracyclines also become dangerous past their expiration dates. While most prescription drugs lose potency after their expiration dates, tetracyclines are known to become toxic over time; expired tetracyclines can cause serious damage to the kidneys.
Miscellaneous: Tetracyclines have also been used for non-antibacterial purposes, having shown properties such as anti-inflammatory activity, immunosuppresion, inhibition of lipase and collagenase activity, and wound healing.
PERTUSSIS
General Pathology
PERTUSSIS (Whooping Cough)
An acute, highly communicable bacterial disease caused by Bordetella pertussis and characterized by a paroxysmal or spasmodic cough that usually ends in a prolonged, high-pitched, crowing inspiration (the whoop).
Transmission is by aspiration of B. pertussis
Symptoms and Signs
The incubation period averages 7 to 14 days (maximum, 3 wk). B. pertussis invades the mucosa of the nasopharynx, trachea, bronchi, and bronchioles, increasing the secretion of mucus, which is initially thin and later viscid and tenacious. The uncomplicated disease lasts about 6 to 10 wk and consists of three stages: catarrhal, paroxysmal, and convalescent.
Dissociation constants
Pharmacology
Dissociation constants
Local anesthetic
pKa
% of base(RN) at pH 7.4
onset of action(min)
Lidocaine
7.8
29
2-4
Bupivacaine
8.1
17
5-8
Mepivacaine
7.7
33
2-4
Prilocaine
7.9
25
2-4
Articaine
7.8
29
2-4
Procaine
9.1
2
14-18
Benzocaine
3.5
100
-
Valvular disease
General Pathology
Valvular disease
A. Generally, there are three types:
1. Stenosis—fibrotic, stiff, and thickened valves, resulting in reduced blood flow through the valve.
2. Regurgitation or valvular insufficiency— valves are unable to close completely, allowing blood to regurgitate.
3. Prolapse—“floppy” valves; may occur with or without regurgitation. The most common valvular defect.