NEET MDS Synopsis
Jaundice
General Pathology
Jaundice, or icterus
a. Characterized by yellowness of tissues, including skin, eyes, and mucous membranes.
b. Caused by excess conjugated and/or unconjugated serum bilirubin. (increased levels of bilirubin in the blood)
lcterus is visible when the serum bilirubin exceeds 2 mg/dl. In unconjugated hyperbilirubinemia, bilirubin is not excreted into the urine because of tight protein binding in serum. In conjugated hyperbilirubinemia, small amounts of bilirubin are excreted in the urine because
it is less tightly protein bound.
NOTE: Concentration of bilirubin in blood plasma does not normally exceed 1 mg/dL (>17µmol/L). A concentration higher than 1.8 mg/dL (>30µmol/L) leads to jaundice.
The conjunctiva of the eye are one of the first tissues to change color as bilirubin levels rise in jaundice. This is sometimes referred to as scleral icterus.
c. Types and causes include:
(1) Hepatocellular jaundice—caused by liver diseases such as cirrhosis and hepatitis.
(2) Hemolytic jaundice—caused by hemolytic anemias.
(3) Obstructive jaundice—caused by blockage of the common bile duct either by gallstones (cholelithiasis) or carcinomas involving the head of
the pancreas.
Differential diagnosis
Jaundice is classified into three categories, depending on which part of the physiological mechanism the pathology affects. The three categories are:
Pre-hepatic → The pathology is occurring prior to the liver.
Hepatic → The pathology is located within the liver.
Post-Hepatic → The pathology is located after the conjugation of bilirubin in the liver.
Pre-hepatic
Pre-hepatic jaundice is caused by anything which causes an increased rate of hemolysis (breakdown of red blood cells).
Certain genetic diseases, such as sickle cell anemia, spherocytosis, thalassemia and glucose 6-phosphate dehydrogenase deficiency can lead to increased red cell lysis and therefore hemolytic jaundice.
Commonly, diseases of the kidney, such as hemolytic uremic syndrome, can also lead to coloration. Defects in bilirubin metabolism also
present as jaundice, as in Gilbert's syndrome (a genetic disorder of bilirubin metabolism which can result in mild jaundice, which is found in about 5% of the population) and Crigler-Najjar syndrome.
In jaundice secondary to hemolysis, the increased production of bilirubin, leads to the increased production of urine-urobilinogen. Bilirubin is not usually found in the urine because unconjugated bilirubin is not water-soluble, so, the combination of increased urine-urobilinogen with no bilirubin (since, unconjugated) in urine is suggestive of hemolytic jaundice.
Laboratory findings include:
• Urine: no bilirubin present, urobilinogen > 2 units (i.e., hemolytic anemia causes increased heme metabolism; exception: infants where gut flora has not developed).
• Serum: increased unconjugated bilirubin.
• Kernicterus is associated with increased unconjugated bilirubin.
Hepatocellular
Hepatocellular (hepatic) jaundice can be caused by acute or chronic hepatitis, hepatotoxicity, cirrhosis, drug induced hepatitis and alcoholic liver disease. Cell necrosis reduces the liver's ability to metabolize and excrete bilirubin leading to a buildup of unconjugated bilirubin in the blood.
Laboratory findings depend on the cause of jaundice.
• Urine: Conjugated bilirubin present, urobilirubin > 2 units but variable (except in children). Kernicterus is a condition not associated with increased conjugated bilirubin.
• Plasma protein show characteristic changes.
• Plasma albumin level is low but plasma globulins are raised due to an increased formation of antibodies.
Bilirubin transport across the hepatocyte may be impaired at any point between the uptake of unconjugated bilirubin into the cell and transport of conjugated bilirubin into biliary canaliculi.
Post-hepatic
Post-hepatic jaundice, also called obstructive jaundice, is caused by an interruption to the drainage of bile in the biliary system. The most common causes are gallstones in the common bile duct, and pancreatic cancer in the head of the pancreas. Also, a group of parasites known as "liver flukes" can live in the common bile duct, causing obstructive jaundice. Other causes include strictures of the common bile duct, biliary atresia, cholangiocarcinoma, pancreatitis and pancreatic pseudocysts. A rare cause of obstructive jaundice is Mirizzi's syndrome.
Pathophysiology
When RBCs are damaged, their membranes become fragile and prone to rupture. As each RBC traverses through the reticuloendothelial system, its cell membrane ruptures when its membrane is fragile enough to allow this.
Hemoglobin, are released into the blood. The hemoglobin is phagocytosed by macrophages, and split into its heme and globin portions. The globin portion, a protein, is degraded into amino acids and plays no role in jaundice.
Two reactions then take place with the heme molecule.
The first oxidation reaction is catalyzed by the microsomal enzyme heme oxygenase and results in biliverdin (green color pigment), iron
and carbon monoxide.
The next step is the reduction of biliverdin to a yellow color tetrapyrol pigment called bilirubin by cytosolic enzyme biliverdin reductase.
This bilirubin is "unconjugated," "free" or "indirect" bilirubin. Approximately 4 mg of bilirubin per kg of blood is produced each day.[11] The majority of this bilirubin comes from the breakdown of heme from expired red blood cells in the process just described.
However approximately 20 percent comes from other heme sources, including ineffective erythropoiesis, and the breakdown of other heme-containing proteins, such as muscle myoglobin and cytochromes.
Hepatic events
The unconjugated bilirubin then travels to the liver through the bloodstream. Because bilirubin is not soluble, however, it is transported through the blood bound to serum albumin.
In Liver, it is conjugated with glucuronic acid (to form bilirubin diglucuronide, or just "conjugated bilirubin") to become more water soluble.
The reaction is catalyzed by the enzyme UDP-glucuronyl transferase.
This conjugated bilirubin is excreted from the liver into the biliary and cystic ducts as part of bile. Intestinal bacteria convert the bilirubin into urobilinogen.
Urobilinogen can take two pathways. It can either be further converted into stercobilinogen, which is then oxidized to stercobilin and passed out in the feces, or it can be reabsorbed by the intestinal cells, transported in the blood to the kidneys, and passed out in the urine as the oxidised product urobilin.
Stercobilin and urobilin are the products responsible for the coloration of feces and urine, respectively.
The Skull
AnatomyThe skull, the skeleton of the head, is the most complex bony structure in the body because it:
Encloses the brain, which is irregular in shape;
Houses the organs of special senses for seeing, hearing, tasting, and smelling; and
Surrounds the openings in to the digestive and respiratory tracts.
In the anatomical position, the skull is oriented so that the inferior margin of the orbit (eye socket) and the superior margin of the external acoustic meatus (auditory canal) are horizontal. This is called the orbitomenial plane (Frankfort plane).
The term cranium (L. skull) is sometimes used when referring to the skull without the mandible (lower jaw), but the cranium is often used when referring to the part of the skull containing the brain.
The superior part is the box-like structure called the calvaria (cranial vault, brain case); the remainder of the cranium, including the maxilla (upper jaw), orbits (eyeball sockets) and nasal cavities, forms the facial skeleton.
The term skullcap (calotte) refers to the superior part of the calvaria, which is removed during autopsies and dissections. The inferior aspect of the cranium is called the cranial base.
Surface Defence Mechanisms
General Pathology
Surface Defence Mechanisms
1. Skin:
(i) Mechanical barrier of keratin and desquamation.
(ii) Resident commensal organisms
(iii)Acidity of sweat.
(iv) Unsaturated fatty acids of sebum
2. Oropharyngeal
(i)Resident flora
(ii) Saliva, rich in lysozyme, mucin and Immunoglobulins (lgA).
3. Gastrointestinal tract.-
(i) Gastric HCI
(ii) Commensal organisms in Intestine
(iii) Bile salts
(iv) IgA.
(v) Diarrhoeal expulsion of irritants.
4. Respiratory tract:
(i) Trapping in turbinates
(ii) Mucus trapping
(iii) Expulsion by coughing and sneezing.
(iv) Ciliary propulsion.
(V) Lysozymes and antibodies in secretion.
(vi) Phagocytosis by alveolar macrophages.
5. Urinary tract:
(i) Flushing action.
(ii) Acidity
(iii) Phagocytosis by urothelial cells.
6. Vagina.-
(i) Desquamation.
(ii) Acid barrier.
(iii) Doderlein's bacilli (Lactobacilli)
7. Conjunctiva:
Lysozymes and IgA in tears
CRUCIBLE FORMER
Dental Materials
CRUCIBLE FORMER
It serves as a base for the casting ring during investing .Usually convex in shape.
May be metal , plastic or rubber .
Shape depends on casting machine used .
Modern machines use tall crucible to enable the pattern to be positioned near the end of the casting machine .
Clinical Signs and Their Significance
Oral and Maxillofacial SurgeryClinical Signs and Their Significance
Understanding various clinical signs is crucial for diagnosing specific
conditions and injuries. Below are descriptions of several important signs,
including Battle sign, Chvostek’s sign, Guerin’s sign, and Tinel’s sign, along
with their clinical implications.
1. Battle Sign
Description: Battle sign refers to ecchymosis
(bruising) in the mastoid region, typically behind the ear.
Clinical Significance: This sign is indicative of a
posterior basilar skull fracture. The bruising occurs due to the
extravasation of blood from the fracture site, which can be a sign of
significant head trauma. It is important to evaluate for other associated
injuries, such as intracranial hemorrhage.
2. Chvostek’s Sign
Description: Chvostek’s sign is characterized by the
twitching of the facial muscles in response to tapping over the area of the
facial nerve (typically in front of the ear).
Clinical Significance: This sign is often observed in
patients who are hypocalcemic (have low calcium levels). The twitching
indicates increased neuromuscular excitability due to low calcium levels,
which can lead to tetany and other complications. It is commonly assessed in
conditions such as hypoparathyroidism.
3. Guerin’s Sign
Description: Guerin’s sign is the presence of
ecchymosis along the posterior soft palate bilaterally.
Clinical Significance: This sign is indicative of
pterygoid plate disjunction or fracture. It suggests significant trauma to
the maxillofacial region, often associated with fractures of the skull base
or facial skeleton. The presence of bruising in this area can help in
diagnosing the extent of facial injuries.
4. Tinel’s Sign
Description: Tinel’s sign is a provocative test where
light percussion over a nerve elicits a distal tingling sensation.
Clinical Significance: This sign is often interpreted
as a sign of small fiber recovery in regenerating nerve sprouts. It is
commonly used in the assessment of nerve injuries, such as carpal tunnel
syndrome or after nerve repair surgeries. A positive Tinel’s sign indicates
that the nerve is healing and that sensory function may be returning.
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).
PROSTHODONTICS QUESTIONS NEET MDS
NEET MDS
1. Following extraction of the molar teeth
A. The ridge height is lost more from the maxilla than from the mandible
B. The maxillary ridge will get more bone lost from the palatal aspect than the
buccal
C. The mandibular arch is relatively narrower than the maxillary arch
D. Compared with the pre-resorption state, the mandibular ridge will lose more
bone from the
lingual aspect than the buccal one
Ans D
2. Which of the following is a major disadvantage to immediate complete
denture therapy
A. Trauma to extraction site
B. Increased the potential of infection
C. Impossibility for anterior try in
D. Excessive resorption of residual ridge
Ans C
3. When repairing a fracture of lower complete denture. Which statement is
correct:
A. Self curing will distort the denture
B. Cold curing will not be strong enough because of small area of attachment
C. There is a possibility of occlusal disharmony
D. none
Ans C
4. The setting expansion of casting investment is approximately
A. 0 to 0.1%
B. 0.1 to 0.5%
C. 0.5 to 1%
D. 1.1 to 1.6%
Ans C
5. The un-polymerized monomer in Self-cured resin is approximately:
A. 0.5%
B. 2.5%
C. 5%
D. 10%
Ans A
6. A volume shrinkage of methyl meta cyrelate monomer when is polymerized:
A. 12%
B. 15%
C. 18%
D. 21%
Ans D
7. All of the following landmarks are included while making a post dam for
maxillary arch except
A) Pterygomaxillary notch
B) Hamular process
C) Fovea palatina
D) Vibrating line
Ans: B
8. The thickness of the spacer used in special tray is
A) 2.5mm
B) 2.0mm
C) 1.5mm
D) 1.0mm
Ans. B,
Wax spacer is used to provide the space in the tray for the final impression
material and allows the tray to be properly positioned in the mouth during
border molding procedures
Base plate wax covers the basal seat area except for labial and buccal
reflections and the posterior palatal seal area
Specific Agents
Pharmacology
Specific Agents
Hydralazine [orally effective]
MOA: Not completely understood. Seems to be partially dependent on the release of EDRF and perhaps partially due to K+-channel activation
- in clinical doses action is manifest primarily on vascular smooth muscle (non-vascular muscle is not much affected).
- Re: Metabolism & Excretion. In cases of renal failure the plasma half life may be substantially increased (4-5 fold). One mode of metabolism is
via N-Acetylation (problem of slow acetylators)
Side Effects
- those typical of vasodilation = headache, nasal congestion, tachycardia etc.
- chronic treatment with high doses > 200 mg/day may induce a rheumatoid-like state which may resemble lupus erythematosus.
Minoxidil (Loniten) [orally effective]
MOA: K+-channel agonist
- very effective antihypertensive. Used primarily to treat life-threatening hypertension or hypertension resistant to other agents.
Side effects - growth of hair
Diazoxide (Hyperstat) [used only IV]
MOA: K+-channel agonist
- Administered by rapid IV injection; action appearing after 3-5 min; action may last from 4 to 12 hours.
Nitroprusside (Nipride) [used only IV]
MOA: increase in cGMP
- unlike the other vasodilators, venous tone is substantially reduced by nitroprusside.
- rapid onset of action (.30 sec); administered as an IV-infusion.
- particularly useful for hypertension associated with left ventricular failure.