NEET MDS Synopsis
Endotracheal intubation (ETI)
Oral and Maxillofacial SurgeryEndotracheal intubation (ETI) is critical in trauma patients for securing the
airway, especially in cases of severe head injury or altered consciousness.
Statistics indicate that approximately 15% of major trauma patients require
urgent intubation, with rates varying widely from 2% to 37% depending on the
setting. Proper airway management is vital to prevent respiratory failure and
improve outcomes.
Importance of Endotracheal Intubation in Trauma Care
Endotracheal intubation (ETI) involves
placing a cuffed tube into the trachea to secure the airway, ensuring
adequate ventilation and oxygenation.
Prevalence: Studies show that between 9% and 28% of
trauma patients undergo ETI, highlighting its significance in emergency
medical care.
Consequences of Failure: The inability to secure a
definitive airway is a leading cause of preventable death in trauma cases.
Effective airway management is crucial for survival.
Indications for Endotracheal Intubation
Clinical Criteria: ETI is indicated in various
scenarios, including:
Severe head injuries with altered consciousness.
Respiratory distress or failure.
Hypoxia despite supplemental oxygen.
Hemodynamic instability (e.g., shock).
Guideline Recommendations: Current guidelines suggest
that ETI should be performed when specific clinical criteria are met, such
as:
Glasgow Coma Scale (GCS) < 9.
Persistent hypotension (systolic blood pressure < 90 mmHg).
Severe respiratory distress.
Challenges in Decision-Making
Complexity of Situations: The decision to intubate is
often complicated by factors such as:
The patient's overall condition and injury severity.
The presence of multiple indications for intubation.
The potential risks associated with the procedure, including
complications like hypoxemia and cardiovascular instability.
Variability in Practice: Despite established guidelines,
the actual intubation rates can vary significantly based on clinical
judgment and the specific circumstances of each case.
Outcomes Associated with Endotracheal Intubation
Impact on Mortality: Research indicates that patients
who undergo ETI may experience higher mortality rates, particularly if
intubation is performed in the absence of other indications. This suggests
that isolated shock may not be a sufficient criterion for intubation.
Length of Stay: Patients requiring ETI often have longer
stays in intensive care units (ICUs) and may experience more complications,
such as coagulopathy and multiple organ failure.
Greenstick Fractures of the Mandible
Oral and Maxillofacial SurgeryManagement of Greenstick/Crack Fractures of the Mandible
Greenstick fractures (or crack fractures) are incomplete
fractures that typically occur in children due to the flexibility of their
bones. Fracture in mandible, can often be managed
conservatively, especially when there is no malocclusion (misalignment of the
teeth).
Conservative Management
No Fixation Required:
For greenstick fractures without malocclusion, surgical fixation is
generally not necessary.
Closed Reduction: The fracture can be managed
through closed reduction, which involves realigning the fractured bone
without surgical exposure.
Dietary Recommendations:
Patients are advised to consume soft foods and
maintain adequate hydration with lots of fluids to
facilitate healing and minimize discomfort during eating.
Surgical Management Options
In cases where surgical intervention is required, or for more complex
fractures, the following methods can be employed:
Kirschner Wire (K-wire) Fixation:
Indications: K-wires can be used for both dentulous
(having teeth) and edentulous (without teeth) mandibles.
Technique: K-wires are inserted through the bone
fragments to stabilize the fracture. This method provides internal
fixation and helps maintain alignment during the healing process.
Circumferential Wiring:
Indications: This technique is also applicable for
both dentulous and edentulous mandibles.
Technique: Circumferential wiring involves wrapping
wire around the mandible to stabilize the fracture. This method can
provide additional support and is often used in conjunction with other
fixation techniques.
External Pin Fixation:
Indications: Primarily used for edentulous
mandibles.
Technique: External pin fixation involves placing
pins into the bone that are connected to an external frame. This method
allows for stabilization of the mandible while avoiding intraoral
fixation, which can be beneficial in certain clinical scenarios.
DYSPLASIA
General Pathology
DYSPLASIA
It is disturbed growth or cells in regard to their size, shape arrangement. In its mild degrees it represents a reversible reaction to chronic inflammation whereas the most severe degrees warrant a labelling of intraepithelial neoplasia. Hence it includes a wide spectrum of changes ranging from a reversible disorientation to 'carcinoma-in-situ'.
Histologically it is characterized by:
o Basal cell hyperplasia.
o Variation in size and shape of cells.
o Disorderly maturation.
o Increased mitotic activity.
o Disorientation of arrangement of cells (loss of polarity)
Dysplasia is commonly seen in:
o Squamous epithelium of cervix.
o Bronchial epithelium in habitual smokers.
o Gastric and colonic mucosa in long standing inflammation
o Oral and vulval leucoplakia
SHOCK
General Surgery
SHOCK
Shock is defined as a pathological state causing inadequate oxygen delivery to the peripheral tissues and resulting in lactic acidosis, cellular hypoxia and disruption of normal metabolic condition.
CLASSIFICATION
Shock is generally classified into three major categories:
1. Hypovolemic shock
2. Cardiogenic shock
3. Distributive shock
Distributive shock is further subdivided into three subgroups:
a. Septic shock
b. Neurogenic shock
c. Anaphylactic shock
Hypovolemic shock is present when marked reduction in oxygen delivery results from diminished cardiac output secondary to inadequate vascular volume. In general, it results from loss of fluid from circulation, either directly or indirectly.
e.g. ? Hemorrhage
• Loss of plasma due to burns
• Loss of water and electrolytes in diarrhea
• Third space loss (Internal fluid shift into inflammatory exudates in
the peritoneum, such as in pancreatitis.)
Cardiogenic shock is present when there is severe reduction in oxygen delivery secondary to impaired cardiac function. Usually it is due to myocardial infarction or pericardial tamponade.
Septic Shock (vasogenic shock) develops as a result of the systemic effect of infection. It is the result of a septicemia with endotoxin and exotoxin release by gram-negative and gram-positive bacteria. Despite normal or increased cardiac output and oxygen delivery, cellular oxygen consumption is less than normal due to impaired extraction as a result of impaired metabolism.
Neurogenic shock results primarily from the disruption of the sympathetic nervous system which may be due to pain or loss of sympathetic tone, as in spinal cord injuries.
PATHO PHYSIOLOGY OF SHOCK
Shock stimulates a physiologic response. This circulatory response to hypotension is to conserve perfusion to the vital organs (heart and brain) at the expense of other tissues. Progressive vasoconstriction of skin, splanchnic and renal vessels leads to renal cortical necrosis and acute renal failure. If not corrected in time, shock leads to organ failure and sets up a vicious circle with hypoxia and acidosis.
CLINICAL FEATURES
The clinical presentation varies according to the cause. But in general patients with hypotension and reduced tissue perfusion presents with:
• Tachycardia
• Feeble pulse
• Narrow pulse pressure
• Cold extremities (except septic shock)
• Sweating, anxiety
• Breathlessness / Hyperventilation
• Confusion leading to unconscious state
PATHO PHYSIOLOGY OF SHOCK
Shock stimulates a physiologic response. This circulatory response to hypotension is to conserve perfusion to the vital organs (heart and brain) at the expense of other tissues. Progressive vasoconstriction of skin, splanchnic and renal vessels leads to renal cortical necrosis and acute renal failure. If not corrected in time, shock leads to organ failure and sets up a vicious circle with hypoxia and acidosis.
CLINICAL FEATURES
The clinical presentation varies according to the cause. But in general patients with hypotension and reduced tissue perfusion presents with:
• Tachycardia
• Feeble pulse
• Narrow pulse pressure
• Cold extremities (except septic shock)
• Sweating, anxiety
• Breathlessness / Hyperventilation
• Confusion leading to unconscious state
Production of Hormones
Physiology
Production of Hormones
The kidneys produce and interact with several hormones that are involved in the control of systems outside of the urinary system.
Calcitriol. Calcitriol is the active form of vitamin D in the human body. It is produced by the kidneys from precursor molecules produced by UV radiation striking the skin. Calcitriol works together with parathyroid hormone (PTH) to raise the level of calcium ions in the bloodstream. When the level of calcium ions in the blood drops below a threshold level, the parathyroid glands release PTH, which in turn stimulates the kidneys to release calcitriol. Calcitriol promotes the small intestine to absorb calcium from food and deposit it into the bloodstream. It also stimulates the osteoclasts of the skeletal system to break down bone matrix to release calcium ions into the blood.
Erythropoietin. Erythropoietin, also known as EPO, is a hormone that is produced by the kidneys to stimulate the production of red blood cells. The kidneys monitor the condition of the blood that passes through their capillaries, including the oxygen-carrying capacity of the blood. When the blood becomes hypoxic, meaning that it is carrying deficient levels of oxygen, cells lining the capillaries begin producing EPO and release it into the bloodstream. EPO travels through the blood to the red bone marrow, where it stimulates hematopoietic cells to increase their rate of red blood cell production. Red blood cells contain hemoglobin, which greatly increases the blood’s oxygen-carrying capacity and effectively ends the hypoxic conditions.
Renin. Renin is not a hormone itself, but an enzyme that the kidneys produce to start the renin-angiotensin system (RAS). The RAS increases blood volume and blood pressure in response to low blood pressure, blood loss, or dehydration. Renin is released into the blood where it catalyzes angiotensinogen from the liver into angiotensin I. Angiotensin I is further catalyzed by another enzyme into Angiotensin II.
Angiotensin II stimulates several processes, including stimulating the adrenal cortex to produce the hormone aldosterone. Aldosterone then changes the function of the kidneys to increase the reabsorption of water and sodium ions into the blood, increasing blood volume and raising blood pressure. Negative feedback from increased blood pressure finally turns off the RAS to maintain healthy blood pressure levels.
Cholecystitis
General Pathology
Cholecystitis
It is inflammation of the gall bladder. It may be acute or chronic.
In 80-90% of cases, it is associated with gall stones (Calcular cholecystis).
Causes and pathogenesis:-
Obstruction of cystic or common bile duct- By stones, strictures, pressure from the outside, tumors etc.
Obstruction , chemical irritation of the gall bladder, Secondary bacterial infection, stone formation, trauma to the wall of gall
bladder
Secondary bacterial infection
Usually by intestinal commensals E.coli, streptococcus fecalis. They reach the gall bladder by lymphatics.
S.typhi reaches the gall bladder after systemic infection
Acute cholecystitis
Gall bladder is enlarged edematous and fiery red in color.
- Wall is edematous, hyperemic, may show abscesses or gangrenous dark brown or green or black foci which may perforate.
Serous covering show fibrinosuppurative inflammation and exudation. Mucosa is edematous, hyperemic and ulcerated.
- If associated with stones, obstruction results in accumulation of pus leading to Empyaema of the gall bladder.
Fate:- Healing by fibrosis and adhesions.
Complications:-
- Pericholecystic abscess.
- Rupture leading to acute peritonitis.
- Ascending suppurative cholangitis and liver abscess
Chronic cholecystitis
May follow Acute cholecystitis or starts chronic. Gall stones are usually present.
Pathology
1. If associated with obstruction: Gall bladder is dilated. Wall may be thickened or thinned out. Contents may be clear, turbid or purulent.
2. If not associated with obstruction: - Gall bladder is contracted, wall is markedly thickened.
3. Serosa is smooth with fibrous adhesions. Draining lymph nodes are enlarged.
4. Wall is thickened, opaque and gray-white with red tinge.
5. Mucosa is gray- red with ulcerations and pouches.
6. Stones are usually present
Speech
Anatomyo English: all speech sounds produced by making exhaled air audible
o Two ways of producing sound
at larynx
further up in vocal tract (tongue, lips)
o How to produce sound at larynx
changes in breathing: regulate airstream from lungs to atmosphere by changing movements of vocal folds, pharynx, soft-palate, tongue, lips and jaws
• inhalation: take in greater volume more quickly, abduct folds
• expiration: variable force; use muscles of inhalation to control rate of expiration, adduct
How to vibrate vocal cords
• NOT rhythmic contraction of laryngeal muscles: would be impossible b/c frequenceies of virbration
• Changes in air pressure cause vibrations
o Adduct folds increase in subglottal pressure force folds apart folds sucked back together (Bernouilli effect)
• The vibration of vocal cords disturbs airareas of low pressure (rarefaction) alternating with areas of high pressure (compression)
• Changes in pressure sound at ears
• Sine waves
o Changes in amplitudes: loudness
o Changes in frequency: pitch
o Normal sounds have fundamental frequency, overtones or harmonics
o Mass of folds: critical in voice
Low pitch of lion’s roar: due to massive fibrous pad that forms part of vocal cords
Men: more massive vocal cords
Larger foldsslow vibrationdeeper voice
o Producing vowels and constants
Most vowels are “voiced”: vocal folds produce sounds
Consonants: can be “voiced” (Z) or “non-voiced” (S)
• Use higher regions of vocal tract to control by stopping, restricting airflow from vocal folds; use lips, teethaperiodic sound
o Vocal folds and resonators emphasize and deemphasize certain frequencies
Never hear sounds produced at vocal foldsevery sound changed by passage thru vocal tract: sinuses/resonating chambers
Howling monkeys: large hyoid bonepowerful resonator
o Age-related changes in voice
Infant larynx is smaller, different proportions
• Arytenoids are proportionately larger
• Smaller vocal apparatushigher pitch
• Larynx sits higher easier to breathe thru nose
Abrupt change in larynx at pubertycan’t control voice
Older adult: normal degenerative changes in lamina propria, ossification of thyroid cartilagechanges in fundamental frequency
Lose your voice vocal fold are irritated
• Can’t adduct foldsair escapes
o Singing v. speaking
Singing: greater thoracic pressure and uneven breathing with changes in resonators
o Whispering
Intercartilaginous portions of vocal folds: open to allow air to escapelesser subglottal pressureslittle vibration of foldslittle tonal quality, low volume
o Falsetto
Allowing only part of vocal folds to vibrate
Increase range by training which part of vocal folds to vibrate
o Colds
Mucus secretions add mass to folds—decrease in pitch, can’t adduct folds as well
o Surgeryscars, fibrotic changes can interfere with voice
FUNGAL INFECTION- Aspergillosis
General Pathology
FUNGAL INFECTION
Aspergillosis
Opportunistic infections caused by Aspergillus sp and inhaled as mold conidia, leading to hyphal growth and invasion of blood vessels, hemorrhagic necrosis, infarction, and potential dissemination to other sites in susceptible patients.
Symptoms and Signs: Noninvasive or, rarely, minimally locally invasive colonization of preexisting cavitary pulmonary lesions also may occur in the form of fungus ball (aspergilloma) formation or chronic progressive aspergillosis.
Primary superficial invasive aspergillosis is uncommon but may occur in burns, beneath occlusive dressings, after corneal trauma (keratitis), or in the sinuses, nose, or ear canal.
Invasive pulmonary aspergillosis usually extends rapidly, causing progressive, ultimately fatal respiratory failure unless treated promptly and aggressively. A. fumigatus is the most common causative species.
Extrapulmonary disseminated aspergillosis may involve the liver, kidneys, brain, or other tissues and is usually fatal. Primary invasive aspergillosis may also begin as an invasive sinusitis, usually caused by A. flavus, presenting as fever with rhinitis and headache